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MOUSE:BAX

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Contents

Species (Taxon ID) Mus musculus (Mouse). (taxon:10090)
Gene Name(s) Bax
Protein Name(s)
  • Apoptosis regulator BAX
External Links
UniProt Identifier BAX_MOUSE
UniProt Accessions Q07813,
EMBL L22472, BC018228, BC053380,
PIR D47538,
RefSeq NP_031553.1,
PDB 2XA0,
IntAct Q07813,
Ensembl ENSMUST00000033093,
Pfam PF00452,

Annotations

Qualifier GO ID GO term name Reference Evidence Code with/from Aspect Notes Status
GO:0046982

protein heterodimerization activity

PMID:7650488[1]

IPI: Inferred from Physical Interaction

UniProtKB:Q64373

F

GO:0005739

mitochondrion

PMID:12847083[2]

IDA: Inferred from Direct Assay

C

GO:0048087

positive regulation of developmental pigmentation

PMID:9241272[3]

IGI: Inferred from Genetic Interaction

P

GO:0010212

response to ionizing radiation

PMID:15578100[4]

IMP: Inferred from Mutant Phenotype

P

GO:0007283

spermatogenesis

PMID:11906913[5]

IMP: Inferred from Mutant Phenotype

P

GO:0046902

regulation of mitochondrial membrane permeability

PMID:14963330[6]

IGI: Inferred from Genetic Interaction

P

GO:0031558

induction of apoptosis in response to chemical stimulus

PMID:14502238[7]

IMP: Inferred from Mutant Phenotype

P

GO:0009651

response to salt stress

PMID:16571598[8]

IGI: Inferred from Genetic Interaction

P

GO:0001844

protein insertion into mitochondrial membrane involved in induction of apoptosis

PMID:12952892[9]

IMP: Inferred from Mutant Phenotype

P

GO:0006808

regulation of nitrogen utilization

PMID:9241272[3]

IGI: Inferred from Genetic Interaction

P

GO:0008635

activation of caspase activity by cytochrome c

PMID:11836241[10]

IMP: Inferred from Mutant Phenotype

P

GO:0009566

fertilization

PMID:10894153[11]

IGI: Inferred from Genetic Interaction

P

GO:0006915

apoptosis

PMID:8358790[12]

IDA: Inferred from Direct Assay

P

GO:0043525

positive regulation of neuron apoptosis

PMID:17192424[13]

IMP: Inferred from Mutant Phenotype

P

GO:0009636

response to toxin

PMID:9454845[14]

IMP: Inferred from Mutant Phenotype

P

GO:0043065

positive regulation of apoptosis

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

P

GO:0010212

response to ionizing radiation

PMID:10639175[16]

IGI: Inferred from Genetic Interaction

P

GO:0051402

neuron apoptosis

PMID:11226327[17]

IMP: Inferred from Mutant Phenotype

P

GO:0005622

intracellular

PMID:9008714[18]

IDA: Inferred from Direct Assay

C

GO:0051402

neuron apoptosis

PMID:12917363[19]

IMP: Inferred from Mutant Phenotype

P

GO:0005625

soluble fraction

PMID:9553144[20]

IDA: Inferred from Direct Assay

C

GO:0042803

protein homodimerization activity

PMID:8631771[21]

IPI: Inferred from Physical Interaction

UniProtKB:Q07813

F

GO:0033599

regulation of mammary gland epithelial cell proliferation

PMID:10363969[22]

IMP: Inferred from Mutant Phenotype

P

GO:0006974

response to DNA damage stimulus

PMID:12952892[9]

IMP: Inferred from Mutant Phenotype

P

GO:0006919

activation of caspase activity

PMID:15776018[23]

IGI: Inferred from Genetic Interaction

P

GO:0030264

nuclear fragmentation involved in apoptotic nuclear change

PMID:12925707[24]

IDA: Inferred from Direct Assay

P

GO:0051402

neuron apoptosis

PMID:15574493[25]

IMP: Inferred from Mutant Phenotype

P

GO:0005515

protein binding

PMID:9463381[26]

IPI: Inferred from Physical Interaction

UniProtKB:P10415

F

GO:0005829

cytosol

PMID:11369777[27]

IDA: Inferred from Direct Assay

C

GO:0006919

activation of caspase activity

PMID:12847083[2]

IGI: Inferred from Genetic Interaction

P

GO:0045136

development of secondary sexual characteristics

PMID:15944391[28]

IMP: Inferred from Mutant Phenotype

P

GO:0006915

apoptosis

PMID:9560217[29]

IDA: Inferred from Direct Assay

P

GO:0005739

mitochondrion

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-0496

C

GO:0051260

protein homooligomerization

PMID:12925707[24]

IDA: Inferred from Direct Assay

P

GO:0035234

germ cell programmed cell death

PMID:14660547[30]

IGI: Inferred from Genetic Interaction

P

GO:0008624

induction of apoptosis by extracellular signals

PMID:14507967[31]

IMP: Inferred from Mutant Phenotype

P

GO:0051402

neuron apoptosis

PMID:11717344[32]

IGI: Inferred from Genetic Interaction

P

GO:0043525

positive regulation of neuron apoptosis

PMID:10762311[33]

IMP: Inferred from Mutant Phenotype

P

GO:0043065

positive regulation of apoptosis

PMID:9988273[34]

IMP: Inferred from Mutant Phenotype

P

GO:0005737

cytoplasm

PMID:16469926[35]

IDA: Inferred from Direct Assay

C

GO:0005829

cytosol

PMID:11864976[36]

IDA: Inferred from Direct Assay

C

GO:0008053

mitochondrial fusion

PMID:17035996[37]

IGI: Inferred from Genetic Interaction

P

GO:0006915

apoptosis

PMID:14963330[6]

IGI: Inferred from Genetic Interaction

P

GO:0005739

mitochondrion

PMID:19139267[38]

IDA: Inferred from Direct Assay

C

GO:0006917

induction of apoptosis

PMID:10479688[39]

IMP: Inferred from Mutant Phenotype

P

GO:0043065

positive regulation of apoptosis

PMID:9241272[3]

IMP: Inferred from Mutant Phenotype

P

GO:0051434

BH3 domain binding

PMID:11060313[40]

IPI: Inferred from Physical Interaction

UniProtKB:Q96BY2

F

GO:0043525

positive regulation of neuron apoptosis

PMID:15947791[41]

IMP: Inferred from Mutant Phenotype

P

GO:0006974

response to DNA damage stimulus

PMID:9454845[14]

IMP: Inferred from Mutant Phenotype

P

GO:0070059

apoptosis in response to endoplasmic reticulum stress

PMID:12847083[2]

IGI: Inferred from Genetic Interaction

P

GO:0043065

positive regulation of apoptosis

PMID:11146002[42]

IMP: Inferred from Mutant Phenotype

P

GO:0043065

positive regulation of apoptosis

PMID:17107997[43]

IGI: Inferred from Genetic Interaction

P

GO:0005741

mitochondrial outer membrane

PMID:12925707[24]

IDA: Inferred from Direct Assay

C

GO:0060041

retina development in camera-type eye

PMID:9699561[44]

IMP: Inferred from Mutant Phenotype

P

GO:0043065

positive regulation of apoptosis

PMID:16571598[8]

IGI: Inferred from Genetic Interaction

P

GO:0005737

cytoplasm

PMID:15528359[45]

IDA: Inferred from Direct Assay

C

GO:0042981

regulation of apoptosis

GO_REF:0000002

IEA: Inferred from Electronic Annotation

InterPro:IPR002475

P

GO:0006917

induction of apoptosis

PMID:8358790[12]

IDA: Inferred from Direct Assay

P

GO:0005783

endoplasmic reticulum

PMID:12847083[2]

IDA: Inferred from Direct Assay

C

GO:0007399

nervous system development

PMID:12810599[46]

IMP: Inferred from Mutant Phenotype

P

GO:0002352

B cell negative selection

PMID:16055554[47]

IGI: Inferred from Genetic Interaction

P

GO:0005739

mitochondrion

PMID:11864976[36]

IDA: Inferred from Direct Assay

C

GO:0002904

positive regulation of B cell apoptosis

PMID:11604501[48]

IGI: Inferred from Genetic Interaction

P

GO:0002262

myeloid cell homeostasis

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

P

GO:0001782

B cell homeostasis

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

P

GO:0001764

neuron migration

PMID:15590937[49]

IMP: Inferred from Mutant Phenotype

P

GO:0043525

positive regulation of neuron apoptosis

PMID:8816704[50]

