This strain is currently unavailable due to replenishing of cryopreserved stocks.
This inbred strain is characterized by increased sensitivity to initiation of skin tumors by carcinogens.Read More +
This strain may be homozygous for Gnat2cpfl3, cone photoreceptor function loss 3, which affects bright light (photopic) vision.
The acronym SENCAR is derived from SENsitivity to CARcinogenesis. SENCAR mice are commonly used for studies of susceptibility and resistance to the induction of skin tumors. Dr. Michael Potter of the National Cancer Institute developed three inbred lines, designated A, B, and C, from random breeding of outbred SENCAR mice. Characterization of these mice for sensitivity to skin tumor development indicated that mice of all three inbred strains displayed increased sensitivity to initiation by 7,12-dimethylbenz[a]anthracene (DMBA), urethane, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Promotion by mezerein as well as carcinogenesis by repeated treatment with DMBA or MNNG produced papillomas with a high frequency of conversion to squamous cell carcinomas (SCCs). Compared with outbred SENCAR mice, development of both squamous papillomas and carcinomas was increased at least two-fold by all protocols tested.
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||age related hearing loss 1; Cdh23ahl|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|Gene Synonym(s)||bob; bustling; bobby; nmf112; nmf252; nmf252; 4930542A03Rik; ahl; 4930542A03Rik; W; sals; mdfw; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; modifier of deaf waddler; age related hearing loss 1; v; USH1D; nmf181; RIKEN cDNA 4930542A03 gene; CDHR23; sals; waltzer; nmf112; nmf181; mdfw; neuroscience mutagenesis facility, 112; bus; ahl; bob; salsa; PITA5|
|Strain of Origin||multiple strains|
|Molecular Note||Genetic complementation tests have shown allelism between the mdfw (modifier of deaf waddler) locus and the ahl locus. Further analysis has shown this is caused by a G to A transition at nucleotide position 753 of Cdh23. This hypomorphic allele causes in frame skipping of exon 7, which is predicted to delete part of the 2nd and 3rd ectodomains, and cause reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD-1, RBF/DnJ, PL/J, AKR/J, RF/J, BALB/cBy, A/WySnJ, P/J, SENCARA/PtJ, DBA/1J, ALS/LtJ, C58/J, C57BLKS/J, 129P1/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129X1/SvJ, NOR/LtJ, A/J, C57BL/6, NOD/LtJ, DBA/2J, ALR/LtJ, C57L/J. Strains classified with ahl that DO NOT carry this mutation include: C3H/HeSnJ, I/LnJ, YBR/Ei, MRL/MpJ.|
|Allele Name||cone photoreceptor function loss 3|
|Allele Synonym(s)||cone photoreceptor function loss 3; Gnat2cpfl3|
|Gene Symbol and Name||Gnat2, guanine nucleotide binding protein, alpha transducing 2|
|Gene Synonym(s)||ACHM4; expressed sequence AW490837; Gt-2; Gnat-2; Tcalpha; Gnat-2; GNATC; AW490837|
|Strain of Origin||various|
|General Note||This allele has been detected in the following strains either by genotyping or complementation testing: ALS/LtJ, SENCARA/PtJ, SENCARB/PtJ, SENCARC/PtJ, PN/nBSwUmabJ. (J:122428) The allele has also been reported in NMRI and CD1 (Lluis Montoliu, J:212307)|
|Molecular Note||A single nucleotide substitution of G to A at position 598 in exon 6. This mutation converts codon 200 from aspartic acid to asparagine.|
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