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|Status||Page||User||Date/Time||GO Term (Aspect)||Reference||Evidence||Notes||Links|
|RAT:P53||Cermakme, MichSt14A 5||2014-04-06 07:14:12 CDT||GO:0009790 embryo development (P)||PMID:23230510||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 3c: Mutant chimeras were created through blastocyte injection. The p53-/ESC- chimeras were the least likely to develop to become neonates when compared to p53+/ESC+ and p53+/ESC- chimeras.
Figure 3d: Of the injected chimeras, p53-/ESC- chimeras were the least likey to have normal body size at the end of embryo development when compared to p53+/ESC+ and p53+/ESC- chimera.
|MOUSE:FAS||Cermakme, MichSt14A 5||2014-04-05 23:53:52 CDT||GO:0030879 mammary gland development (P)||PMID:24668799||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 6: Average mammary gland lumen size was measured on various days of lactation across three pregnancies in FASN null mutants and wild type lactating mice. The FASN null mutant mice had decreased mammary gland lumen size when compared to wild type lumen size supporting that FASN is involved in mammary gland development.
|?||Cermakme, MichSt14A 5||2014-04-05 23:38:14 CDT||GO:0018991 oviposition (Figure 1: PAK1 Deficient strains of C. elegans (RB689) have decreased numbers of eggs laid per female worm compared to wild type worms.)||PMID:23524941||IMP: Inferred from Mutant Phenotype||challenge|
|MOUSE:BMAL1||Cermakme, MichSt14A 5||2014-04-05 14:20:44 CDT||GO:0060137 maternal process involved in parturition (P)||PMID:22697126||ECO:0000315 mutant phenotype evidence used in manual assertion|
Table 1: Pregnant female rats with disrupted copies of Bmal1 were significantly less likely rats with normal copies of Bmal1 to give birth at a normal (expected) time.
|MOUSE:CUL4A||Cermakme, MichSt14A 5||2014-04-05 13:48:43 CDT||GO:0001701 in utero embryonic development (P)||PMID:12077329||ECO:0000315 mutant phenotype evidence used in manual assertion|
Table 1: In the group of offspring produced from heterozygous CUL4A mutant crosses, no homozygous CUL4A mutants were viable past the blastocyte stage. There were also significanly fewer heterozygote pups than expected based on mendialian genetics. This shows that CUL4A plays an important role in embryo development.
|MOUSE:GCST||Cermakme, MichSt14A 5||2014-04-05 13:19:14 CDT||PMID:22171071||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 4: Mice that were heterozygous for the AMT- mutation had significantly decreased glycine cleavage system activity than wild type mice. Mice that were homozygous for the AMT- mutation had undetectable levels of GCS activity.
|CAMJE:Q0PBH4||Cermakme, MichSt14A 5||2014-04-04 15:43:54 CDT||GO:1902210 positive regulation of bacterial-type flagellum assembly (P)||PMID:12055288||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 2: Electron microscopy images show that C. jejuni flhB mutants lack flagella while wild type C. jejuni have normal flagella and normal cell shape.
Figure 3a: Western immunoblot probed with a flagellum-specific monoclonal antibody (P2D3) show that flhB mutants do not express FlaA (a flagellar protein). This decreased expression of flagellar proteins in flhB mutants is believed to partly cause the lack of motility.
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