IMP: Inferred from Mutant Phenotype

P

GO:0006687

glycosphingolipid metabolic process

PMID:18308723[51]

IMP: Inferred from Mutant Phenotype

P

GO:0043065

positive regulation of apoptosis

PMID:17068116[52]

IMP: Inferred from Mutant Phenotype

P

GO:0043525

positive regulation of neuron apoptosis

PMID:10683286[53]

IMP: Inferred from Mutant Phenotype

P

GO:0001836

release of cytochrome c from mitochondria

PMID:17052454[54]

IGI: Inferred from Genetic Interaction

P

GO:0001541

ovarian follicle development

PMID:17244737[55]

IMP: Inferred from Mutant Phenotype

P

GO:0001541

ovarian follicle development

PMID:10894153[11]

IGI: Inferred from Genetic Interaction

P

GO:0006915

apoptosis

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-0053

P

GO:0005737

cytoplasm

PMID:10931486[56]

IDA: Inferred from Direct Assay

C

GO:0007283

spermatogenesis

PMID:10894153[11]

IGI: Inferred from Genetic Interaction

P

GO:0048678

response to axon injury

PMID:16103918[57]

IMP: Inferred from Mutant Phenotype

P

GO:0007548

sex differentiation

PMID:15342910[58]

IMP: Inferred from Mutant Phenotype

P

GO:0010524

positive regulation of calcium ion transport into cytosol

PMID:15613488[59]

IGI: Inferred from Genetic Interaction

P

GO:0006915

apoptosis

PMID:10618441[60]

IMP: Inferred from Mutant Phenotype

P

GO:0048515

spermatid differentiation

PMID:16270031[61]

IMP: Inferred from Mutant Phenotype

P

GO:0033137

negative regulation of peptidyl-serine phosphorylation

PMID:15613488[59]

IGI: Inferred from Genetic Interaction

P

GO:0044445

cytosolic part

PMID:9553144[20]

IDA: Inferred from Direct Assay

C

GO:0009791

post-embryonic development

PMID:9241272[3]

IGI: Inferred from Genetic Interaction

P

GO:0043525

positive regulation of neuron apoptosis

PMID:10639175[16]

IGI: Inferred from Genetic Interaction

P

GO:0008285

negative regulation of cell proliferation

PMID:10762311[33]

IMP: Inferred from Mutant Phenotype

P

GO:0048872

homeostasis of number of cells

PMID:11163212[62]

IGI: Inferred from Genetic Interaction

P

GO:0070059

apoptosis in response to endoplasmic reticulum stress

PMID:15776018[23]

IGI: Inferred from Genetic Interaction

P

GO:0005737

cytoplasm

PMID:11226327[17]

IDA: Inferred from Direct Assay

C

GO:0008283

cell proliferation

PMID:9176392[63]

IDA: Inferred from Direct Assay

P

GO:0009611

response to wounding

PMID:14507967[31]

IMP: Inferred from Mutant Phenotype

P

GO:0043525

positive regulation of neuron apoptosis

PMID:10744634[64]

IGI: Inferred from Genetic Interaction

P

GO:0043525

positive regulation of neuron apoptosis

PMID:15944391[28]

IMP: Inferred from Mutant Phenotype

P

GO:0019987

negative regulation of anti-apoptosis

PMID:8798452[65]

IGI: Inferred from Genetic Interaction

P

GO:0006919

activation of caspase activity

PMID:14502238[7]

IMP: Inferred from Mutant Phenotype

P

GO:0005829

cytosol

PMID:12925707[24]

IDA: Inferred from Direct Assay

C

GO:0005737

cytoplasm

GO_REF:0000023

IEA: Inferred from Electronic Annotation

SP_SL:SL-0086

C

GO:0001776

leukocyte homeostasis

PMID:11163212[62]

IGI: Inferred from Genetic Interaction

P

GO:0001836

release of cytochrome c from mitochondria

PMID:14614769[66]

IDA: Inferred from Direct Assay

P

GO:0007281

germ cell development

PMID:10894153[11]

IGI: Inferred from Genetic Interaction

P

GO:0001777

T cell homeostatic proliferation

PMID:9241272[3]

IMP: Inferred from Mutant Phenotype

P

GO:0001836

release of cytochrome c from mitochondria

PMID:9560217[29]

IDA: Inferred from Direct Assay

P

GO:0008629

induction of apoptosis by intracellular signals

PMID:12952892[9]

IMP: Inferred from Mutant Phenotype

P

GO:0001782

B cell homeostasis

PMID:16055554[47]

IMP: Inferred from Mutant Phenotype

P

GO:0043525

positive regulation of neuron apoptosis

PMID:15590937[49]

IMP: Inferred from Mutant Phenotype

P

GO:0005829

cytosol

PMID:12847083[2]

IDA: Inferred from Direct Assay

C

GO:0005739

mitochondrion

PMID:11369777[27]

IDA: Inferred from Direct Assay

C

GO:0048873

homeostasis of number of cells within a tissue

PMID:15342910[58]

IMP: Inferred from Mutant Phenotype

P

GO:0043065

positive regulation of apoptosis

PMID:10995754[67]

IMP: Inferred from Mutant Phenotype

P

GO:0048597

post-embryonic camera-type eye morphogenesis

PMID:15955981[68]

IGI: Inferred from Genetic Interaction

P

GO:0032471

reduction of endoplasmic reticulum calcium ion concentration

PMID:15613488[59]

IGI: Inferred from Genetic Interaction

P

GO:0042981

regulation of apoptosis

GO_REF:0000002

IEA: Inferred from Electronic Annotation

InterPro:IPR020717

P

GO:0043525

positive regulation of neuron apoptosis

PMID:14502238[7]

IMP: Inferred from Mutant Phenotype

P

GO:0042803

protein homodimerization activity

PMID:8631771[21]

IMP: Inferred from Mutant Phenotype

F

GO:0008635

activation of caspase activity by cytochrome c

PMID:9560217[29]

IDA: Inferred from Direct Assay

P

GO:0043525

positive regulation of neuron apoptosis

PMID:16103918[57]

IMP: Inferred from Mutant Phenotype

P

GO:0043525

positive regulation of neuron apoptosis

PMID:9699561[44]

IMP: Inferred from Mutant Phenotype

P

GO:0046666

retinal cell programmed cell death

PMID:14517994[69]

IMP: Inferred from Mutant Phenotype

P

GO:0006919

activation of caspase activity

PMID:14561915[70]

IMP: Inferred from Mutant Phenotype

P

GO:0005739

mitochondrion

PMID:15528359[45]

IDA: Inferred from Direct Assay

C

GO:0005737

cytoplasm

PMID:10486519[71]

IDA: Inferred from Direct Assay

C

GO:0043525

positive regulation of neuron apoptosis

PMID:11150333[72]

IMP: Inferred from Mutant Phenotype

P

GO:0006915

apoptosis

PMID:10201940[73]

IMP: Inferred from Mutant Phenotype

P

GO:0016020

membrane

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-0472

C

GO:0042981

regulation of apoptosis

GO_REF:0000002

IEA: Inferred from Electronic Annotation

InterPro:IPR020728

P

GO:0021987

cerebral cortex development

PMID:15342910[58]

IMP: Inferred from Mutant Phenotype

P

GO:0007283

spermatogenesis

PMID:7569956[74]

IMP: Inferred from Mutant Phenotype

P

GO:0005515

protein binding

PMID:9843949[75]

IPI: Inferred from Physical Interaction

UniProtKB:P21796

F

GO:0046982

protein heterodimerization activity

PMID:11226327[17]

IPI: Inferred from Physical Interaction

UniProtKB:P10417

F

GO:0005741

mitochondrial outer membrane

PMID:12910269[76]

IDA: Inferred from Direct Assay

C

GO:0006915

apoptosis

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

P

GO:0005829

cytosol

PMID:15989966[77]

IDA: Inferred from Direct Assay

C

GO:0048872

homeostasis of number of cells

PMID:10931486[56]

IMP: Inferred from Mutant Phenotype

P

GO:0005741

mitochondrial outer membrane

GO_REF:0000023

IEA: Inferred from Electronic Annotation

SP_SL:SL-0172

C

GO:0043065

positive regulation of apoptosis

PMID:15955981[68]

IGI: Inferred from Genetic Interaction

P

GO:0005829

cytosol

PMID:11980919[78]

IDA: Inferred from Direct Assay

C

GO:0060058

positive regulation of apoptosis involved in mammary gland involution

PMID:10363969[22]

