MOUSE:PTEN

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Species (Taxon ID)	Mus musculus (Mouse). ([1])
Gene Name(s)	Pten (synonyms: Mmac1)
Protein Name(s)	Phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN Mutated in multiple advanced cancers 1 Phosphatase and tensin homolog
External Links
EMBL	U92437 AK076980 AK088717 AK148736 BC021445
IPI	IPI00114410
RefSeq	NP_032986.1
UniGene	Mm.245395 Mm.444861
ProteinModelPortal	O08586
SMR	O08586
DIP	DIP-38740N
IntAct	O08586
MINT	MINT-128418
STRING	O08586
PhosphoSite	O08586
PRIDE	O08586
Ensembl	ENSMUST00000013807
GeneID	19211
KEGG	mmu:19211
UCSC	uc008hfr.1
CTD	5728
MGI	MGI:109583
eggNOG	roNOG17599
HOGENOM	HBG745257
HOVERGEN	HBG000239
InParanoid	O08586
OMA	TRREDKH
OrthoDB	EOG434W64
PhylomeDB	O08586
NextBio	295956
ArrayExpress	O08586
Bgee	O08586
CleanEx	MM_PTEN
Genevestigator	O08586
GermOnline	ENSMUSG00000013663
GO	GO:0035749 GO:0016605 GO:0043220 GO:0051717 GO:0000287 GO:0030165 GO:0016314 GO:0051800 GO:0004438 GO:0004722 GO:0004725 GO:0008138 GO:0007092 GO:0001525 GO:0006915 GO:0048738 GO:0007417 GO:0043542 GO:0006917 GO:0046855 GO:0043066 GO:0090344 GO:0030336 GO:0050680 GO:0051895 GO:0051898 GO:0046856 GO:0008284 GO:0060736 GO:0002902 GO:0033032 GO:0010975
InterPro	IPR017361 IPR008973 IPR000340 IPR014019 IPR014020 IPR016130
Pfam	PF00782 PF10409
PIRSF	PIRSF038025
SUPFAM	SSF49562
PROSITE	PS51182 PS51181

