IMPC phenotypes (gene matching)
B6.129P2-Acvr1ctm1Cfi/Kctt
| Status | Available to order |
| EMMA ID | EM:02574 |
| Citation information | RRID:IMSR_EM:02574 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-Acvr1ctm1Cfi/Kctt |
| Alternative name | Alk7 knock-out mice |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Acvr1ctm1Cfi |
| Gene/Transgene symbol | Acvr1c |
Information from provider
| Provider | Carlos Ibanez |
| Provider affiliation | Neuroscience, Karolinska Institutet |
| Genetic information | A targeting vector was designed to insert a lacZ gene (followed by a reverse-oriented neomycin cassette) in frame with the start codon of the Alk-7 gene (Acvr1c). This also deleted a portion of exon 1 and intron 1 (75 bp after the ATG start codon in the 3' end of the first exon and 664 bp from the 5' end of the first intron). |
| Phenotypic information | Increased serum insulin levels, decreased white fat deposition and partial resistance to high fat diet-induced obesity. Mutant mice harbor a beta-galactosidase "knock-in" allele that also abolishes endogenous gene function. |
| Breeding history | The construct was electroporated into 129P2/OlaHsd-derived E14 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts and chimeric males were bred with either 129/Sv or C57BL/6 to establish the colony. Mice were then backcrossed to C57BL/6 for 11 generations. |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | not known |
Information from EMMA
| Archiving centre | Karolinska Institutet, Stockholm, Sweden |
Disease and phenotype information
MGI phenotypes (gene matching)
- no abnormal phenotype detected / MGI
Literature references
- ALK7, a receptor for nodal, is dispensable for embryogenesis and left-right patterning in the mouse.;Jörnvall Henrik, Reissmann Eva, Andersson Olov, Mehrkash Mehrnaz, Ibáñez Carlos F, ;2004;Molecular and cellular biology;24;9383-9; 15485907
- Activin B receptor ALK7 is a negative regulator of pancreatic beta-cell function.;Bertolino Philippe, Holmberg Rebecka, Reissmann Eva, Andersson Olov, Berggren Per-Olof, Ibáñez Carlos F, ;2008;Proceedings of the National Academy of Sciences of the United States of America;105;7246-51; 18480258
- Growth/differentiation factor 3 signals through ALK7 and regulates accumulation of adipose tissue and diet-induced obesity.;Andersson Olov, Korach-Andre Marion, Reissmann Eva, Ibáñez Carlos F, Bertolino Philippe, ;2008;Proceedings of the National Academy of Sciences of the United States of America;105;7252-6; 18480259
- A novel type I receptor serine-threonine kinase predominantly expressed in the adult central nervous system.;Rydén M, Imamura T, Jörnvall H, Belluardo N, Neveu I, Trupp M, Okadome T, ten Dijke P, Ibáñez C F, ;1996;The Journal of biological chemistry;271;30603-9; 8940033
- The orphan receptor ALK7 and the Activin receptor ALK4 mediate signaling by Nodal proteins during vertebrate development.;Reissmann E, Jörnvall H, Blokzijl A, Andersson O, Chang C, Minchiotti G, Persico M G, Ibáñez C F, Brivanlou A H, ;2001;Genes & development;15;2010-22; 11485994
- ALK7 protects against pathological cardiac hypertrophy in mice.;Huang He, Tang Yanhong, Wu Gang, Mei Yang, Liu Wanli, Liu Xiaoxiong, Wan Nian, Liu Yu, Huang Congxin, ;2015;Cardiovascular research;108;50-61; 26249805