IMP: Inferred from Mutant Phenotype

P

GO:0051281

positive regulation of release of sequestered calcium ion into cytosol

PMID:15947791[41]

IMP: Inferred from Mutant Phenotype

P

GO:0051726

regulation of cell cycle

PMID:16055554[47]

IGI: Inferred from Genetic Interaction

P

GO:0005737

cytoplasm

PMID:10464378[79]

IDA: Inferred from Direct Assay

C

GO:0043525

positive regulation of neuron apoptosis

PMID:10884318[80]

IGI: Inferred from Genetic Interaction

P

GO:0048873

homeostasis of number of cells within a tissue

PMID:11413548[81]

IMP: Inferred from Mutant Phenotype

P

GO:0043524

negative regulation of neuron apoptosis

PMID:8625820[82]

IDA: Inferred from Direct Assay

P

GO:0035234

germ cell programmed cell death

PMID:17107997[43]

IGI: Inferred from Genetic Interaction

P

GO:0051881

regulation of mitochondrial membrane potential

PMID:14614769[66]

IDA: Inferred from Direct Assay

P

GO:0031966

mitochondrial membrane

PMID:11369777[27]

IDA: Inferred from Direct Assay

C

GO:0042981

regulation of apoptosis

GO_REF:0000002

IEA: Inferred from Electronic Annotation

InterPro:IPR000712

P

GO:0060011

Sertoli cell proliferation

PMID:11784036[83]

IGI: Inferred from Genetic Interaction

P

GO:0008584

male gonad development

PMID:9241272[3]

IGI: Inferred from Genetic Interaction

P

GO:0005737

cytoplasm

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-0963

C

GO:0043525

positive regulation of neuron apoptosis

PMID:9096145[84]

IGI: Inferred from Genetic Interaction

P

GO:0043065

positive regulation of apoptosis

PMID:15753097[85]

IDA: Inferred from Direct Assay

P

GO:0043065

positive regulation of apoptosis

PMID:15578100[4]

IMP: Inferred from Mutant Phenotype

P

GO:0031966

mitochondrial membrane

PMID:11980919[78]

IDA: Inferred from Direct Assay

C

GO:0042803

protein homodimerization activity

PMID:10582606[86]

IPI: Inferred from Physical Interaction

UniProtKB:P10417

F

GO:0043525

positive regulation of neuron apoptosis

PMID:9454852[87]

IMP: Inferred from Mutant Phenotype

P

GO:0008584

male gonad development

PMID:16270031[61]

IMP: Inferred from Mutant Phenotype

P

GO:0042981

regulation of apoptosis

GO_REF:0000002

IEA: Inferred from Electronic Annotation

InterPro:IPR020726

P

GO:0043065

positive regulation of apoptosis

PMID:11906913[5]

IMP: Inferred from Mutant Phenotype

P

GO:0051402

neuron apoptosis

PMID:17077143[88]

IGI: Inferred from Genetic Interaction

P

GO:0043525

positive regulation of neuron apoptosis

PMID:15869495[89]

IMP: Inferred from Mutant Phenotype

P

GO:0008053

mitochondrial fusion

PMID:16893972[90]

IGI: Inferred from Genetic Interaction

P

GO:0043281

regulation of caspase activity

PMID:14507967[31]

IMP: Inferred from Mutant Phenotype

P

GO:0005739

mitochondrion

PMID:18614015[91]

IDA: Inferred from Direct Assay

C

GO:0042475

odontogenesis of dentine-containing tooth

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

P

GO:0005622

intracellular

PMID:11146504[92]

IDA: Inferred from Direct Assay

C

GO:0008624

induction of apoptosis by extracellular signals

PMID:12925707[24]

IMP: Inferred from Mutant Phenotype

P

GO:0001836

release of cytochrome c from mitochondria

PMID:14963330[6]

IGI: Inferred from Genetic Interaction

P

GO:0001776

leukocyte homeostasis

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

P

GO:0001783

B cell apoptosis

PMID:16055554[47]

IGI: Inferred from Genetic Interaction

P

GO:0001836

release of cytochrome c from mitochondria

PMID:12925707[24]

IDA: Inferred from Direct Assay

P

GO:0005829

cytosol

PMID:16227588[93]

IDA: Inferred from Direct Assay

C

GO:0001777

T cell homeostatic proliferation

PMID:7569956[74]

IMP: Inferred from Mutant Phenotype

P

GO:0001974

blood vessel remodeling

PMID:15955981[68]

IGI: Inferred from Genetic Interaction

P

GO:0005739

mitochondrion

PMID:14651853[94]

IDA: Inferred from Direct Assay

C

GO:0002358

B cell homeostatic proliferation

PMID:7569956[74]

IMP: Inferred from Mutant Phenotype

P

GO:0001101

response to acid

PMID:7675327[95]

IDA: Inferred from Direct Assay

P

GO:0001822

kidney development

PMID:9241272[3]

IGI: Inferred from Genetic Interaction

P

GO:0051402

neuron apoptosis

PMID:10762311[33]

IGI: Inferred from Genetic Interaction

P

GO:0005739

mitochondrion

PMID:16469926[35]

IDA: Inferred from Direct Assay

C

GO:0021854

hypothalamus development

PMID:15342910[58]

IMP: Inferred from Mutant Phenotype

P

GO:0034644

cellular response to UV

PMID:14963330[6]

IGI: Inferred from Genetic Interaction

P

GO:0005741

mitochondrial outer membrane

PMID:16227588[93]

IDA: Inferred from Direct Assay

C

GO:0010332

response to gamma radiation

PMID:17068116[52]

IMP: Inferred from Mutant Phenotype

P

GO:0035108

limb morphogenesis

PMID:11163212[62]

IGI: Inferred from Genetic Interaction

P

GO:0016021

integral to membrane

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-0812

C

GO:0008283

cell proliferation

PMID:10762311[33]

IGI: Inferred from Genetic Interaction

P

GO:0046982

protein heterodimerization activity

PMID:8798452[65]

IPI: Inferred from Physical Interaction

UniProtKB:Q64373-1

F

GO:0005829

cytosol

PMID:19139267[38]

IDA: Inferred from Direct Assay

C

GO:0005741

mitochondrial outer membrane

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-1000

C

GO:0031966

mitochondrial membrane

PMID:14614769[66]

IDA: Inferred from Direct Assay

C

GO:0043065

positive regulation of apoptosis

PMID:9056387[96]

IGI: Inferred from Genetic Interaction

P

GO:0060068

vagina development

PMID:11163212[62]

IGI: Inferred from Genetic Interaction

P

GO:0008637

apoptotic mitochondrial changes

PMID:12925707[24]

IDA: Inferred from Direct Assay

P

GO:0048147

negative regulation of fibroblast proliferation

PMID:12952892[9]

IMP: Inferred from Mutant Phenotype

P

GO:0007283

spermatogenesis

PMID:7569956[74]

IMP: Inferred from Mutant Phenotype

P

Fig 2 A, C-J, Fig 3) Bax- mutants were incapable of spermatogenesis.

complete

GO:0001101

response to acid

PMID:7675327[95]

IDA: Inferred from Direct Assay

P

GO:0001541

ovarian follicle development

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0001541

ovarian follicle development

PMID:10894153[11]

IGI: Inferred from Genetic Interaction

MGI:MGI:2176699

P

GO:0001541

ovarian follicle development

PMID:17244737[55]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0001764

neuron migration

PMID:15590937[49]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0001776

leukocyte homeostasis

PMID:11163212[62]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0001776

leukocyte homeostasis

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

MGI:MGI:1197519

P

GO:0001777

T cell homeostatic proliferation

PMID:7569956[74]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0001777

T cell homeostatic proliferation

PMID:9241272[3]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0001782

B cell homeostasis

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

MGI:MGI:1197519

P

GO:0001782

B cell homeostasis

PMID:16055554[47]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0001783

B cell apoptosis

PMID:16055554[47]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0001822

kidney development

PMID:9241272[3]

IGI: Inferred from Genetic Interaction

MGI:MGI:88138

P

GO:0001836

release of cytochrome c from mitochondria

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0001836

release of cytochrome c from mitochondria

PMID:12925707[24]

IDA: Inferred from Direct Assay

P

GO:0001836

release of cytochrome c from mitochondria

PMID:14614769[66]

IDA: Inferred from Direct Assay

P

GO:0001836

release of cytochrome c from mitochondria

PMID:14963330[6]