Annotations

Qualifier	GO ID	GO term name	Reference	Evidence Code	with/from	Aspect	Notes	Status
	GO:0000287	magnesium ion binding	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	F	Seeded From UniProt
	GO:0001525	angiogenesis	PMID:16107612^[1]	IMP: Inferred from Mutant Phenotype	MGI:MGI:2136412	P	Seeded From UniProt
	GO:0001525	angiogenesis	PMID:16107612^[1]	IMP: Inferred from Mutant Phenotype	MGI:MGI:2182005	P	Seeded From UniProt
	GO:0001933	negative regulation of protein phosphorylation	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0002902	regulation of B cell apoptosis	PMID:9990064^[2]	IMP: Inferred from Mutant Phenotype	MGI:MGI:1857466	P	Seeded From UniProt
	GO:0004438	phosphatidylinositol-3-phosphatase activity	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	F	Seeded From UniProt
	GO:0004438	phosphatidylinositol-3-phosphatase activity	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	F	Seeded From UniProt
	GO:0004721	phosphoprotein phosphatase activity	GO_REF:0000003	IEA: Inferred from Electronic Annotation	EC:3.1.3.16	F	Seeded From UniProt
	GO:0004721	phosphoprotein phosphatase activity	GO_REF:0000004	IEA: Inferred from Electronic Annotation	SP_KW:KW-0904	F	Seeded From UniProt
	GO:0004721	phosphoprotein phosphatase activity	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	F	Seeded From UniProt
	GO:0004722	protein serine/threonine phosphatase activity	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	F	Seeded From UniProt
	GO:0004722	protein serine/threonine phosphatase activity	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	F	Seeded From UniProt
	GO:0004725	protein tyrosine phosphatase activity	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR016130	F	Seeded From UniProt
	GO:0004725	protein tyrosine phosphatase activity	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	F	Seeded From UniProt
	GO:0004725	protein tyrosine phosphatase activity	GO_REF:0000003	IEA: Inferred from Electronic Annotation	EC:3.1.3.48	F	Seeded From UniProt
	GO:0004725	protein tyrosine phosphatase activity	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	F	Seeded From UniProt
	GO:0004725	protein tyrosine phosphatase activity	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	F	Seeded From UniProt
	GO:0005515	protein binding	PMID:16456542^[3]	IPI: Inferred from Physical Interaction	UniProtKB:P70441	F	Seeded From UniProt
	GO:0005515	protein binding	PMID:16456542^[3]	IPI: Inferred from Physical Interaction	UniProtKB:Q9JHL1	F	Seeded From UniProt
	GO:0005515	protein binding	PMID:17218262^[4]	IPI: Inferred from Physical Interaction	UniProtKB:P49452	F	Seeded From UniProt
	GO:0005515	protein binding	PMID:18190691^[5]	IPI: Inferred from Physical Interaction	UniProtKB:P70441	F	Seeded From UniProt
	GO:0005634	nucleus	GO_REF:0000004	IEA: Inferred from Electronic Annotation	SP_KW:KW-0539	C	Seeded From UniProt
	GO:0005634	nucleus	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	C	Seeded From UniProt
	GO:0005634	nucleus	GO_REF:0000023	IEA: Inferred from Electronic Annotation	SP_SL:SL-0191	C	Seeded From UniProt
	GO:0005634	nucleus	PMID:14522255^[6]	IDA: Inferred from Direct Assay		C	Seeded From UniProt
	GO:0005634	nucleus	PMID:18332125^[7]	IDA: Inferred from Direct Assay		C	Seeded From UniProt
	GO:0005634	nucleus	PMID:18562292^[8]	IDA: Inferred from Direct Assay		C	Seeded From UniProt
	GO:0005737	cytoplasm	GO_REF:0000004	IEA: Inferred from Electronic Annotation	SP_KW:KW-0963	C	Seeded From UniProt
	GO:0005737	cytoplasm	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	C	Seeded From UniProt
	GO:0005737	cytoplasm	GO_REF:0000023	IEA: Inferred from Electronic Annotation	SP_SL:SL-0086	C	Seeded From UniProt
	GO:0005737	cytoplasm	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	C	Seeded From UniProt
	GO:0005737	cytoplasm	PMID:14522255^[6]	IDA: Inferred from Direct Assay		C	Seeded From UniProt
	GO:0005737	cytoplasm	PMID:18562292^[8]	IDA: Inferred from Direct Assay		C	Seeded From UniProt
	GO:0006470	protein dephosphorylation	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR000340	P	Seeded From UniProt
	GO:0006470	protein dephosphorylation	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	P	Seeded From UniProt
	GO:0006470	protein dephosphorylation	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0006470	protein dephosphorylation	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	P	Seeded From UniProt
	GO:0006629	lipid metabolic process	GO_REF:0000004	IEA: Inferred from Electronic Annotation	SP_KW:KW-0443	P	Seeded From UniProt
	GO:0006915	apoptosis	GO_REF:0000004	IEA: Inferred from Electronic Annotation	SP_KW:KW-0053	P	Seeded From UniProt
	GO:0006917	induction of apoptosis	PMID:9778245^[9]	IMP: Inferred from Mutant Phenotype	MGI:MGI:1857937	P	Seeded From UniProt
	GO:0007092	activation of mitotic anaphase-promoting complex activity	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0007092	activation of mitotic anaphase-promoting complex activity	PMID:21241890^[10]	IMP: Inferred from Mutant Phenotype		P	Seeded From UniProt
	GO:0007399	nervous system development	GO_REF:0000004	IEA: Inferred from Electronic Annotation	SP_KW:KW-0524	P	Seeded From UniProt
	GO:0007417	central nervous system development	PMID:12091320^[11]	IMP: Inferred from Mutant Phenotype	MGI:MGI:2183285	P	Seeded From UniProt
	GO:0007507	heart development	PMID:15755804^[12]	IMP: Inferred from Mutant Phenotype	MGI:MGI:3578141	P	Seeded From UniProt
	GO:0008138	protein tyrosine/serine/threonine phosphatase activity	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR000340	F	Seeded From UniProt
