- abnormal mammary gland development / MGI
- abnormal ovarian folliculogenesis / MGI
- abnormal ovarian follicle morphology / MGI
- absent mature ovarian follicles / MGI
- absent corpus luteum / MGI
- abnormal vagina epithelium morphology / MGI
- decreased body weight / MGI
- increased incidence of induced tumors / MGI
- ovary atrophy / MGI
- uterus atrophy / MGI
- reproductive system phenotype / MGI
- adrenal gland hyperplasia / MGI
- absent nipple / MGI
- increased mammary gland tumor incidence / MGI
- mammary gland hyperplasia / MGI
- anemia / MGI
- premature death / MGI
- increased intestinal adenoma incidence / MGI
- increased intestinal adenocarcinoma incidence / MGI
- abnormal pregnancy / MGI
- extended life span / MGI
- aneuploidy / MGI
- increased incidence of tumors by chemical induction / MGI
- decreased intestinal adenoma incidence / MGI
- decreased hematocrit / MGI
- hyperlipidemia / MGI
- melena / MGI
- rectal prolapse / MGI
- abnormal intestinal mucosa morphology / MGI
- increased mammary adenocarcinoma incidence / MGI
- intestinal obstruction / MGI
- abnormal intestinal goblet cell morphology / MGI
- abnormal large intestine crypts of Lieberkuhn morphology / MGI
- intestine polyps / MGI
- abnormal enterocyte proliferation / MGI
- decreased T cell number / MGI
- decreased NK cell number / MGI
- decreased splenocyte number / MGI
- neoplasm / MGI
- increased circulating triglyceride level / MGI
- increased circulating free fatty acid level / MGI
- postnatal growth retardation / MGI
- increased colonic adenoma incidence / MGI
- hepatic steatosis / MGI
- decreased macrophage cell number / MGI
- increased prostaglandin level / MGI
- abnormal embryo development / MGI
- abnormal embryo size / MGI
- abnormal egg cylinder morphology / MGI
- abnormal cell physiology / MGI
- embryonic lethality, complete penetrance / MGI
- decreased embryo size / MGI
- embryonic lethality between implantation and placentation / MGI
- absent mandible / MGI
- abnormal brain development / MGI
- acrania / MGI
- perinatal lethality, complete penetrance / MGI
- lethality throughout fetal growth and development, incomplete penetrance / MGI
- absent midbrain / MGI
- absent forebrain / MGI
- decreased susceptibility to experimental autoimmune encephalomyelitis / MGI
- decreased T cell proliferation / MGI
- abnormal digestive system physiology / MGI
- immune system phenotype / MGI
- abnormal T-helper 1 physiology / MGI
- abnormal T-helper 2 physiology / MGI
B6Rcc.Cg-Cd44tm1.1Ugu ApcMin/Cnrm
Status | Available to order |
EMMA ID | EM:02001 |
International strain name | B6Rcc.Cg-Cd44tm1.1Ugu ApcMin/Cnrm |
Alternative name | C57 BL/6RCC Min/+ CD44v6v7-/- |
Strain type | Induced Mutant Strains : Chemically-induced |
Allele/Transgene symbol | ApcMin, |
Gene/Transgene symbol | Apc |
Information from provider
Provider | Ursula Günthert |
Provider affiliation | Institut für Pathologie, University of Basel |
Genetic information | Ethylnitrosurea induced mutation. A transversion point mutation in the Apc (adenomatosis polyposis coli) gene that alters nucleotide 2549 from a T to an A and converts codon 850 from one encoding a leucine to a stop codon, generating the mutant allele ApcMin(adenomatosis polyposis coli; multiple intestinal neoplasia). A loxP site was inserted 3' of exon v6 and a neomycin resistance cassette, with a 5' loxP site, was inserted 5' of exon v6 of the Cd44 gene. During insertion, 1.6 kb of sequence was lost in the exon v7 region; cre recombinase was transiently expressed in ES cells allowing the removal of neomycin cassette and exon v6. Mice lack both exon v6 and v7. |
Phenotypic information | Min/+: Development of early stages of colon carcinoma: polyps. Cd44v6v7-/-: Expression of Cd44v6 is an independent prognostic factor for a poor prognosis in colon carcinoma. Expression of Cd44v6 isoforms has been shown to be an independent prognostic factor for a poor prognosis in human colon carcinoma (Mulder et al., 1994). To determine whether and to what extent Cd44v6/v7-containing isoforms are involved in the early stages of adenoma formation, we crossbred ApcMin mice with mice bearing deletions for Cd44v6/v7. While Min/+ x Cd44v6/v7 wild-type mice developed on the average more than 50 adenomas at an age of 12-18 weeks, Min/+ x Cd44v6/v7 knock-out mice developed fewer than 10 adenomas, and many had no polyps at all. Moreover, the life span of Min/+ x Cd44v6/v7 null mice increased substantially to more than 60 weeks (p |
Breeding history | 10 generations backcrossed onto C57BL/6Rcc; currently maintained as C57BL/6Rcc Min/+ Cd44v6v7-/-. |
References |
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Information from EMMA
Archiving centre | CNR, Consiglio Nazionale delle Ricerche, Monterotondo, Italy |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- Desmoid tumor / Orphanet_873
- Cenani-Lenz syndrome / Orphanet_3258
- Turcot syndrome with polyposis / Orphanet_99818
- Gastric adenocarcinoma and proximal polyposis of the stomach / Orphanet_314022
- Gardner syndrome / Orphanet_79665
- APC-related attenuated familial adenomatous polyposis / Orphanet_247806
MGI phenotypes (allele matching)
Literature references
- Abrogation of experimental colitis correlates with increased apoptosis in mice deficient for CD44 variant exon 7 (CD44v7).;Wittig B M, Johansson B, Zöller M, Schwärzler C, Günthert U, ;2000;The Journal of experimental medicine;191;2053-64; 10859330
- A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse.;Moser A R, Pitot H C, Dove W F, ;1990;Science (New York, N.Y.);247;322-4; 2296722
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