IGI: Inferred from Genetic Interaction

MGI:MGI:98834

P

GO:0001836

release of cytochrome c from mitochondria

PMID:17052454[54]

IGI: Inferred from Genetic Interaction

MGI:MGI:108093

P

GO:0001836

release of cytochrome c from mitochondria

PMID:9560217[29]

IDA: Inferred from Direct Assay

P

GO:0001844

protein insertion into mitochondrial membrane involved in induction of apoptosis

PMID:12952892[9]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0001974

blood vessel remodeling

PMID:15955981[68]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0002262

myeloid cell homeostasis

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

MGI:MGI:1197519

P

GO:0002352

B cell negative selection

PMID:16055554[47]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0002358

B cell homeostatic proliferation

PMID:7569956[74]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0002904

positive regulation of B cell apoptosis

PMID:11604501[48]

IGI: Inferred from Genetic Interaction

MGI:MGI:97250

P

GO:0005515

protein binding

PMID:9463381[26]

IPI: Inferred from Physical Interaction

UniProtKB:P10415

F

GO:0005515

protein binding

PMID:9843949[75]

IPI: Inferred from Physical Interaction

UniProtKB:P21796

F

GO:0005622

intracellular

PMID:11146504[92]

IDA: Inferred from Direct Assay

C

GO:0005622

intracellular

PMID:9008714[18]

IDA: Inferred from Direct Assay

C

GO:0005625

soluble fraction

PMID:9553144[20]

IDA: Inferred from Direct Assay

C

GO:0005737

cytoplasm

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-0963

C

GO:0005737

cytoplasm

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

C

GO:0005737

cytoplasm

GO_REF:0000023

IEA: Inferred from Electronic Annotation

SP_SL:SL-0086

C

GO:0005737

cytoplasm

PMID:10464378[79]

IDA: Inferred from Direct Assay

C

GO:0005737

cytoplasm

PMID:10486519[71]

IDA: Inferred from Direct Assay

C

GO:0005737

cytoplasm

PMID:10931486[56]

IDA: Inferred from Direct Assay

C

GO:0005737

cytoplasm

PMID:11226327[17]

IDA: Inferred from Direct Assay

C

GO:0005737

cytoplasm

PMID:15528359[45]

IDA: Inferred from Direct Assay

C

GO:0005737

cytoplasm

PMID:16469926[35]

IDA: Inferred from Direct Assay

C

GO:0005739

mitochondrion

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-0496

C

GO:0005739

mitochondrion

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

C

GO:0005739

mitochondrion

PMID:11369777[27]

IDA: Inferred from Direct Assay

C

GO:0005739

mitochondrion

PMID:11864976[36]

IDA: Inferred from Direct Assay

C

GO:0005739

mitochondrion

PMID:12847083[2]

IDA: Inferred from Direct Assay

C

GO:0005739

mitochondrion

PMID:14651853[94]

IDA: Inferred from Direct Assay

C

GO:0005739

mitochondrion

PMID:15528359[45]

IDA: Inferred from Direct Assay

C

GO:0005739

mitochondrion

PMID:16469926[35]

IDA: Inferred from Direct Assay

C

GO:0005739

mitochondrion

PMID:18614015[91]

IDA: Inferred from Direct Assay

C

GO:0005739

mitochondrion

PMID:19139267[38]

IDA: Inferred from Direct Assay

C

GO:0005741

mitochondrial outer membrane

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-1000

C

GO:0005741

mitochondrial outer membrane

GO_REF:0000023

IEA: Inferred from Electronic Annotation

SP_SL:SL-0172

C

GO:0005741

mitochondrial outer membrane

PMID:12910269[76]

IDA: Inferred from Direct Assay

C

GO:0005741

mitochondrial outer membrane

PMID:12925707[24]

IDA: Inferred from Direct Assay

C

GO:0005741

mitochondrial outer membrane

PMID:16227588[93]

IDA: Inferred from Direct Assay

C

GO:0005783

endoplasmic reticulum

PMID:12847083[2]

IDA: Inferred from Direct Assay

C

GO:0005829

cytosol

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

C

GO:0005829

cytosol

PMID:11369777[27]

IDA: Inferred from Direct Assay

C

GO:0005829

cytosol

PMID:11864976[36]

IDA: Inferred from Direct Assay

C

GO:0005829

cytosol

PMID:11980919[78]

IDA: Inferred from Direct Assay

C

GO:0005829

cytosol

PMID:12847083[2]

IDA: Inferred from Direct Assay

C

GO:0005829

cytosol

PMID:12925707[24]

IDA: Inferred from Direct Assay

C

GO:0005829

cytosol

PMID:15989966[77]

IDA: Inferred from Direct Assay

C

GO:0005829

cytosol

PMID:16227588[93]

IDA: Inferred from Direct Assay

C

GO:0005829

cytosol

PMID:19139267[38]

IDA: Inferred from Direct Assay

C

GO:0006687

glycosphingolipid metabolic process

PMID:18308723[51]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0006808

regulation of nitrogen utilization

PMID:9241272[3]

IGI: Inferred from Genetic Interaction

MGI:MGI:88138

P

GO:0006915

apoptosis

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-0053

P

GO:0006915

apoptosis

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0006915

apoptosis

PMID:10201940[73]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0006915

apoptosis

PMID:10618441[60]

IMP: Inferred from Mutant Phenotype

P

GO:0006915

apoptosis

PMID:14963330[6]

IGI: Inferred from Genetic Interaction

MGI:MGI:98834

P

GO:0006915

apoptosis

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

MGI:MGI:1197519

P

GO:0006915

apoptosis

PMID:8358790[12]

IDA: Inferred from Direct Assay

P

GO:0006915

apoptosis

PMID:9560217[29]

IDA: Inferred from Direct Assay

P

GO:0006917

induction of apoptosis

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0006917

induction of apoptosis

PMID:10479688[39]

IMP: Inferred from Mutant Phenotype

P

GO:0006917

induction of apoptosis

PMID:8358790[12]

IDA: Inferred from Direct Assay

P

GO:0006919

activation of caspase activity

PMID:12847083[2]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0006919

activation of caspase activity

PMID:14502238[7]

IMP: Inferred from Mutant Phenotype

MGI:MGI:2158306

P

GO:0006919

activation of caspase activity

PMID:14561915[70]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0006919

activation of caspase activity

PMID:15776018[23]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0006919

activation of caspase activity

PMID:16735463[97]

IDA: Inferred from Direct Assay

P

GO:0006974

response to DNA damage stimulus

PMID:12952892[9]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0006974

response to DNA damage stimulus

PMID:9454845[14]

IMP: Inferred from Mutant Phenotype

P

GO:0007007

inner mitochondrial membrane organization

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0007008

outer mitochondrial membrane organization

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0007281

germ cell development

PMID:10894153[11]

IGI: Inferred from Genetic Interaction

MGI:MGI:2176699

P

GO:0007283

spermatogenesis

PMID:10894153[11]

IGI: Inferred from Genetic Interaction

MGI:MGI:2176699

P

GO:0007283

spermatogenesis

PMID:11906913[5]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0007283

spermatogenesis

PMID:7569956[74]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0007399

nervous system development

PMID:12810599[46]

IMP: Inferred from Mutant Phenotype

MGI:MGI:2387665

P

GO:0007420

brain development

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0007548

sex differentiation

PMID:15342910[58]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0008283

cell proliferation

PMID:10762311[33]

IGI: Inferred from Genetic Interaction

MGI:MGI:88138

P

GO:0008283

cell proliferation

PMID:9176392[63]

IDA: Inferred from Direct Assay

P

GO:0008285

negative regulation of cell proliferation

PMID:10762311[33]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0008584

male gonad development

PMID:16270031[61]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0008584

male gonad development

PMID:9241272[3]

IGI: Inferred from Genetic Interaction

MGI:MGI:88138

P

GO:0008624

induction of apoptosis by extracellular signals

PMID:12925707[24]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0008624

induction of apoptosis by extracellular signals

PMID:14507967[31]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0008629

induction of apoptosis by intracellular signals

PMID:12952892[9]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0008635

activation of caspase activity by cytochrome c

PMID:11836241[10]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0008635

activation of caspase activity by cytochrome c

PMID:9560217[29]

IDA: Inferred from Direct Assay

P

GO:0008637

apoptotic mitochondrial changes

PMID:12925707[24]

IDA: Inferred from Direct Assay

P

GO:0009566

fertilization

PMID:10894153[11]