	GO:0008284	positive regulation of cell proliferation	PMID:21241890^[10]	IMP: Inferred from Mutant Phenotype		P	Seeded From UniProt
	GO:0008285	negative regulation of cell proliferation	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	P	Seeded From UniProt
	GO:0008285	negative regulation of cell proliferation	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0008285	negative regulation of cell proliferation	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	P	Seeded From UniProt
	GO:0008285	negative regulation of cell proliferation	PMID:16027168^[13]	IGI: Inferred from Genetic Interaction	MGI:MGI:102548	P	Seeded From UniProt
	GO:0008285	negative regulation of cell proliferation	PMID:16027169^[14]	IMP: Inferred from Mutant Phenotype	MGI:MGI:1857936	P	Seeded From UniProt
	GO:0009898	internal side of plasma membrane	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	C	Seeded From UniProt
	GO:0010975	regulation of neuron projection development	PMID:19778506^[15]	IMP: Inferred from Mutant Phenotype		P	Seeded From UniProt
	GO:0010997	anaphase-promoting complex binding	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	F	Seeded From UniProt
	GO:0016311	dephosphorylation	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR016130	P	Seeded From UniProt
	GO:0016314	phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase activity	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	F	Seeded From UniProt
	GO:0016314	phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase activity	GO_REF:0000003	IEA: Inferred from Electronic Annotation	EC:3.1.3.67	F	Seeded From UniProt
	GO:0016314	phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase activity	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	F	Seeded From UniProt
	GO:0016314	phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase activity	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	F	Seeded From UniProt
	GO:0016314	phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase activity	PMID:9778245^[9]	IDA: Inferred from Direct Assay		F	Seeded From UniProt
	GO:0016477	cell migration	PMID:12091320^[11]	IMP: Inferred from Mutant Phenotype	MGI:MGI:2183285	P	Seeded From UniProt
	GO:0016605	PML body	GO_REF:0000023	IEA: Inferred from Electronic Annotation	SP_SL:SL-0465	C	Seeded From UniProt
	GO:0016787	hydrolase activity	GO_REF:0000004	IEA: Inferred from Electronic Annotation	SP_KW:KW-0378	F	Seeded From UniProt
	GO:0016791	phosphatase activity	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR016130	F	Seeded From UniProt
	GO:0019899	enzyme binding	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	F	Seeded From UniProt
	GO:0030165	PDZ domain binding	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	F	Seeded From UniProt
	GO:0030165	PDZ domain binding	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	F	Seeded From UniProt
	GO:0030165	PDZ domain binding	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	F	Seeded From UniProt
	GO:0030336	negative regulation of cell migration	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	P	Seeded From UniProt
	GO:0030336	negative regulation of cell migration	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0030336	negative regulation of cell migration	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	P	Seeded From UniProt
	GO:0031647	regulation of protein stability	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	P	Seeded From UniProt
	GO:0031647	regulation of protein stability	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0031647	regulation of protein stability	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	P	Seeded From UniProt
	GO:0031658	negative regulation of cyclin-dependent protein kinase activity involved in G1/S	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0033032	regulation of myeloid cell apoptosis	PMID:9990064^[2]	IMP: Inferred from Mutant Phenotype	MGI:MGI:1857466	P	Seeded From UniProt
	GO:0035335	peptidyl-tyrosine dephosphorylation	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0035335	peptidyl-tyrosine dephosphorylation	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	P	Seeded From UniProt
	GO:0035749	myelin sheath adaxonal region	PMID:20237282^[16]	IDA: Inferred from Direct Assay		C	Seeded From UniProt
	GO:0043066	negative regulation of apoptosis	PMID:10339565^[17]	IMP: Inferred from Mutant Phenotype		P	Seeded From UniProt
	GO:0043220	Schmidt-Lanterman incisure	PMID:20237282^[16]	IDA: Inferred from Direct Assay		C	Seeded From UniProt
	GO:0043542	endothelial cell migration	PMID:16107612^[1]	IMP: Inferred from Mutant Phenotype	MGI:MGI:2136412	P	Seeded From UniProt
	GO:0043542	endothelial cell migration	PMID:16107612^[1]	IMP: Inferred from Mutant Phenotype	MGI:MGI:2182005	P	Seeded From UniProt
	GO:0046855	inositol phosphate dephosphorylation	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	P	Seeded From UniProt
	GO:0046855	inositol phosphate dephosphorylation	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0046855	inositol phosphate dephosphorylation	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	P	Seeded From UniProt
	GO:0046856	phosphatidylinositol dephosphorylation	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	P	Seeded From UniProt
	GO:0046856	phosphatidylinositol dephosphorylation	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0046856	phosphatidylinositol dephosphorylation	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	P	Seeded From UniProt
	GO:0048738	cardiac muscle tissue development	PMID:16107612^[1]	IMP: Inferred from Mutant Phenotype	MGI:MGI:2136412	P	Seeded From UniProt
