Apcmin mice

Manufactured by Jackson ImmunoResearch

Sourced in United States, Montenegro, China

The ApcMin/+ mice are a genetically engineered mouse model used in research. These mice carry a mutation in the Apc gene, which is involved in tumor suppression. This mutation leads to the development of multiple intestinal neoplasia (MIN) in the mice.

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64 protocols using apcmin mice

Circadian Knockout Impacts Intestinal Tumorigenesis

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Mice were housed on a 12-hour light/12-hour dark cycle with ad libitum food in a barrier facility. Apc^min mice (#002020; Jackson Labs, Bar Harbor, ME) were crossed with Bmal1^+/- null mutant mice (#009100; Jackson Labs). Progeny were back-crossed for 7 generations to generate a genetically pure strain before experiments began. Bmal1^flox/flox mice (#007668; Jackson Labs) were crossed with Villin^Cre/+ mice (#021504; Jackson Labs), or Apc^min mice, then the 2 strains were crossed to obtain the Apc^min/+; Bmal1^flox/flox and Apc^min/+; Vil^Cre/+; Bmal1^flox/flox for the cKO experiments. Genotyping was performed according to protocols available at Jackson Labs (www.jax.org). All animals were tested for tumor initiation at 1 or 3 months of age. Mice maintained under constant light (LL) were housed in these conditions from 21 days of age to 3 months of age. Light levels were approximately 700 Lux, measured at the back of each cage, and all objects were removed so that light fully penetrated throughout each cage. Mice were maintained under Canadian Council for Animal Care guidelines (University of Windsor: AUPP 17-21).

Stokes K., Nunes M., Trombley C., Flôres D.E., Wu G., Taleb Z., Alkhateeb A., Banskota S., Harris C., Love O.P., Khan W.I., Rueda L., Hogenesch J.B, & Karpowicz P. (2021). The Circadian Clock Gene, Bmal1, Regulates Intestinal Stem Cell Signaling and Represses Tumor Initiation. Cellular and Molecular Gastroenterology and Hepatology, 12(5), 1847-1872.e0.

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Xenograft Mouse Models of Colorectal Cancer

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All animal experiments conform to our animal protocols that were approved by the Institutional Animal Care and Use Committee at Arizona State University. NSG and Apc^Min/+ mice were obtained from Jackson Laboratory (Bar Harbor, Maine). For the subcutaneous (sub-Q) injection, indicated cell numbers were injected into the flanks of male NSG mice at age of 7 weeks old. For the orthotopic mouse model, 1 × 10⁴ of cells derived from LS-174T, LS-174T/vector, LS-174T/shp65, or 5 × 10⁵ of cells derived from human primary CRC specimen were injected into the cecal wall of male NSG mice at age of 7 weeks old. Additional information on animal treatments is provided in Supplemental Methods.

Wang D., Fu L., Sun H., Guo L, & DuBois R.N. (2015). Prostaglandin E2 Promotes Colorectal Cancer Stem Cell Expansion and Metastasis in Mice. Gastroenterology, 149(7), 1884-1895.e4.

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Ghrelin Knockout Mouse Model for Colorectal Cancer

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All animal experiments were approved by the Institutional Animal Care and Use Committee of the University of Miyazaki. Mice were housed in plastic cages (four or five mice per cage) in a specific pathogen-free condition with free access to drinking water and a basal diet (Oriental Yeast Co., Ltd., Tokyo, Japan). C57BL/6 mice were obtained from Kyudo (Saga, Japan). Ghrelin knockout (Ghrl^−/−) mice were described previously.21 (link)
Apc^Min/+ mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA). Ghrelin-deleted Apc mutant mice were established by crossing Ghrl^−/− and Apc^Min/+ mice.

Kawaguchi M., Kanemaru A., Fukushima T., Yamamoto K., Tanaka H., Haruyama Y., Itoh H., Matsumoto N., Kangawa K., Nakazato M, & Kataoka H. (2015). Ghrelin administration suppresses inflammation-associated colorectal carcinogenesis in mice. Cancer Science, 106(9), 1130-1136.