IGI: Inferred from Genetic Interaction

MGI:MGI:2176699

P

GO:0009611

response to wounding

PMID:14507967[31]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0009636

response to toxin

PMID:9454845[14]

IMP: Inferred from Mutant Phenotype

P

GO:0009791

post-embryonic development

PMID:9241272[3]

IGI: Inferred from Genetic Interaction

MGI:MGI:88138

P

GO:0010212

response to ionizing radiation

PMID:10639175[16]

IGI: Inferred from Genetic Interaction

MGI:MGI:107202

P

GO:0010212

response to ionizing radiation

PMID:15578100[4]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0010332

response to gamma radiation

PMID:17068116[52]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0010524

positive regulation of calcium ion transport into cytosol

PMID:15613488[59]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0016020

membrane

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-0472

C

GO:0016021

integral to membrane

GO_REF:0000004

IEA: Inferred from Electronic Annotation

SP_KW:KW-0812

C

GO:0019987

negative regulation of anti-apoptosis

PMID:8798452[65]

IGI: Inferred from Genetic Interaction

MGI:MGI:88139

P

GO:0021854

hypothalamus development

PMID:15342910[58]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0021987

cerebral cortex development

PMID:15342910[58]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0030264

nuclear fragmentation involved in apoptotic nuclear change

PMID:12925707[24]

IDA: Inferred from Direct Assay

P

GO:0031072

heat shock protein binding

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

F

GO:0031558

induction of apoptosis in response to chemical stimulus

PMID:14502238[7]

IMP: Inferred from Mutant Phenotype

MGI:MGI:2158306

P

GO:0031966

mitochondrial membrane

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

C

GO:0031966

mitochondrial membrane

PMID:11369777[27]

IDA: Inferred from Direct Assay

C

GO:0031966

mitochondrial membrane

PMID:11980919[78]

IDA: Inferred from Direct Assay

C

GO:0031966

mitochondrial membrane

PMID:14614769[66]

IDA: Inferred from Direct Assay

C

GO:0032471

reduction of endoplasmic reticulum calcium ion concentration

PMID:15613488[59]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0033137

negative regulation of peptidyl-serine phosphorylation

PMID:15613488[59]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0033599

regulation of mammary gland epithelial cell proliferation

PMID:10363969[22]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0034349

glial cell apoptosis

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0034644

cellular response to UV

PMID:14963330[6]

IGI: Inferred from Genetic Interaction

MGI:MGI:98834

P

GO:0035108

limb morphogenesis

PMID:11163212[62]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0035234

germ cell programmed cell death

PMID:14660547[30]

IGI: Inferred from Genetic Interaction

MGI:MGI:96677

P

GO:0035234

germ cell programmed cell death

PMID:14660547[30]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0035234

germ cell programmed cell death

PMID:17107997[43]

IGI: Inferred from Genetic Interaction

MGI:MGI:96974

P

GO:0042220

response to cocaine

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0042475

odontogenesis of dentine-containing tooth

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

MGI:MGI:1197519

P

GO:0042493

response to drug

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0042803

protein homodimerization activity

PMID:10582606[86]

IPI: Inferred from Physical Interaction

UniProtKB:P10417

F

GO:0042803

protein homodimerization activity

PMID:8631771[21]

IMP: Inferred from Mutant Phenotype

F

GO:0042803

protein homodimerization activity

PMID:8631771[21]

IPI: Inferred from Physical Interaction

UniProtKB:Q07813

F

GO:0042981

regulation of apoptosis

GO_REF:0000002

IEA: Inferred from Electronic Annotation

InterPro:IPR000712

P

GO:0042981

regulation of apoptosis

GO_REF:0000002

IEA: Inferred from Electronic Annotation

InterPro:IPR002475

P

GO:0042981

regulation of apoptosis

GO_REF:0000002

IEA: Inferred from Electronic Annotation

InterPro:IPR020717

P

GO:0042981

regulation of apoptosis

GO_REF:0000002

IEA: Inferred from Electronic Annotation

InterPro:IPR020726

P

GO:0042981

regulation of apoptosis

GO_REF:0000002

IEA: Inferred from Electronic Annotation

InterPro:IPR020728

P

GO:0043065

positive regulation of apoptosis

PMID:10995754[67]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043065

positive regulation of apoptosis

PMID:11146002[42]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043065

positive regulation of apoptosis

PMID:11906913[5]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043065

positive regulation of apoptosis

PMID:15578100[4]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043065

positive regulation of apoptosis

PMID:15753097[85]

IDA: Inferred from Direct Assay

P

GO:0043065

positive regulation of apoptosis

PMID:15955981[68]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0043065

positive regulation of apoptosis

PMID:15967824[15]

IGI: Inferred from Genetic Interaction

MGI:MGI:1197519

P

GO:0043065

positive regulation of apoptosis

PMID:17068116[52]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043065

positive regulation of apoptosis

PMID:17107997[43]

IGI: Inferred from Genetic Interaction

MGI:MGI:96974

P

GO:0043065

positive regulation of apoptosis

PMID:9056387[96]

IGI: Inferred from Genetic Interaction

MGI:MGI:98834

P

GO:0043065

positive regulation of apoptosis

PMID:9241272[3]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043065

positive regulation of apoptosis

PMID:9988273[34]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043281

regulation of caspase activity

PMID:14507967[31]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043524

negative regulation of neuron apoptosis

PMID:8625820[82]

IDA: Inferred from Direct Assay

P

GO:0043525

positive regulation of neuron apoptosis

PMID:10639175[16]

IGI: Inferred from Genetic Interaction

MGI:MGI:107202

P

GO:0043525

positive regulation of neuron apoptosis

PMID:10683286[53]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043525

positive regulation of neuron apoptosis

PMID:10744634[64]

IGI: Inferred from Genetic Interaction

MGI:MGI:95824

P

GO:0043525

positive regulation of neuron apoptosis

PMID:10762311[33]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043525

positive regulation of neuron apoptosis

PMID:10884318[80]

IGI: Inferred from Genetic Interaction

MGI:MGI:95813

P

GO:0043525

positive regulation of neuron apoptosis

PMID:11150333[72]

IMP: Inferred from Mutant Phenotype

MGI:MGI:2158306

P

GO:0043525

positive regulation of neuron apoptosis

PMID:14502238[7]

IMP: Inferred from Mutant Phenotype

MGI:MGI:2158306

P

GO:0043525

positive regulation of neuron apoptosis

PMID:15590937[49]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043525

positive regulation of neuron apoptosis

PMID:15869495[89]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043525

positive regulation of neuron apoptosis

PMID:15944391[28]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043525

positive regulation of neuron apoptosis

PMID:15947791[41]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043525

positive regulation of neuron apoptosis

PMID:16103918[57]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043525

positive regulation of neuron apoptosis

PMID:17192424[13]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043525

positive regulation of neuron apoptosis

PMID:8816704[50]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043525

positive regulation of neuron apoptosis

PMID:9096145[84]

IGI: Inferred from Genetic Interaction

MGI:MGI:88139

P

GO:0043525

positive regulation of neuron apoptosis

PMID:9454852[87]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0043525

positive regulation of neuron apoptosis

PMID:9699561[44]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0044445

cytosolic part

PMID:9553144[20]

IDA: Inferred from Direct Assay

C

GO:0045136

development of secondary sexual characteristics

PMID:15944391[28]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0045333

cellular respiration

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0046666

retinal cell programmed cell death

PMID:14517994[69]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0046688

response to copper ion

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0046982

protein heterodimerization activity

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

F

GO:0046982

protein heterodimerization activity

PMID:11226327[17]

IPI: Inferred from Physical Interaction

UniProtKB:P10417

F

GO:0046982

protein heterodimerization activity

PMID:7650488[1]

IPI: Inferred from Physical Interaction

UniProtKB:Q64373

F

GO:0046982

protein heterodimerization activity

PMID:7834748[98]

IPI: Inferred from Physical Interaction

UniProtKB:Q64373

F

GO:0046982

protein heterodimerization activity

PMID:8798452[65]

IPI: Inferred from Physical Interaction

UniProtKB:Q64373-1

F

GO:0048087

positive regulation of developmental pigmentation

PMID:9241272[3]