	GO:0048738	cardiac muscle tissue development	PMID:16107612^[1]	IMP: Inferred from Mutant Phenotype	MGI:MGI:2182005	P	Seeded From UniProt
	GO:0050680	negative regulation of epithelial cell proliferation	PMID:15994948^[18]	IMP: Inferred from Mutant Phenotype	MGI:MGI:2183284	P	Seeded From UniProt
	GO:0050821	protein stabilization	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0051091	positive regulation of sequence-specific DNA binding transcription factor activity	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0051717	inositol-1,3,4,5-tetrakisphosphate 3-phosphatase activity	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	F	Seeded From UniProt
	GO:0051717	inositol-1,3,4,5-tetrakisphosphate 3-phosphatase activity	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	F	Seeded From UniProt
	GO:0051726	regulation of cell cycle	PMID:18332125^[7]	IGI: Inferred from Genetic Interaction	MGI:MGI:98834	P	Seeded From UniProt
	GO:0051800	phosphatidylinositol-3,4-bisphosphate 3-phosphatase activity	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	F	Seeded From UniProt
	GO:0051800	phosphatidylinositol-3,4-bisphosphate 3-phosphatase activity	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	F	Seeded From UniProt
	GO:0051800	phosphatidylinositol-3,4-bisphosphate 3-phosphatase activity	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	F	Seeded From UniProt
	GO:0051895	negative regulation of focal adhesion assembly	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	P	Seeded From UniProt
	GO:0051895	negative regulation of focal adhesion assembly	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0051895	negative regulation of focal adhesion assembly	GO_REF:0000024	ISS: Inferred from Sequence or Structural Similarity	UniProtKB:P60484	P	Seeded From UniProt
	GO:0051898	negative regulation of protein kinase B signaling cascade	GO_REF:0000002	IEA: Inferred from Electronic Annotation	InterPro:IPR017361	P	Seeded From UniProt
	GO:0051898	negative regulation of protein kinase B signaling cascade	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0051898	negative regulation of protein kinase B signaling cascade	PMID:10339565^[17]	IMP: Inferred from Mutant Phenotype		P	Seeded From UniProt
	GO:0060070	canonical Wnt receptor signaling pathway	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0060736	prostate gland growth	PMID:15994948^[18]	IMP: Inferred from Mutant Phenotype	MGI:MGI:2183284	P	Seeded From UniProt
	GO:0090344	negative regulation of cell aging	PMID:21241890^[10]	IMP: Inferred from Mutant Phenotype		P	Seeded From UniProt
	GO:2000060	positive regulation of protein ubiquitination involved in ubiquitin-dependent protein catabolic process	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:2000134	negative regulation of G1/S transition of mitotic cell cycle	GO_REF:0000019	IEA: Inferred from Electronic Annotation	Ensembl:ENSP00000361021	P	Seeded From UniProt
	GO:0019717	synaptosome	PMID:21664258^[19]	IMP: Inferred from Mutant Phenotype		C	Synaptosomal fraction from brain of wild type mice, figure 5A	complete
	GO:0051898	negative regulation of protein kinase B signaling cascade	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	Pten mutant mice showed increase phosphor-Ser473-Akt (P-Akt) which is a marker for Akt activation in the dentate gyrus. Therefore Pten has a negative regulation role in the PIK3/Akt signalling pathway compared to wild type. Figure 1C.	complete
	GO:0035176	social behavior	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	Control mice exposed to novel mice exhibited typical behaviour of approaching and sniffing (typical social behaviour for mice) but this initial social interaction was decreased in mutant Pten mice, figure 2A. When control mice re-exposed to same mouse, social interaction decreased from initial interaction indicating recognition of familiar mouse showing normal social learning. However this decrease was not seen in mutant mice showing impaired social initial interaction. Similar result seen in figure 2E. In the test there are two cages one with a adult mouse and another cage with a inanimate object. Control mice spent more time interacting with social target than inanimate target. However Pten mutant mice showed decreased interaction with social target compared to control. Pten mutant mice spent equal amount of time with social target and inanimate target. Figure 2F, Same result results were in a three roomed chamber. When mice were exposed to novel mouse and familiar mouse, control mouse spend more time with novel mouse than familiar mouse but the Pten mutant mice showed no preference of either novel or familiar mouse figure 2G.	complete
	GO:0030534	adult behavior	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	Figure 2B, control mice showed immediate activity of nest formation but mutant mice showed litter nest forming activity. I used the term adult behaviour because building a nest occurs at the adult stage of mice. But a new GO term as a child term for adult behaviour can be nest building or can be a child term for the GO term behaviour.	complete
	GO:0060179	male mating behavior	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	Control male mouse made females pregnant but mutant Pten males did not made female mice pregnant. Figure 2H.	complete
	GO:0042711	maternal behavior	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	When Pten mutant female mice were pregnant and delivered normal size pups, after 5 days the survival rate of pups were decreased in Pten females pups compared to wild type, figure 2H.	complete