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Conditional Deletion of Dnmt1 in Intestine

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Dnmt1^loxP/loxP mice were provided by Rudolf Jaenisch (20 (link)), Villin-Cre-ERT2 mice were received from Sylvia Robine (21 (link)), and Apc^Min/+ mice from the Jackson Laboratories (10 (link),12 (link)). For Dnmt1 deletion experiments, Cre-recombination activity was induced by three daily intraperitoneal injections of 1.6 mg tamoxifen (Sigma) in an ethanol/sunflower oil mixture. In all experiments, littermate controls without the VillinCreERT2 transgene were also tamoxifen treated. All procedures involving mice were conducted in accordance with approved Institutional Animal Care and Use Committee protocols.

Sheaffer K.L., Elliott E.N, & Kaestner K.H. (2016). DNA hypomethylation contributes to genomic instability and intestinal cancer initiation. Cancer prevention research (Philadelphia, Pa.), 9(7), 534-546.

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Genetic Mouse Models for Immunology Research

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Foxp3^Cre and Foxp3^Cre-ERT2 mice were described previously^{17 (link), 44}. Il2ra^fl mice were generated by J.D.F. Stat5a/b^fl mice were provided by L Henninghausen. Apc^Min mice were purchased from the Jackson Laboratory. The targeting strategies to generate Il2rb^fl (generated by U.K.) and Rosa26^Stat5bCA alleles are shown in Supplementary Fig. 7. Tcra^fl mice were described previously^{34 (link)}. The experimental mice were either generated on or backcrossed onto a C57BL/6J (B6) background, bred and housed in the specific pathogen-free animal facility at Memorial Sloan Kettering Cancer Center (MSKCC). All animal experiments were approved by institutional animal care and use committee at MSKCC and were performed in accordance with the institutional guidelines. For survival analysis, mice were monitored daily and unhealthy mice were euthanized once they are found lethargic and counted as non-survivors. For tamoxifen treatment, tamoxifen (Sigma-Aldrich) was dissolved in olive oil at a concentration of 40 mg/ml. Mice were given oral gavage of 100 μl of tamoxifen emulsion per treatment. In EAE and infection experiments, mice were challenged 2 to 3 months after a single tamoxifen gavage and assessed as described previously^{38 (link)}.

Chinen T., Kannan A.K., Levine A.G., Fan X., Klein U., Zheng Y., Gasteiger G., Feng Y., Fontenot J.D, & Rudensky A.Y. (2016). An essential role for IL-2 receptor in regulatory T cell function. Nature immunology, 17(11), 1322-1333.

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Preclinical Evaluation of PG545 in Colorectal Cancer

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Cells were detached with trypsin/EDTA, washed with PBS, and cell suspension was inoculated subcutaneously at the right flank of 6-week-old SCID/NOD (SW480; 5×10⁶) or Balb/C (CT26; 1×10⁵) mice. PG545 was administrated (i.p.; 20 mg/kg, once weekly) once tumors became palpable. Xenografts size was determined by externally measuring tumors in 2 dimensions using a caliper. At the end of the experiment, mice were sacrificed; tumor xenografts were removed, weighed, and fixed in formalin. Paraffin-embedded 5 μm sections were subjected to immunostaining with the indicated antibody using the Envision kit according to the manufacturer's (Dako) instructions, as described previously [23] (link), [24] (link).
APC Min^+/− mice were obtained from Jackson Laboratories (Bar Harbor, ME). In a tumor prevention experiment, PG545 (20 mg/kg; once weekly) was administrated to APC Min^+/− mice (n = 8) starting at 4 weeks of age. In a treatment setting, PG545 was given starting at 9 weeks of age (n = 10). In both settings, experiments were terminated at 19 weeks of age. Mice were then sacrificed, the colon and small bowel were exposed, and the number and size of polyps was evaluated. Polyps were immediately homogenized for RNA and protein extraction, or were fixed in formalin for histological and immunostaining analyses as described above.

Singh P., Blatt A., Feld S., Zohar Y., Saadi E., Barki-Harrington L., Hammond E., Ilan N., Vlodavsky I., Chowers Y, & Half E. (2017). The Heparanase Inhibitor PG545 Attenuates Colon Cancer Initiation and Growth, Associating with Increased p21 Expression. Neoplasia (New York, N.Y.), 19(3), 175-184.