IGI: Inferred from Genetic Interaction

MGI:MGI:99702

P

GO:0048147

negative regulation of fibroblast proliferation

PMID:12952892[9]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0048515

spermatid differentiation

PMID:16270031[61]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0048597

post-embryonic camera-type eye morphogenesis

PMID:15955981[68]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0048678

response to axon injury

PMID:16103918[57]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0048872

homeostasis of number of cells

PMID:10931486[56]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0048872

homeostasis of number of cells

PMID:11163212[62]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0048873

homeostasis of number of cells within a tissue

PMID:11413548[81]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0048873

homeostasis of number of cells within a tissue

PMID:15342910[58]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857249

P

GO:0051087

chaperone binding

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

F

GO:0051260

protein homooligomerization

PMID:12925707[24]

IDA: Inferred from Direct Assay

P

GO:0051281

positive regulation of release of sequestered calcium ion into cytosol

PMID:15947791[41]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0051400

BH domain binding

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

F

GO:0051402

neuron apoptosis

PMID:10762311[33]

IGI: Inferred from Genetic Interaction

MGI:MGI:88138

P

GO:0051402

neuron apoptosis

PMID:11226327[17]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0051402

neuron apoptosis

PMID:12917363[19]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0051402

neuron apoptosis

PMID:15574493[25]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0051402

neuron apoptosis

PMID:17077143[88]

IGI: Inferred from Genetic Interaction

MGI:MGI:95819

P

GO:0051412

response to corticosterone stimulus

GO_REF:0000019

IEA: Inferred from Electronic Annotation

Ensembl:ENSRNOP00000028328

P

GO:0051434

BH3 domain binding

PMID:11060313[40]

IPI: Inferred from Physical Interaction

UniProtKB:Q96BY2

F

GO:0051726

regulation of cell cycle

PMID:16055554[47]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0060041

retina development in camera-type eye

PMID:9699561[44]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0060058

positive regulation of apoptosis involved in mammary gland involution

PMID:10363969[22]

IMP: Inferred from Mutant Phenotype

MGI:MGI:1857429

P

GO:0060068

vagina development

PMID:11163212[62]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

GO:0070059

apoptosis in response to endoplasmic reticulum stress

PMID:12847083[2]

IGI: Inferred from Genetic Interaction

MGI:MGI:1097161

P

NOT

GO:0051881

regulation of mitochondrial membrane potential

PMID:14614769[66]

IDA: Inferred from Direct Assay

P


Notes

References

See Help:References for how to manage references in GONUTS.