	GO:0007626	locomotory behavior	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	Mutant mice showed hyperactivity in more stressful conditions such as being in a bright environment of open field, therefore traveling further and at a increased average speed, figure 3A. But locomotor activity was normal in dark enclosed environment Figure supplementary data 1A and 1B.	complete
	GO:0060134	prepulse inhibition	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	Figure 3B: Pten mutant mice increased initial startle response compared to control. Sensorimotor gating was measured by prepulse inhibition (PPI) paradigm which was impaired in mutant Pten mice compared to control figure 3C	complete
	GO:0007611	learning or memory	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	In Morris water maze, when the platform was submerged, Pten mutant mice did not learn as quickly in terms of time and distance compared to control, figure 3G. In figure 3H, control mice spent more time in target quadrant compared to mutant Pten mice where no preference was shown.	complete
	GO:0001966	thigmotaxis	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	In the Morris water maze, mutant Pten mice showed to swim more long the edge of the maze which was also seen in the open field test compared to control, figure 3I.	complete
	GO:0048853	forebrain morphogenesis	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	Mutant Pten mice showed progressive macrocephaly (abnormal large head) compared to control (figure 4A). Progressive macrocephaly was seen in the forebrain area (cortex and hippocampus figure 4b and C)	complete
	GO:0045792	negative regulation of cell size	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	Supplementary figure S2A-C shows that aging mice as increase in soma hypertrophy of Pten mutant mice compared to control.	complete
	GO:0021955	central nervous system neuron axonogenesis	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	Figure 5A showed abnormal axonal processes in mutant Pten mice compared to control. Also figure 5B shows abnormal axonal projection in dentate gyrus mossy fiber tracts. Adult mutant Pten mice showed enlargement of mossy fiber tract (supplementary figure 3A and B)	complete
	GO:2000808	negative regulation of synaptic vesicle clustering	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	Figure 5C shows Pten mutant mice had increase presynaptic vesicles compared to control.	complete
	GO:0061002	negative regulation of dendritic spine morphogenesis	PMID:16675393^[20]	IMP: Inferred from Mutant Phenotype		P	Figure 6A, showed 3 month old mutant Pten mice had thickened elongated processes. Also dendritic hypertrophy seen in adult mutant Pten mice in the dentate gyrus, figure 6B. Also figure 6C shows increase of 24.9% in dendritic spine density in mutant Pten mice compared to control mice.	complete
	GO:0060024	rhythmic synaptic transmission	PMID:17706614^[21]	IMP: Inferred from Mutant Phenotype		P	Figure 1C: seizure activity increased with age in mutant Pten mice compared to control resulting in abnormal rhythmic synaptic transmission	complete
	GO:0021542	dentate gyrus development	PMID:17706614^[21]	IMP: Inferred from Mutant Phenotype		P	Pten mutant mice showed dispersion of dentate granule neurons in mutant Pten mice compared to control, figure3. Possibly a better new GO term would be ‘dentate gyrus morphogenesis’ since there was dispersion of dentate granules.	complete
	GO:0045475	locomotor rhythm	PMID:17706614^[21]	IMP: Inferred from Mutant Phenotype		P	Figure 4A, Pten mutant mice showed increase locomotor activity compared to control in the dark but no difference in the light. Similar results seen in wheel running task, figure 5. Figure 6A and B, difference in locomotor activity, Pten mutant mice showed more breaks in the dark compared wild type where wild type mice showed constant rate of locomotor activity.	complete
	GO:0032535	regulation of cellular component size	PMID:18082964^[22]	IMP: Inferred from Mutant Phenotype		P	GFAP-crecombinase was used to knockout Pten in mice hippocampus neurons. Used electron microscopy, found changes in knockout PTEN pyramidal neurons in cerebral cortex compared to control. There was increase in nuclei and somata of neurons in knockout Pten mice compared to control, figure 1A and B. In addition, mitochondria of knockout Pten mice were enlarged. New GO term can be regulation of mitochondria size, regulation of nucleus size. Similar result were seen in Pten knockout mice in cerebellar granule neurons, where there was enlargement in nuclear size (figure 4A and B)	complete
	GO:0090071	negative regulation of ribosome biogenesis	PMID:18082964^[22]	IMP: Inferred from Mutant Phenotype		P	Figure 1C and D shows increase of ribosome density into dendritic and axonal projections proximal to the somata of Pten knockout mice compared to control. This was not due to increase in number of nucleoli, figure 1F.	complete
	GO:0060997	dendritic spine morphogenesis	PMID:18082964^[22]	IMP: Inferred from Mutant Phenotype		P	Figure 2C and 2D, Pten knockout mice showed enlarge dendritic projections and increase in density of dendritic spines compared to control. In addition the morphology was abnormal and lacked distinct mushroom shaped termini.	complete
	GO:0097105	presynaptic membrane assembly	PMID:18082964^[22]	IMP: Inferred from Mutant Phenotype		P	Figure 3 A-D, Pten knockout mice had presynaptic terminal present but enlarged and densely packed with increase number of synaptic vesicles compared to control. Similar result were seen in Pten knockout mice in cerebellar granule neurons, figure 4C and E.	complete