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Conditional Epsin Double Knockout Mice

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We reported a strategy to generate an epsins 1 and 2 global double knockout (DKO) mouse model^{34 (link)}. We used a similar strategy with modifications to create a conditional knockout of epsin 1 (Epn1^fl/fl mice)^{34 (link),37 (link)}. Epn1^fl/fl mice were mated with Epn2^−/− null mice to generate Epn1^fl/fl;Epn2^−/− mice. Tamoxifen-inducible intestinal epithelial cell-specific DKO (IEpC-iDKO) mice were obtained by crossing Epn1^fl/fl;Epn2^−/− mice with Villin-ER^T2 Cre deleter mice which express Cre recombinase specifically in the IEpCs^{44 (link)}. To induce postnatal deletion of IEpC epsin 1, we administered 5 mg kg-1 (body weight) of 4-hydroxytamoxifen by intraperitoneal-injection into 10-week-old WT or Epn1^fl/fl;Epn2^−/−;Villin-ER^T2 mice every-second-day for two weeks. To generate the Apc^Min/IEpC-iDKO mice, we crossed our Epn1^fl/fl;Epn2^−/−;Villin-ER^T2 mice with Apc^Min mice purchased from Jackson Laboratories. All vertebrate procedures were performed in accordance with the Guide for the Care and Use of Laboratory Animals and were approved by the Institutional Animal Care and Use Committee at Oklahoma Medical Research Foundation.

Chang B., Tessneer K.L., McManus J., Liu X., Hahn S., Pasula S., Wu H., Song H., Chen Y., Cai X., Dong Y., Brophy M.L., Rahman R., Ma J.X., Xia L, & Chen H. (2015). Epsin is required for Dishevelled stability and Wnt signaling activation in colon cancer development. Nature communications, 6, 6380.

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Genetically Modified Mouse Models

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Mice were bred under specific pathogen-free conditions in the Animal Facility at Kobe University Graduate School of Medicine. Villin-Cre and Apc^Min/+ mice (strain #004586 and #002020, respectively) were purchased from the Jackson Laboratory (Bar Harbor, ME, USA). LAT1^fl/fl mice were generated as previously described [19 (link)], and LAT1^fl/fl; vil-cre; Apc^Min/+ and LAT1^fl/fl; Apc^Min/+ mice were generated by breeding these strains. All mice were of a C57BL/6J background, and both female and male mice were used in all experiments. All animal experiments were approved by the Institutional Animal Care and Use Committee of Kobe University (approval number: P190307).

Sui Y., Hoshi N., Ohgaki R., Kong L., Yoshida R., Okamoto N., Kinoshita M., Miyazaki H., Ku Y., Tokunaga E., Ito Y., Watanabe D., Ooi M., Shinohara M., Sasaki K., Zen Y., Kotani T., Matozaki T., Tian Z., Kanai Y, & Kodama Y. (2023). LAT1 expression influences Paneth cell number and tumor development in ApcMin/+ mice. Journal of Gastroenterology, 58(5), 444-457.

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Transgenic Mouse Characterization Protocol

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The C57BL/6J mice were obtained from the Guangdong Medical Laboratory Animal Center. The Apc^Min/+ mice were obtained from the Jackson Laboratory (Bar. Harbor, Maine, USA). The Slit2 transgenic mice were generated and donated by Dr. Jianguo Geng (University of Michigan, USA) according to the published procedures [40 (link)], and more detailed description of the experimental procedures is provided as the Supplementary Materials and Methods. Verification of the successful transgene expression is provided as the Supplementary Figures 2 A-C. Use of the animals in this project was approved by the Ethics Committee of the Center of Laboratory Animals, Guangdong Pharmaceutical University. All mice were maintained under a 12-h light/dark cycle in a climate-controlled room at 24 ± 2°C and 60 ± 5% humidity. All surgical procedures were performed under diethylether anesthesia. BrdU was intraperitoneally injected into the mice at a dose of 0.1 mg/g body weight 1.5 hours before sacrifice.

Zhang Q.Q., Zhou D.L., Lei Y., Zheng L., Chen S.X., Gou H.J., Gu Q.L., He X.D., Lan T., Qi C.L., Li J.C., Ding Y.Q., Qiao L, & Wang L.J. (2014). Slit2/Robo1 signaling promotes intestinal tumorigenesis through Src-mediated activation of the Wnt/β-catenin pathway. Oncotarget, 6(5), 3123-3135.

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Genetic Mouse Models for Immunology Research

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