Strain Data Sheet

RBRC01872

Strain Information

Image
BRC No.RBRC01872
TypeTargeted MutationCartagena
SpeciesMus musculus
Strain nameFVB;129P2(Cg)-Apc<tm2.1Cip>/GvnRbrc
Former Common nameApcFlox14
H-2 Haplotype
ES Cell line
Background strain
Appearancealbino [A/A B/B c/c D/D P/P]
Strain developmentDeveloped by Dr. Marco Giovannini, INSRM France. FVB/N background.
Strain descriptionFVB.Cg-Apc<tm2.1Cip>. Apc, adenomatosis polyposis coli is a member of the Wnt signaling pathway that is involved in development and tumorigenesis. This conditional knockout mice have a loxP-flanked Apc allele. Conditional Apc deficient mice can be generated by crossing with tissue-specific Cre mice.
Colony maintenanceSibling Mating
References
Liver-targeted disruption of Apc in mice activates beta-catenin signaling and leads to hepatocellular carcinomas.
Colnot S, Decaens T, Niwa-Kawakita M, Godard C, Hamard G, Kahn A, Giovannini M, Perret C
Proc. Natl. Acad. Sci. USA, 101, 17216-17221 (2004). 15563600

Colorectal cancers in a new mouse model of familial adenomatous polyposis: influence of genetic and environmental modifiers.
Colnot S, Niwa-Kawakita M, Hamard G, Godard C, Le Plenier S, Houbron C, Romagnolo B, Berrebi D, Giovannini M, Perret C
Lab Invest., 84, 1619-1930 (2004). 15502862

Health Report

Examination Date / Room / Rack

Gene

Gene SymbolGene NameChr.Allele SymbolAllele NameCommon NamesPromoterDiseases Related to This Gene
Apc
MGI:88039		APC, WNT signaling pathway regulator18Apc<tm2.1Cip>
MGI:3521822		targeted mutation 2.1, Christine Perret
  • classic familial adenomatous polyposis(DisGeNET)

  • colorectal cancer(MedGEN)

  • colorectal carcinoma(DisGeNET)
    • more 5 Diseases
  • desmoid tumor(DisGeNET)

  • familial adenomatous polyposis 1(MedGEN)

  • gastric adenocarcinoma and proximal polyposis of the stomach(MedGEN)

  • gastric cancer(MedGEN)

  • hepatocellular carcinoma(MedGEN)
    • loxP phage P1 loxP18loxP
    loxP phage P1 loxP18loxP

    Phenotype

    Annotation by Mammalian phenotyhpe ontology
  • abnormal NK T cell physiology(MP:0008042)

  • abnormal autophagy(MP:0008260)

  • abnormal colon morphology(MP:0000495)

  • abnormal gut flora balance(MP:0010377)

  • abnormal intestinal epithelium morphology(MP:0000488)
    • more 17 phenotypes
  • abnormal intestinal goblet cell morphology(MP:0003449)

  • abnormal liver morphology(MP:0000598)

  • abnormal small intestine crypts of Lieberkuhn morphology(MP:0004841)

  • cachexia(MP:0005150)

  • decreased NK T cell number(MP:0008040)

  • enlarged liver(MP:0000599)

  • increased colon adenoma incidence(MP:0002044)

  • increased hepatocellular carcinoma incidence(MP:0003331)

  • increased interferon-gamma secretion(MP:0008566)

  • increased interleukin-4 secretion(MP:0008699)

  • increased intestinal adenocarcinoma incidence(MP:0002957)

  • increased intestinal adenoma incidence(MP:0002404)

  • intestine polyps(MP:0008011)

  • liver hyperplasia(MP:0005141)

  • liver inflammation(MP:0001860)

  • premature death(MP:0002083)

  • rectal prolapse(MP:0000493)
    • Detailed phenotype data

    Ordering Information

    Donor DNAPhage P1 loxP sites, mouse Apc genomic DNA
    Research applicationCre/loxP system
    Specific Term and ConditionsIn publishing the research results obtained by use of the BIOLOGICAL RESOURCE, a citation of the following literature(s) designated by the DEPOSITOR is requested. Proc. Natl. Acad. Sci., 101, 17216-17221 (2004). Lab Invest., 84, 1619-1930 (2004). In publishing the research results to be obtained by use of the BIOLOGICAL RESOURCE, an acknowledgment to the DEPOSITOR is requested. RECIPIENT shall keep DEPOSITOR apprised of any results obtained from the BIOLOGICAL RESOURCE in the course of the research, as soon as they are available. Moreover, if the research results in a potential invention or a substance that may have potential commercial value (hereinafter referred as to the "Invention") RECIPIENT will promptly disclose this Invention to DEPOSITOR with samples thereof for DEPOSITOR's internal use.
    RECIPIENT and DEPOSITOR will consult together and agree about the possibility of filing one or more patent application to Invention conceived by one or more employees of Recipients that directly arise out of the research. The Parties will negotiate in good faith the conditions of such patent application according to each party's inventiveness contribution in the Invention.
    In case of such Invention, patentable or not, reduced in practice or developed in the course of the research that could not have been obtained, reduced to practice or developed but from using the Material and/or Confidential Information, RECIPIENT and DEPOSITOR shall confer with one another as regards licensing and commercialization of such Invention to negotiate in good faith the terms of an institutional agreement as regards said matters.
    DepositorMarco Giovannini (INSERM)
    Strain Statusan icon for Frozen embryosFrozen embryos
    Strain AvailabilityRecovered litters from cryopreserved embryos (2 to 4 months)
    Cryopreserved embryos (within 1 month)
    Additional Info.Necessary documents for ordering:
    1. Order form (Japanese / English)
    2. Category I MTA: MTA for distribution with RIKEN BRC (Japanese / English)
    3. Acceptance of responsibility for living modified organism (Japanese / English)

    Genotyping protocol -PCR-

    BRC mice in Publications

    Ishibashi F, Shimizu H, Nakata T, Fujii S, Suzuki K, Kawamoto A, Anzai S, Kuno R, Nagata S, Ito G, Murano T, Mizutani T, Oshima S, Tsuchiya K, Nakamura T, Watanabe M, Okamoto R.
    Contribution of ATOH1+ Cells to the Homeostasis, Repair, and Tumorigenesis of the Colonic Epithelium.
    Stem Cell Reports 10(1) 27-42(2018) 29233556
    Nakata T, Shimizu H, Nagata S, Ito G, Fujii S, Suzuki K, Kawamoto A, Ishibashi F, Kuno R, Anzai S, Murano T, Mizutani T, Oshima S, Tsuchiya K, Nakamura T, Hozumi K, Watanabe M, Okamoto R.
    Indispensable role of Notch ligand-dependent signaling in the proliferation and stem cell niche maintenance of APC-deficient intestinal tumors.
    Biochem Biophys Res Commun 482(4) 1296-1303(2017) 27939883
    Funato Y, Yamazaki D, Mizukami S, Du L, Kikuchi K, Miki H.
    Membrane protein CNNM4-dependent Mg2+ efflux suppresses tumor progression.
    J Clin Invest 124(12) 5398-410(2014) 25347473