	GO:2000808	negative regulation of synaptic vesicle clustering	PMID:18082964^[22]	IMP: Inferred from Mutant Phenotype		P	Figure 3 A-D, Pten knockout mice had presynaptic terminal present but enlarged and densely packed with increase number of synaptic vesicles compared to control. Figure 3E and F show Pten knockout mice enlarged presynaptic terminals with increase synaptic vesicles seen by increase immunofluorescent staining synaptic vesicles marker (synaptophysin) in cerebral cortex compared to control. Similar results were seen in Pten knockout mice in cerebellar granule neurons, figure 4C and E.	complete
	GO:0097107	postsynaptic density assembly	PMID:18082964^[22]	IMP: Inferred from Mutant Phenotype		P	Figure 3B, Pten knockout showed that in greater than 60% enlarge presynaptic terminals, there was no postsynaptic density. Similar result were seen in Pten knockout mice in cerebellar granule neurons, figure 4D and F	complete
	GO:0060074	synapse maturation	PMID:18082964^[22]	IMP: Inferred from Mutant Phenotype		P	Figure 3D, mutant Pten mice showed abnormal synaptic connections when postsynaptic density was present with abnormal structure with increase in size compared to control. Similar results were seen in Pten knockout mice in cerebellar granule neurons, figure 4F.	complete
	GO:0007270	neuron-neuron synaptic transmission	PMID:18082964^[22]	IMP: Inferred from Mutant Phenotype		P	Synaptic transmission measured at excitatory synapses between CA3 and CA1 neurons of the hippocampus. Figure 5A showed decrease in synaptic transmission. A new child term can be: regulation of neuron-neuron synaptic transmission and then a child term to describe this experimental evidence can be positive regulation of neuron-neuron synaptic transmission	complete
	GO:2000463	positive regulation of excitatory postsynaptic membrane potential	PMID:18082964^[22]	IMP: Inferred from Mutant Phenotype		P	Figure 5 A-C, fEPSP were significantly impaired in Pten knockout mice compared to wild type.	complete
	GO:0060291	long-term synaptic potentiation	PMID:18082964^[22]	IMP: Inferred from Mutant Phenotype		P	To investigate if synaptic transmission is impaired due to presynaptic function, pair-pulse ratio was used. No difference was seen between wild type and Pten knockout mice. There was no impairment in neurotransmitter release from presynaptic terminal, figure 5B. Therefore synaptic plasticity was investigated by measuring long-term potentiation (LTP) at CA3-CA1 synapse. Figure 5C shows decrease in LTP in Pten knockout mice compared to wild type, reduced by more than 70%	complete
	GO:0032286	central nervous system myelin maintenance	PMID:18082964^[22]	IMP: Inferred from Mutant Phenotype		P	Figure 6B and D shows thickening of myelin sheath and regions of unravelling myelin compared to wild type where myelin was tightly wrapped in the corpus callosum figure 6A and C. Figure 7J shows that Pten mice show enlarged oligodendrocytes compared to wild type. Therefore loss of functional oligodendrocytes leads to myelination defects. New GO term: oligodendrocytes development child term of ‘central nervous system myelin maintenance’	complete
	GO:0048854	brain morphogenesis	PMID:19208814^[23]	IMP: Inferred from Mutant Phenotype		P	Heterozygous Pten mice resulted in macrocephaly in males and females, figure 1A-C. There was increase in brain size; therefore Pten has a negative regulation on brain growth.	complete
	GO:0046621	negative regulation of organ growth	PMID:19208814^[23]	IMP: Inferred from Mutant Phenotype		P	Heterozygous Pten mice resulted in macrocephaly in males and females, figure 1A-C. There was increase in brain size; therefore Pten has a negative regulation on brain growth. Perhaps a new GO term can be ‘brain growth’ as a child term for ‘organ growth’. Then negative regulation term can be added to brain growth.	complete
	GO:0035176	social behavior	PMID:19208814^[23]	IMP: Inferred from Mutant Phenotype		P	To measure social behaviour an apparatus that contained two chambers, one with a mouse and the other chamber with inanimate object (figure 2A). Wild type Pten mice spend more time with novel mouse instead of inanimate object whereas mutant Pten female mice did not show preference over the social and non-social chamber, figure 2B.	complete
	GO:0060134	prepulse inhibition	PMID:19208814^[23]	IMP: Inferred from Mutant Phenotype		P	Figure 2D shows Pten mutant mice was impaired in prepluse inhibition of acoustic startle response compared to control.	complete
	GO:0045792	negative regulation of cell size	PMID:21411674^[24]	IMP: Inferred from Mutant Phenotype		P	Figure 2A, Pten knockdown granule cells showed increase in cross-sectional area compared to control.	complete
	GO:0060997	dendritic spine morphogenesis	PMID:21411674^[24]	IMP: Inferred from Mutant Phenotype		P	Figure 2B, Pten knockdown neurons were thicker dendrites with more filopodial-like protrusion and aberrant protrusion extruding from existing spines Pten knockdown granule cells. Figure 2B also shows increase in spine density in Pten knockdown compared to control.	complete
	GO:0090394	negative regulation of excitatory postsynaptic membrane potential	PMID:21411674^[24]	IMP: Inferred from Mutant Phenotype		P	Examine synaptic activity. Pten knockdown mice showed increase mEPSC frequency, compared to control, figure 6B, C, figure 7A.	complete
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Notes