  1. ↑ 1.0 1.1 Chao DT et al. (1995) Bcl-XL and Bcl-2 repress a common pathway of cell death. J Exp Med 182: 821-8 PubMed GONUTS page
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Zong WX et al. (2003) Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis. J Cell Biol 162: 59-69 PubMed GONUTS page
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 Knudson CM & Korsmeyer SJ (1997) Bcl-2 and Bax function independently to regulate cell death. Nat Genet 16: 358-63 PubMed GONUTS page
  4. ↑ 4.0 4.1 4.2 4.3 Tessner TG et al. (2004) Prostaglandin E2 reduces radiation-induced epithelial apoptosis through a mechanism involving AKT activation and bax translocation. J Clin Invest 114: 1676-85 PubMed GONUTS page
  5. ↑ 5.0 5.1 5.2 5.3 Russell LD et al. (2002) Bax-dependent spermatogonia apoptosis is required for testicular development and spermatogenesis. Biol Reprod 66: 950-8 PubMed GONUTS page
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 Chipuk JE et al. (2004) Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis. Science 303: 1010-4 PubMed GONUTS page
  7. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 Young C et al. (2003) Ethanol-induced neuronal apoptosis in vivo requires BAX in the developing mouse brain. Cell Death Differ 10: 1148-55 PubMed GONUTS page
  8. ↑ 8.0 8.1 Fan H et al. (2006) Susceptibility to metanephric apoptosis in bradykinin B2 receptor null mice via the p53-Bax pathway. Am J Physiol Renal Physiol 291: F670-82 PubMed GONUTS page
  9. ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 Shibue T et al. (2003) Integral role of Noxa in p53-mediated apoptotic response. Genes Dev 17: 2233-8 PubMed GONUTS page
  10. ↑ 10.0 10.1 Degenhardt K et al. (2002) Bax and Bak independently promote cytochrome C release from mitochondria. J Biol Chem 277: 14127-34 PubMed GONUTS page
  11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 Rucker EB 3rd et al. (2000) Bcl-x and Bax regulate mouse primordial germ cell survival and apoptosis during embryogenesis. Mol Endocrinol 14: 1038-52 PubMed GONUTS page
  12. ↑ 12.0 12.1 12.2 12.3 Oltvai ZN et al. (1993) Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell 74: 609-19 PubMed GONUTS page
  13. ↑ 13.0 13.1 Buss RR et al. (2006) Neuromuscular development in the absence of programmed cell death: phenotypic alteration of motoneurons and muscle. J Neurosci 26: 13413-27 PubMed GONUTS page
  14. ↑ 14.0 14.1 14.2 14.3 Xiang H et al. (1998) Bax involvement in p53-mediated neuronal cell death. J Neurosci 18: 1363-73 PubMed GONUTS page
  15. ↑ 15.00 15.01 15.02 15.03 15.04 15.05 15.06 15.07 15.08 15.09 15.10 15.11 Hutcheson J et al. (2005) Combined loss of proapoptotic genes Bak or Bax with Bim synergizes to cause defects in hematopoiesis and in thymocyte apoptosis. J Exp Med 201: 1949-60 PubMed GONUTS page
  16. ↑ 16.0 16.1 16.2 16.3 Chong MJ et al. (2000) Atm and Bax cooperate in ionizing radiation-induced apoptosis in the central nervous system. Proc Natl Acad Sci U S A 97: 889-94 PubMed GONUTS page
  17. ↑ 17.0 17.1 17.2 17.3 17.4 17.5 Vila M et al. (2001) Bax ablation prevents dopaminergic neurodegeneration in the 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease. Proc Natl Acad Sci U S A 98: 2837-42 PubMed GONUTS page
  18. ↑ 18.0 18.1 Amling M et al. (1997) Bcl-2 lies downstream of parathyroid hormone-related peptide in a signaling pathway that regulates chondrocyte maturation during skeletal development. J Cell Biol 136: 205-13 PubMed GONUTS page
  19. ↑ 19.0 19.1 Sun W et al. (2003) Neuromuscular development after the prevention of naturally occurring neuronal death by Bax deletion. J Neurosci 23: 7298-310 PubMed GONUTS page
  20. ↑ 20.0 20.1 20.2 20.3 Hsu YT & Youle RJ (1998) Bax in murine thymus is a soluble monomeric protein that displays differential detergent-induced conformations. J Biol Chem 273: 10777-83 PubMed GONUTS page
  21. ↑ 21.0 21.1 21.2 21.3 Zha H et al. (1996) Proapoptotic protein Bax heterodimerizes with Bcl-2 and homodimerizes with Bax via a novel domain (BH3) distinct from BH1 and BH2. J Biol Chem 271: 7440-4 PubMed GONUTS page
  22. ↑ 22.0 22.1 22.2 22.3 Schorr K et al. (1999) Gain of Bcl-2 is more potent than bax loss in regulating mammary epithelial cell survival in vivo. Cancer Res 59: 2541-5 PubMed GONUTS page
  23. ↑ 23.0 23.1 23.2 Ruiz-Vela A et al. (2005) Proapoptotic BAX and BAK control multiple initiator caspases. EMBO Rep 6: 379-85 PubMed GONUTS page
  24. ↑ 24.00 24.01 24.02 24.03 24.04 24.05 24.06 24.07 24.08 24.09 24.10 24.11 24.12 24.13 Valentijn AJ et al. (2003) Spatial and temporal changes in Bax subcellular localization during anoikis. J Cell Biol 162: 599-612 PubMed GONUTS page
  25. ↑ 25.0 25.1 Weiner JA et al. (2005) Gamma protocadherins are required for synaptic development in the spinal cord. Proc Natl Acad Sci U S A 102: 8-14 PubMed GONUTS page
  26. ↑ 26.0 26.1 Huang DC et al. (1998) The conserved N-terminal BH4 domain of Bcl-2 homologues is essential for inhibition of apoptosis and interaction with CED-4. EMBO J 17: 1029-39 PubMed GONUTS page
  27. ↑ 27.0 27.1 27.2 27.3 27.4 27.5 Zhao Y et al. (2001) Activation of pro-death Bcl-2 family proteins and mitochondria apoptosis pathway in tumor necrosis factor-alpha-induced liver injury. J Biol Chem 276: 27432-40 PubMed GONUTS page
  28. ↑ 28.0 28.1 28.2 28.3 Jacob DA et al. (2005) Effects of Bax gene deletion on muscle and motoneuron degeneration in a sexually dimorphic neuromuscular system. J Neurosci 25: 5638-44 PubMed GONUTS page
  29. ↑ 29.0 29.1 29.2 29.3 29.4 29.5 Jürgensmeier JM et al. (1998) Bax directly induces release of cytochrome c from isolated mitochondria. Proc Natl Acad Sci U S A 95: 4997-5002 PubMed GONUTS page
  30. ↑ 30.0 30.1 30.2 Stallock J et al. (2003) The pro-apoptotic gene Bax is required for the death of ectopic primordial germ cells during their migration in the mouse embryo. Development 130: 6589-97 PubMed GONUTS page
  31. ↑ 31.0 31.1 31.2 31.3 31.4 31.5 Dong H et al. (2003) Enhanced oligodendrocyte survival after spinal cord injury in Bax-deficient mice and mice with delayed Wallerian degeneration. J Neurosci 23: 8682-91 PubMed GONUTS page
  32. ↑ Laforet GA et al. (2001) Changes in cortical and striatal neurons predict behavioral and electrophysiological abnormalities in a transgenic murine model of Huntington's disease. J Neurosci 21: 9112-23 PubMed GONUTS page
  33. ↑ 33.0 33.1 33.2 33.3 33.4 33.5 33.6 33.7 Middleton G et al. (2000) Differences in bcl-2- and bax-independent function in regulating apoptosis in sensory neuron populations. Eur J Neurosci 12: 819-27 PubMed GONUTS page
  34. ↑ 34.0 34.1 Perez GI et al. (1999) Prolongation of ovarian lifespan into advanced chronological age by Bax-deficiency. Nat Genet 21: 200-3 PubMed GONUTS page
  35. ↑ 35.0 35.1 35.2 35.3 Lakhani SA et al. (2006) Caspases 3 and 7: key mediators of mitochondrial events of apoptosis. Science 311: 847-51 PubMed GONUTS page
  36. ↑ 36.0 36.1 36.2 36.3 Karpinich NO et al. (2002) The course of etoposide-induced apoptosis from damage to DNA and p53 activation to mitochondrial release of cytochrome c. J Biol Chem 277: 16547-52 PubMed GONUTS page
  37. ↑ Karbowski M et al. (2006) Role of Bax and Bak in mitochondrial morphogenesis. Nature 443: 658-62 PubMed GONUTS page
  38. ↑ 38.0 38.1 38.2 38.3 Wang X et al. (2009) Mitochondrial degeneration and not apoptosis is the primary cause of embryonic lethality in ceramide transfer protein mutant mice. J Cell Biol 184: 143-58 PubMed GONUTS page
  39. ↑ 39.0 39.1 Cregan SP et al. (1999) Bax-dependent caspase-3 activation is a key determinant in p53-induced apoptosis in neurons. J Neurosci 19: 7860-9 PubMed GONUTS page
  40. ↑ 40.0 40.1 Tan KO et al. (2001) MAP-1, a novel proapoptotic protein containing a BH3-like motif that associates with Bax through its Bcl-2 homology domains. J Biol Chem 276: 2802-7 PubMed GONUTS page
  41. ↑ 41.0 41.1 41.2 41.3 Shi J et al. (2005) Bax limits adult neural stem cell persistence through caspase and IP3 receptor activation. Cell Death Differ 12: 1601-12 PubMed GONUTS page
  42. ↑ 42.0 42.1 Dargusch R et al. (2001) The role of Bax in glutamate-induced nerve cell death. J Neurochem 76: 295-301 PubMed GONUTS page
  43. ↑ 43.0 43.1 43.2 43.3 Runyan C et al. (2006) Steel factor controls midline cell death of primordial germ cells and is essential for their normal proliferation and migration. Development 133: 4861-9 PubMed GONUTS page
  44. ↑ 44.0 44.1 44.2 44.3 Mosinger Ogilvie J et al. (1998) Suppression of developmental retinal cell death but not of photoreceptor degeneration in Bax-deficient mice. Invest Ophthalmol Vis Sci 39: 1713-20 PubMed GONUTS page
  45. ↑ 45.0 45.1 45.2 45.3 Parikh N et al. (2004) The Bax N terminus is required for negative regulation by the mitogen-activated protein kinase kinase and Akt signaling pathways in T cells. J Immunol 173: 6220-7 PubMed GONUTS page
  46. ↑ 46.0 46.1 Ma L et al. (2003) Brn3a regulation of TrkA/NGF receptor expression in developing sensory neurons. Development 130: 3525-34 PubMed GONUTS page
  47. ↑ 47.0 47.1 47.2 47.3 47.4 47.5 47.6 47.7 Takeuchi O et al. (2005) Essential role of BAX,BAK in B cell homeostasis and prevention of autoimmune disease. Proc Natl Acad Sci U S A 102: 11272-7 PubMed GONUTS page
  48. ↑ 48.0 48.1 Eischen CM et al. (2001) Bax loss impairs Myc-induced apoptosis and circumvents the selection of p53 mutations during Myc-mediated lymphomagenesis. Mol Cell Biol 21: 7653-62 PubMed GONUTS page
