- abnormal kidney development / MGI
- abnormal telencephalon morphology / MGI
- abnormal midbrain morphology / MGI
- abnormal brain development / MGI
- exencephaly / MGI
- pulmonary hypoplasia / MGI
- edema / MGI
- respiratory failure / MGI
- abnormal kidney morphology / MGI
- dilated renal tubules / MGI
- renal hypoplasia / MGI
- single kidney / MGI
- decreased renal glomerulus number / MGI
- impaired branching involved in ureteric bud morphogenesis / MGI
- impaired lung alveolus development / MGI
- abnormal ureteric bud morphology / MGI
- decreased susceptibility to neuronal excitotoxicity / MGI
- small ureteric bud / MGI
- abnormal ureteric bud elongation / MGI
- impaired branching involved in terminal bronchiole morphogenesis / MGI
- neonatal lethality, complete penetrance / MGI
- lethality throughout fetal growth and development, incomplete penetrance / MGI
- renal glomerulus hypertrophy / MGI
- increased kidney apoptosis / MGI
- increased kidney cell proliferation / MGI
B6.129P2-Bag6tm1Mak/Cnbc
Status | Available to order |
EMMA ID | EM:07234 |
Citation information | RRID:IMSR_EM:07234 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
International strain name | B6.129P2-Bag6tm1Mak/Cnbc |
Alternative name | Bat 3 |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Bag6tm1Mak |
Gene/Transgene symbol | Bag6 |
Information from provider
Provider | Tak W Mak |
Provider affiliation | Division of Stem Cell and Developmental Biology, Advanced Medical Discovery Institute/Ontario Cancer Institute |
Genetic information | Targeting construct deletes exons 2-6 with neomycin cassette. |
Phenotypic information | Thymocytes from Bag6 (Bat3) deficient mice exhibit reduced induction of Bbc3 (Puma) and Cdkn1 (p21/CDKI/WAF1), and are resistant to DNA damage-induced apoptosis in vivo. Our data indicate that Bat3 is a novel and essential regulator of Trp53 (p53)-mediated responses to genotoxic stress, and that Bat3 controls DNA damage-induced acetylation of p53. |
Breeding history | Backcrossed 10 times to C57BL/6. |
References |
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Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | not known |
Information from EMMA
Archiving centre | CNB-CSIC, Centro Nacional de Biotecnologia, Madrid, Spain |
Animals used for archiving | heterozygous C57BL/6J males |
Disease and phenotype information
MGI phenotypes (gene matching)
Literature references
- Requirement for Casper (c-FLIP) in regulation of death receptor-induced apoptosis and embryonic development.;Yeh W C, Itie A, Elia A J, Ng M, Shu H B, Wakeham A, Mirtsos C, Suzuki N, Bonnard M, Goeddel D V, Mak T W, ;2000;Immunity;12;633-42; 10894163
- HLA-B-associated transcript 3 (Bat3)/Scythe is essential for p300-mediated acetylation of p53.;Sasaki Toru, Gan Eugene C, Wakeham Andrew, Kornbluth Sally, Mak Tak W, Okada Hitoshi, ;2007;Genes & development;21;848-61; 17403783
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