References

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

↑ ^1.0 ^1.1 ^1.2 ^1.3 ^1.4 ^1.5 Hamada K et al. (2005) The PTEN/PI3K pathway governs normal vascular development and tumor angiogenesis. Genes Dev 19: 2054-65 PubMed GONUTS page
↑ ^2.0 ^2.1 Podsypanina K et al. (1999) Mutation of Pten/Mmac1 in mice causes neoplasia in multiple organ systems. Proc Natl Acad Sci U S A 96: 1563-8 PubMed GONUTS page
↑ ^3.0 ^3.1 Takahashi Y et al. (2006) PTEN tumor suppressor associates with NHERF proteins to attenuate PDGF receptor signaling. EMBO J 25: 910-20 PubMed GONUTS page
↑ Shen WH et al. (2007) Essential role for nuclear PTEN in maintaining chromosomal integrity. Cell 128: 157-70 PubMed GONUTS page
↑ Pan Y et al. (2008) Na+/H+ exchanger regulatory factor 1 inhibits platelet-derived growth factor signaling in breast cancer cells. Breast Cancer Res 10: R5 PubMed GONUTS page
↑ ^6.0 ^6.1 Wang S et al. (2003) Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer. Cancer Cell 4: 209-21 PubMed GONUTS page
↑ ^7.0 ^7.1 Chang CJ et al. (2008) PTEN nuclear localization is regulated by oxidative stress and mediates p53-dependent tumor suppression. Mol Cell Biol 28: 3281-9 PubMed GONUTS page
↑ ^8.0 ^8.1 Fouladkou F et al. (2008) The ubiquitin ligase Nedd4-1 is dispensable for the regulation of PTEN stability and localization. Proc Natl Acad Sci U S A 105: 8585-90 PubMed GONUTS page
↑ ^9.0 ^9.1 Stambolic V et al. (1998) Negative regulation of PKB/Akt-dependent cell survival by the tumor suppressor PTEN. Cell 95: 29-39 PubMed GONUTS page
↑ ^10.0 ^10.1 ^10.2 Song MS et al. (2011) Nuclear PTEN regulates the APC-CDH1 tumor-suppressive complex in a phosphatase-independent manner. Cell 144: 187-99 PubMed GONUTS page
↑ ^11.0 ^11.1 Marino S et al. (2002) PTEN is essential for cell migration but not for fate determination and tumourigenesis in the cerebellum. Development 129: 3513-22 PubMed GONUTS page
↑ García-García MJ et al. (2005) Analysis of mouse embryonic patterning and morphogenesis by forward genetics. Proc Natl Acad Sci U S A 102: 5913-9 PubMed GONUTS page
↑ Ma L et al. (2005) Genetic analysis of Pten and Tsc2 functional interactions in the mouse reveals asymmetrical haploinsufficiency in tumor suppression. Genes Dev 19: 1779-86 PubMed GONUTS page
↑ Manning BD et al. (2005) Feedback inhibition of Akt signaling limits the growth of tumors lacking Tsc2. Genes Dev 19: 1773-8 PubMed GONUTS page
↑ Kim JY et al. (2009) DISC1 regulates new neuron development in the adult brain via modulation of AKT-mTOR signaling through KIAA1212. Neuron 63: 761-73 PubMed GONUTS page
↑ ^16.0 ^16.1 Ozçelik M et al. (2010) Pals1 is a major regulator of the epithelial-like polarization and the extension of the myelin sheath in peripheral nerves. J Neurosci 30: 4120-31 PubMed GONUTS page
↑ ^17.0 ^17.1 Sun H et al. (1999) PTEN modulates cell cycle progression and cell survival by regulating phosphatidylinositol 3,4,5,-trisphosphate and Akt/protein kinase B signaling pathway. Proc Natl Acad Sci U S A 96: 6199-204 PubMed GONUTS page
↑ ^18.0 ^18.1 Ma X et al. (2005) Targeted biallelic inactivation of Pten in the mouse prostate leads to prostate cancer accompanied by increased epithelial cell proliferation but not by reduced apoptosis. Cancer Res 65: 5730-9 PubMed GONUTS page
↑ Ventruti A et al. (2011) Reelin deficiency causes specific defects in the molecular composition of the synapses in the adult brain. Neuroscience 189: 32-42 PubMed GONUTS page
↑ ^20.00 ^20.01 ^20.02 ^20.03 ^20.04 ^20.05 ^20.06 ^20.07 ^20.08 ^20.09 ^20.10 ^20.11 ^20.12 ^20.13 Kwon CH et al. (2006) Pten regulates neuronal arborization and social interaction in mice. Neuron 50: 377-88 PubMed GONUTS page
↑ ^21.0 ^21.1 ^21.2 Ogawa S et al. (2007) A seizure-prone phenotype is associated with altered free-running rhythm in Pten mutant mice. Brain Res 1168: 112-23 PubMed GONUTS page
↑ ^22.00 ^22.01 ^22.02 ^22.03 ^22.04 ^22.05 ^22.06 ^22.07 ^22.08 ^22.09 ^22.10 Fraser MM et al. (2008) Phosphatase and tensin homolog, deleted on chromosome 10 deficiency in brain causes defects in synaptic structure, transmission and plasticity, and myelination abnormalities. Neuroscience 151: 476-88 PubMed GONUTS page
↑ ^23.0 ^23.1 ^23.2 ^23.3 Page DT et al. (2009) Haploinsufficiency for Pten and Serotonin transporter cooperatively influences brain size and social behavior. Proc Natl Acad Sci U S A 106: 1989-94 PubMed GONUTS page
↑ ^24.0 ^24.1 ^24.2 Luikart BW et al. (2011) Pten knockdown in vivo increases excitatory drive onto dentate granule cells. J Neurosci 31: 4345-54 PubMed GONUTS page

[PMID:16107612-0] 1.0 ^1.1 ^1.2 ^1.3 ^1.4 ^1.5 Hamada K et al. (2005) The PTEN/PI3K pathway governs normal vascular development and tumor angiogenesis. Genes Dev 19: 2054-65 PubMed GONUTS page

[PMID:9990064-1] 2.0 ^2.1 Podsypanina K et al. (1999) Mutation of Pten/Mmac1 in mice causes neoplasia in multiple organ systems. Proc Natl Acad Sci U S A 96: 1563-8 PubMed GONUTS page

[PMID:16456542-2] 3.0 ^3.1 Takahashi Y et al. (2006) PTEN tumor suppressor associates with NHERF proteins to attenuate PDGF receptor signaling. EMBO J 25: 910-20 PubMed GONUTS page

[PMID:17218262-3] Shen WH et al. (2007) Essential role for nuclear PTEN in maintaining chromosomal integrity. Cell 128: 157-70 PubMed GONUTS page

[PMID:18190691-4] Pan Y et al. (2008) Na+/H+ exchanger regulatory factor 1 inhibits platelet-derived growth factor signaling in breast cancer cells. Breast Cancer Res 10: R5 PubMed GONUTS page