  49. ↑ 49.0 49.1 49.2 49.3 Sun W et al. (2004) Programmed cell death of adult-generated hippocampal neurons is mediated by the proapoptotic gene Bax. J Neurosci 24: 11205-13 PubMed GONUTS page
  50. ↑ 50.0 50.1 Deckwerth TL et al. (1996) BAX is required for neuronal death after trophic factor deprivation and during development. Neuron 17: 401-11 PubMed GONUTS page
  51. ↑ 51.0 51.1 Rabionet M et al. (2008) Male germ cells require polyenoic sphingolipids with complex glycosylation for completion of meiosis: a link to ceramide synthase-3. J Biol Chem 283: 13357-69 PubMed GONUTS page
  52. ↑ 52.0 52.1 52.2 52.3 Przemeck SM et al. (2007) Radiation-induced gastric epithelial apoptosis occurs in the proliferative zone and is regulated by p53, bak, bax, and bcl-2. Am J Physiol Gastrointest Liver Physiol 292: G620-7 PubMed GONUTS page
  53. ↑ 53.0 53.1 Werth JL et al. (2000) Reversible physiological alterations in sympathetic neurons deprived of NGF but protected from apoptosis by caspase inhibition or Bax deletion. Exp Neurol 161: 203-11 PubMed GONUTS page
  54. ↑ 54.0 54.1 Walensky LD et al. (2006) A stapled BID BH3 helix directly binds and activates BAX. Mol Cell 24: 199-210 PubMed GONUTS page
  55. ↑ 55.0 55.1 Greenfeld CR et al. (2007) BAX is involved in regulating follicular growth, but is dispensable for follicle atresia in adult mouse ovaries. Reproduction 133: 107-16 PubMed GONUTS page
  56. ↑ 56.0 56.1 56.2 56.3 Zeng Q et al. (2000) Gustatory innervation and bax-dependent caspase-2: participants in the life and death pathways of mouse taste receptor cells. J Comp Neurol 424: 640-50 PubMed GONUTS page
  57. ↑ 57.0 57.1 57.2 57.3 Libby RT et al. (2005) Susceptibility to neurodegeneration in a glaucoma is modified by Bax gene dosage. PLoS Genet 1: 17-26 PubMed GONUTS page
  58. ↑ 58.0 58.1 58.2 58.3 58.4 58.5 58.6 58.7 Forger NG et al. (2004) Deletion of Bax eliminates sex differences in the mouse forebrain. Proc Natl Acad Sci U S A 101: 13666-71 PubMed GONUTS page
  59. ↑ 59.0 59.1 59.2 59.3 59.4 59.5 Oakes SA et al. (2005) Proapoptotic BAX and BAK regulate the type 1 inositol trisphosphate receptor and calcium leak from the endoplasmic reticulum. Proc Natl Acad Sci U S A 102: 105-10 PubMed GONUTS page
  60. ↑ 60.0 60.1 Roth KA et al. (2000) Epistatic and independent functions of caspase-3 and Bcl-X(L) in developmental programmed cell death. Proc Natl Acad Sci U S A 97: 466-71 PubMed GONUTS page
  61. ↑ 61.0 61.1 61.2 61.3 Coultas L et al. (2005) Concomitant loss of proapoptotic BH3-only Bcl-2 antagonists Bik and Bim arrests spermatogenesis. EMBO J 24: 3963-73 PubMed GONUTS page
  62. ↑ 62.0 62.1 62.2 62.3 62.4 62.5 62.6 62.7 Lindsten T et al. (2000) The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues. Mol Cell 6: 1389-99 PubMed GONUTS page
  63. ↑ 63.0 63.1 Tzung SP et al. (1997) Expression of Bcl-2 family during liver regeneration and identification of Bcl-x as a delayed early response gene. Am J Pathol 150: 1985-95 PubMed GONUTS page
  64. ↑ 64.0 64.1 Almeida OF et al. (2000) Subtle shifts in the ratio between pro- and antiapoptotic molecules after activation of corticosteroid receptors decide neuronal fate. FASEB J 14: 779-90 PubMed GONUTS page
  65. ↑ 65.0 65.1 65.2 65.3 Simonian PL et al. (1996) Bax can antagonize Bcl-XL during etoposide and cisplatin-induced cell death independently of its heterodimerization with Bcl-XL. J Biol Chem 271: 22764-72 PubMed GONUTS page
  66. ↑ 66.0 66.1 66.2 66.3 66.4 66.5 Heimlich G et al. (2004) Bax-induced cytochrome c release from mitochondria depends on alpha-helices-5 and -6. Biochem J 378: 247-55 PubMed GONUTS page
  67. ↑ 67.0 67.1 Chi MM et al. (2000) Decreased glucose transporter expression triggers BAX-dependent apoptosis in the murine blastocyst. J Biol Chem 275: 40252-7 PubMed GONUTS page
  68. ↑ 68.0 68.1 68.2 68.3 68.4 68.5 Hahn P et al. (2005) Persistent fetal ocular vasculature in mice deficient in bax and bak. Arch Ophthalmol 123: 797-802 PubMed GONUTS page
  69. ↑ 69.0 69.1 Péquignot MO et al. (2003) Major role of BAX in apoptosis during retinal development and in establishment of a functional postnatal retina. Dev Dyn 228: 231-8 PubMed GONUTS page
  70. ↑ 70.0 70.1 Robinson AM et al. (2003) Olfactory neurons in bax knockout mice are protected from bulbectomy-induced apoptosis. Neuroreport 14: 1891-4 PubMed GONUTS page
  71. ↑ 71.0 71.1 Abdelwahid E et al. (1999) Apoptosis in the pattern formation of the ventricular wall during mouse heart organogenesis. Anat Rec 256: 208-17 PubMed GONUTS page
  72. ↑ 72.0 72.1 Zaidi AU et al. (2001) Bcl-X(L)-caspase-9 interactions in the developing nervous system: evidence for multiple death pathways. J Neurosci 21: 169-75 PubMed GONUTS page
  73. ↑ 73.0 73.1 Hotchkiss RS et al. (1999) Overexpression of Bcl-2 in transgenic mice decreases apoptosis and improves survival in sepsis. J Immunol 162: 4148-56 PubMed GONUTS page
  74. ↑ 74.0 74.1 74.2 74.3 74.4 74.5 74.6 Knudson CM et al. (1995) Bax-deficient mice with lymphoid hyperplasia and male germ cell death. Science 270: 96-9 PubMed GONUTS page
  75. ↑ 75.0 75.1 Narita M et al. (1998) Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria. Proc Natl Acad Sci U S A 95: 14681-6 PubMed GONUTS page
  76. ↑ 76.0 76.1 Zhou Z et al. (2003) Cidea-deficient mice have lean phenotype and are resistant to obesity. Nat Genet 35: 49-56 PubMed GONUTS page
  77. ↑ 77.0 77.1 Yuan X et al. (2005) Genetic inactivation of the transcription factor TIF-IA leads to nucleolar disruption, cell cycle arrest, and p53-mediated apoptosis. Mol Cell 19: 77-87 PubMed GONUTS page
  78. ↑ 78.0 78.1 78.2 78.3 Putcha GV et al. (2002) Intrinsic and extrinsic pathway signaling during neuronal apoptosis: lessons from the analysis of mutant mice. J Cell Biol 157: 441-53 PubMed GONUTS page
  79. ↑ 79.0 79.1 Zeng Q & Oakley B (1999) p53 and Bax: putative death factors in taste cell turnover. J Comp Neurol 413: 168-80 PubMed GONUTS page
  80. ↑ 80.0 80.1 Selimi F et al. (2000) Bax inactivation in lurcher mutants rescues cerebellar granule cells but not purkinje cells or inferior olivary neurons. J Neurosci 20: 5339-45 PubMed GONUTS page
  81. ↑ 81.0 81.1 Fan H et al. (2001) Elimination of Bax expression in mice increases cerebellar purkinje cell numbers but not the number of granule cells. J Comp Neurol 436: 82-91 PubMed GONUTS page
  82. ↑ 82.0 82.1 Middleton G et al. (1996) Bax promotes neuronal survival and antagonises the survival effects of neurotrophic factors. Development 122: 695-701 PubMed GONUTS page
  83. ↑ Ross AJ et al. (2001) BCLW mediates survival of postmitotic Sertoli cells by regulating BAX activity. Dev Biol 239: 295-308 PubMed GONUTS page
  84. ↑ 84.0 84.1 Shindler KS et al. (1997) Bax deficiency prevents the increased cell death of immature neurons in bcl-x-deficient mice. J Neurosci 17: 3112-9 PubMed GONUTS page
  85. ↑ 85.0 85.1 Li A & Harris DA (2005) Mammalian prion protein suppresses Bax-induced cell death in yeast. J Biol Chem 280: 17430-4 PubMed GONUTS page
  86. ↑ 86.0 86.1 Vukosavic S et al. (1999) Bax and Bcl-2 interaction in a transgenic mouse model of familial amyotrophic lateral sclerosis. J Neurochem 73: 2460-8 PubMed GONUTS page
  87. ↑ 87.0 87.1 White FA et al. (1998) Widespread elimination of naturally occurring neuronal death in Bax-deficient mice. J Neurosci 18: 1428-39 PubMed GONUTS page
  88. ↑ 88.0 88.1 de Rivero Vaccari JC et al. (2006) NMDA receptors promote survival in somatosensory relay nuclei by inhibiting Bax-dependent developmental cell death. Proc Natl Acad Sci U S A 103: 16971-6 PubMed GONUTS page
  89. ↑ 89.0 89.1 Guo H et al. (2005) Development of pontine noradrenergic A5 neurons requires brain-derived neurotrophic factor. Eur J Neurosci 21: 2019-23 PubMed GONUTS page
  90. ↑ Pardo J et al. (2006) The mitochondrial protein Bak is pivotal for gliotoxin-induced apoptosis and a critical host factor of Aspergillus fumigatus virulence in mice. J Cell Biol 174: 509-19 PubMed GONUTS page
  91. ↑ 91.0 91.1 Pagliarini DJ et al. (2008) A mitochondrial protein compendium elucidates complex I disease biology. Cell 134: 112-23 PubMed GONUTS page
  92. ↑ 92.0 92.1 Dominov JA et al. (2001) Pro- and anti-apoptotic members of the Bcl-2 family in skeletal muscle: a distinct role for Bcl-2 in later stages of myogenesis. Dev Dyn 220: 18-26 PubMed GONUTS page
  93. ↑ 93.0 93.1 93.2 93.3 Takahashi Y et al. (2005) Loss of Bif-1 suppresses Bax/Bak conformational change and mitochondrial apoptosis. Mol Cell Biol 25: 9369-82 PubMed GONUTS page
  94. ↑ 94.0 94.1 Mootha VK et al. (2003) Integrated analysis of protein composition, tissue diversity, and gene regulation in mouse mitochondria. Cell 115: 629-40 PubMed GONUTS page
  95. ↑ 95.0 95.1 Gillardon F et al. (1995) Up-regulation of bax and down-regulation of bcl-2 is associated with kainate-induced apoptosis in mouse brain. Neurosci Lett 192: 85-8 PubMed GONUTS page
  96. ↑ 96.0 96.1 Popper P et al. (1997) TRPM-2 expression and tunel staining in neurodegenerative diseases: studies in wobbler and rd mice. Exp Neurol 143: 246-54 PubMed GONUTS page
  97. ↑ Dziarmaga A et al. (2006) Neuronal apoptosis inhibitory protein is expressed in developing kidney and is regulated by PAX2. Am J Physiol Renal Physiol 291: F913-20 PubMed GONUTS page
  98. ↑ Yang E et al. (1995) Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death. Cell 80: 285-91 PubMed GONUTS page
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