C57BL/6J-ApcMin/5H

Status

Available to order

EMMA IDEM:01724
International strain nameC57BL/6J-ApcMin/5H
Alternative nameApc<Min>, Line V
Strain typeInduced Mutant Strains : Chemically-induced
Allele/Transgene symbolApcMin,
Gene/Transgene symbolApc

Information from provider

ProviderMichelle Ellender
Provider affiliationHealth Protection Agency, Chilton, Didcot, Oxon OX11 0RQ
Genetic informationIntestinal polyposis (high multiplicity). The mutation is on chromosome 18 and is a transversion point mutation that alters nucleotide 2549 from a T to an A (mRNA: NM_001360980.1; protein: NM_007462.3). This converts codon 850 from one encoding a leucine to a stop codon (p.Leu850*), truncating the expected polypeptide. The Apc mutation is the homologue of the human APC (adenomatous polyposis coli) gene and the Min (multiple intestinal neoplasia) mice are highly susceptible to spontaneous intestinal tumour formation. This line (#5 or V) is distinct from the other ApcMin line (#2 or II) also submitted to EMMA (strain ID EM:01715). These different ApcMin lines have been described as having different severity of phenotype (Haines J et al., PNAS, 2005, doi: 10.1073/pnas.0500039102).
Phenotypic informationMice develop life-shortening intestinal polyposis.
References
  • 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
  • Genetic basis of variation in adenoma multiplicity in ApcMin/+ Mom1S mice.;Haines Jackie, Johnson Victoria, Pack Kevin, Suraweera Nirosha, Slijepcevic Predrag, Cabuy Erik, Coster Margaret, Ilyas Mohammad, Wilding Jennifer, Sieber Oliver, Bodmer Walter, Tomlinson Ian, Silver Andrew, ;2005;Proceedings of the National Academy of Sciences of the United States of America;102;2868-73; 15710876

Information from EMMA

Archiving centreMary Lyon Centre at MRC Harwell, Oxford, United Kingdom

Disease and phenotype information

MGI allele-associated human disease models

Orphanet associated rare diseases, based on orthologous gene matching

MGI phenotypes (allele matching)
  • 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

Literature references

  • 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
  • Genetic basis of variation in adenoma multiplicity in ApcMin/+ Mom1S mice.;Haines Jackie, Johnson Victoria, Pack Kevin, Suraweera Nirosha, Slijepcevic Predrag, Cabuy Erik, Coster Margaret, Ilyas Mohammad, Wilding Jennifer, Sieber Oliver, Bodmer Walter, Tomlinson Ian, Silver Andrew, ;2005;Proceedings of the National Academy of Sciences of the United States of America;102;2868-73; 15710876

Order

Availabilities

Requesting frozen sperm or embryos is generally advisable wherever possible, in order to minimise the shipment of live mice.

  • Frozen embryos. Delivered in 4 weeks (after paperwork in place). €1740*
  • Rederivation of mice from frozen stock, delivery time available upon request . €3880*

Due to the dynamic nature of our processes strain availability may change at short notice. The local repository manager will advise you in these circumstances.

* In addition users have to cover all the shipping costs (including the cost for returning dry-shippers, where applicable).

More details on pricing and delivery times

Practical information

Example health report
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Material Transfer Agreement (MTA)
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