[PMID:14522255-5] 6.0 ^6.1 Wang S et al. (2003) Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer. Cancer Cell 4: 209-21 PubMed GONUTS page

[PMID:18332125-6] 7.0 ^7.1 Chang CJ et al. (2008) PTEN nuclear localization is regulated by oxidative stress and mediates p53-dependent tumor suppression. Mol Cell Biol 28: 3281-9 PubMed GONUTS page

[PMID:18562292-7] 8.0 ^8.1 Fouladkou F et al. (2008) The ubiquitin ligase Nedd4-1 is dispensable for the regulation of PTEN stability and localization. Proc Natl Acad Sci U S A 105: 8585-90 PubMed GONUTS page

[PMID:9778245-8] 9.0 ^9.1 Stambolic V et al. (1998) Negative regulation of PKB/Akt-dependent cell survival by the tumor suppressor PTEN. Cell 95: 29-39 PubMed GONUTS page

[PMID:21241890-9] 10.0 ^10.1 ^10.2 Song MS et al. (2011) Nuclear PTEN regulates the APC-CDH1 tumor-suppressive complex in a phosphatase-independent manner. Cell 144: 187-99 PubMed GONUTS page

[PMID:12091320-10] 11.0 ^11.1 Marino S et al. (2002) PTEN is essential for cell migration but not for fate determination and tumourigenesis in the cerebellum. Development 129: 3513-22 PubMed GONUTS page

[PMID:15755804-11] García-García MJ et al. (2005) Analysis of mouse embryonic patterning and morphogenesis by forward genetics. Proc Natl Acad Sci U S A 102: 5913-9 PubMed GONUTS page

[PMID:16027168-12] Ma L et al. (2005) Genetic analysis of Pten and Tsc2 functional interactions in the mouse reveals asymmetrical haploinsufficiency in tumor suppression. Genes Dev 19: 1779-86 PubMed GONUTS page

[PMID:16027169-13] Manning BD et al. (2005) Feedback inhibition of Akt signaling limits the growth of tumors lacking Tsc2. Genes Dev 19: 1773-8 PubMed GONUTS page

[PMID:19778506-14] Kim JY et al. (2009) DISC1 regulates new neuron development in the adult brain via modulation of AKT-mTOR signaling through KIAA1212. Neuron 63: 761-73 PubMed GONUTS page

[PMID:20237282-15] 16.0 ^16.1 Ozçelik M et al. (2010) Pals1 is a major regulator of the epithelial-like polarization and the extension of the myelin sheath in peripheral nerves. J Neurosci 30: 4120-31 PubMed GONUTS page

[PMID:10339565-16] 17.0 ^17.1 Sun H et al. (1999) PTEN modulates cell cycle progression and cell survival by regulating phosphatidylinositol 3,4,5,-trisphosphate and Akt/protein kinase B signaling pathway. Proc Natl Acad Sci U S A 96: 6199-204 PubMed GONUTS page

[PMID:15994948-17] 18.0 ^18.1 Ma X et al. (2005) Targeted biallelic inactivation of Pten in the mouse prostate leads to prostate cancer accompanied by increased epithelial cell proliferation but not by reduced apoptosis. Cancer Res 65: 5730-9 PubMed GONUTS page

[PMID:21664258-18] Ventruti A et al. (2011) Reelin deficiency causes specific defects in the molecular composition of the synapses in the adult brain. Neuroscience 189: 32-42 PubMed GONUTS page

[PMID:16675393-19] 20.00 ^20.01 ^20.02 ^20.03 ^20.04 ^20.05 ^20.06 ^20.07 ^20.08 ^20.09 ^20.10 ^20.11 ^20.12 ^20.13 Kwon CH et al. (2006) Pten regulates neuronal arborization and social interaction in mice. Neuron 50: 377-88 PubMed GONUTS page

[PMID:17706614-20] 21.0 ^21.1 ^21.2 Ogawa S et al. (2007) A seizure-prone phenotype is associated with altered free-running rhythm in Pten mutant mice. Brain Res 1168: 112-23 PubMed GONUTS page

[PMID:18082964-21] 22.00 ^22.01 ^22.02 ^22.03 ^22.04 ^22.05 ^22.06 ^22.07 ^22.08 ^22.09 ^22.10 Fraser MM et al. (2008) Phosphatase and tensin homolog, deleted on chromosome 10 deficiency in brain causes defects in synaptic structure, transmission and plasticity, and myelination abnormalities. Neuroscience 151: 476-88 PubMed GONUTS page

[PMID:19208814-22] 23.0 ^23.1 ^23.2 ^23.3 Page DT et al. (2009) Haploinsufficiency for Pten and Serotonin transporter cooperatively influences brain size and social behavior. Proc Natl Acad Sci U S A 106: 1989-94 PubMed GONUTS page

[PMID:21411674-23] 24.0 ^24.1 ^24.2 Luikart BW et al. (2011) Pten knockdown in vivo increases excitatory drive onto dentate granule cells. J Neurosci 31: 4345-54 PubMed GONUTS page

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MOUSE:PTEN

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