B6.Cg-Bclaf1tm1Lfmp Tg(Vav1-cre)1Cgp/Ieg
Status | Available to order |
EMMA ID | EM:04562 |
Citation information | RRID:IMSR_EM:04562 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.Cg-Bclaf1tm1Lfmp Tg(Vav1-cre)1Cgp/Ieg |
Alternative name | Bclaf1 x Tg Vav cre C57BL/6 |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Bclaf1tm1Lfmp, Tg(Vav1-cre)1Cgp |
Gene/Transgene symbol | Bclaf1, Tg(Vav1-cre)1Cgp |
Information from provider
Provider | Rosel Blasig |
Provider affiliation | Research Institute of Molecular Pharmacology |
Genetic information | Promoterless reporter gene (NotI-NheI fragment of the pSA-betaGeo-lox2PGKDTA vector) containing a loxP-flanked cassette of splice acceptor, beta-galactosidase/lacZ gene and neo gene; inserted into intron between Bclaf1 exon 3 (translation start at ATG) and exon 4 by targeted mutagenesis. After breeding of heterozygous mice with transgenic Vav-cre mice on C57BL/6 genetic background the Bclaf1-/- Vav-cre+ mice are chimeras. Where the Vav promotor-driven cre recombinase is well expressed (bone marrow, spleen, blood cells, heart and lung), the Bclaf1 genotype switches from -/- via -/del to del/del (wild-type with an additional loxP site in the intron between exon 3 and 4 due to removal of loxP-flanked marker cassette). In organs without Vav promotor-driven cre recombinase expression (ear, eye, tong, optic nerve) the genotype of the mice is Bclaf1-/- Vav-cre+. |
Phenotypic information | All Bclaf1-/- Vav-cre+ mice survive to normal life span with normal body weight. The males and females are fertile. Bclaf1-/- Vav cre-(minus) mice survive only 2-4 weeks and have 70-80% body size at birth and 35-75% body weight at 14 d age compared to littermates. If older than 2 weeks they move slowly, lay sometimes for a short time on the side, some behave sometimes like epileptically for a short time; they do not learn rearing and climbing; lower body temperature starts 4 days postnatally, lower blood glucose starts 7 days postnatally. The Bclaf1 Vav cre-(minus) mice are deposited as Bclaf1 RK BL6 on C57BL/6 background, at EMMA since 2006 (strain EM:01978). |
Breeding history | Bclaf1 knock-out line backcrossed to C57BL/6 more than 10 generations (inbred); breeding with transgenic line expressing cre recombinase under Vav1 oncogene (Vav-cre) on C57BL/6 background. |
References |
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Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | Helmholtz Zentrum Muenchen - German Research Center for Environmental Health (GmbH), Oberschleißheim, Germany |
Animals used for archiving | heterozygous C57BL/6 males, wild-type C57BL/6 females |
Stage of embryos | 2-cell |
Disease and phenotype information
IMPC phenotypes (gene matching)
MGI phenotypes (allele matching)
- no phenotypic analysis / MGI
MGI phenotypes (gene matching)
- polydactyly / MGI
- abnormal lung development / MGI
- decreased body size / MGI
- no phenotypic analysis / MGI
- increased B cell number / MGI
- decreased T cell proliferation / MGI
- decreased CD8-positive, alpha-beta T cell number / MGI
- absent gastric milk in neonates / MGI
- postnatal lethality, complete penetrance / MGI
- thick lung-associated mesenchyme / MGI
- abnormal mesenchymal cell differentiation involved in lung development / MGI
Literature references
- Hematopoietic stem cell transplantation without irradiation.;Waskow Claudia, Madan Vikas, Bartels Susanne, Costa Céline, Blasig Rosel, Rodewald Hans-Reimer, ;2009;Nature methods;6;267-9; 19270698
- Essential role for Bclaf1 in lung development and immune system function.;McPherson J Peter, Sarras H, Lemmers B, Tamblyn L, Migon E, Matysiak-Zablocki E, Hakem A, Azami S Alizadeh, Cardoso R, Fish J, Sanchez O, Post M, Hakem R, ;2009;Cell death and differentiation;16;331-9; 19008920
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