P53flox

Manufactured by Jackson ImmunoResearch

Sourced in United States

P53flox is a DNA sequence used in genetic engineering. It contains the gene for the p53 protein, which is a tumor suppressor. The sequence is designed to be incorporated into cells or organisms to study the function and regulation of the p53 gene.

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Lab products found in correlation

5 protocols using p53flox

Genetically Engineered Mouse Models for Lung Cancer

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Kras^LSL-G12D (JAX #008179 (ref. [16 (link)])) (Jackson Laboratory, Bar Harbor, ME, USA), p53^flox (JAX #008462 (ref. [40 (link)])), FVB Kras^LSL-G12Dp53^flox (gift from F. Slack), and Gata6^flox (JAX #008196 (ref. [18 (link)])) mice were backcrossed to FVB or C57Bl/6 background for ten generations to obtain FVB and C57Bl/6 KP, KPG, K, and KG lines. Tumors were initiated by intratracheal infection of mice with viral vectors expressing Cre. Additional details are included in Supplementary Table 5. For syngeneic grafts, 6-week-old C57Bl/6 (JAX #00064) mice were injected subcutaneously with SPC-Cre tumor cells. For delayed expression of shRNAs, 7-week-old Athymic NCr-nu/nu (Charles River NCI #553) mice were injected subcutaneously with SPC-Cre cells containing doxycycline inducible shRNAs. Tumor growth was measured by bioluminescent imaging using an IVIS Spectrum or calipers. All animal studies were approved by the Yale University Institutional Animal Care and Use Committee.

Arnal-Estapé A., Cai W.L., Albert A.E., Zhao M., Stevens L.E., López-Giráldez F., Patel K.D., Tyagi S., Schmitt E.M., Westbrook T.F, & Nguyen D.X. (2020). Tumor progression and chromatin landscape of lung cancer are regulated by the lineage factor GATA6. Oncogene, 39(18), 3726-3737.

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Induced p53 Ablation and ApoE Deficiency in Mice

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All animal procedures were carried out in accordance with CCAC guidelines and Queen’s University Animal Care Committee (UACC), Kingston, Ontario, Canada specifically approved this study (protocol: Mak-2011-002-Or-A1).In order to ameliorate suffering, the health status of mice was monitored daily by animal care staff and if mice were found to be experiencing undue suffering, they were euthanized immediately. Mice on a C57BL/6 genetic background p53 Flox (stock 8462 Jackson Laboratories), Apoe^tm1Unc (stock 2052 Jackson Laboratories) or αSMA-Cre-ER^T2 (Pierre Chambon, IGBMC Strasbourg, France) were crossbred to create the various genotypes required for this study (Fig 1A). Mice (ApoE, p53 and Cre recombinase) were genotyped by PCR analyses using primers and protocols from The Jackson Laboratory. Mice were kept on a 12-hour light/dark schedule for the duration of the study and fed normal mouse chow (5015, PMI, St. Louis Missouri). Six week-old mice were intraperitoneally injected with five daily injections of 1 mg tamoxifen to induce p53 ablation as previously described [16 (link),21 (link)]. At the age of 7 weeks, experimental mice were switched to a Western diet (TD88137, Harlan Teklad) for 6, 10 or 15 weeks as indicated. Food and water were available ad libitum.

Cao R.Y., Eves R., Jia L., Funk C.D., Jia Z, & Mak A.S. (2017). Effects of p53-knockout in vascular smooth muscle cells on atherosclerosis in mice. PLoS ONE, 12(3), e0175061.

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Mouse lines for genetic studies

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Wild type C57BL/6J mice and the following mutant mouse lines were obtained from The Jackson Laboratory: Pten^flox (stock # 004597) (Groszer et al., 2001 (link)), p53^flox (stock # 008462) (Marino et al., 2000 (link)), p21 KO (stock # 003263) (Brugarolas et al., 1995 (link)), mGfap-Cre line 77.6 (stock # 024098) (Gregorian et al., 2009 (link)), Thy1-STOP-YFP (stock # 005630) (Buffelli et al., 2003 (link)), and Rosa-tdT (stock # 007914) (Madisen et al., 2010 (link)). Unless otherwise stated, both male and female mice at 8 weeks and older were used for all experiments. All mice were housed under a controlled temperature and a 12-h light/dark cycle with free access to water and food in an animal facility at UT Southwestern. The sample sizes were empirically determined. The experiments were not randomized and the researchers were not blinded to the allocation of animals during experiments and outcome assessment. All experimental procedures and protocols were approved by the Institutional Animal Care and Use Committee at UT Southwestern.

Wang L.L., Su Z., Tai W., Zou Y., Xu X.M, & Zhang C.L. (2016). The p53 pathway controls SOX2-mediated reprogramming in the mouse adult spinal cord. Cell reports, 17(3), 891-903.

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Genetically Engineered Mice for Oncology Research

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Runx3^flox (Jax 008773), p53^flox (Jax 008462), K-Ras^LSL-G12D (Jax 008179), K-Ras^LA1 (Johnson et al., 2001), Rosa26R-Tomato (Jax 007914), and Flp^ERT2 (R26^FlpoER, Jax 019016) mice were obtained from Jackson Laboratory (Bar Harbor, ME, USA). Runx3^{Frt-Stop-Frt/+} (Runx3^FSF/+) mice originated from Macrogen (Seoul, Republic of Korea). All mice analyzed had mixed genetic backgrounds and were age matched (6–8 weeks old) unless mentioned specifically. Sample size was determined based on our experience and previous experiments. No data were excluded from analysis. Animal experiments described were repeated with at least three independent replicates with significant results in the same direction as those represented in the figures. All animal studies were randomized in ‘control’ or ‘treated’ groups. However, all animals housed within the same cage were generally placed within the same treatment group. For analysis of tumor samples, identities were blinded from histopathological assessment. All animals were housed in SPF (Specific Pathogen Free) facilities. The animal studies were approved by the Institutional Animal Care Committee of Chungbuk National University.

Lee J.Y., Lee J.W., Park T.G., Han S.H., Yoo S.Y., Jung K.M., Kim D.M., Lee O.J., Kim D., Chi X.Z., Kim E.G., Lee Y.S, & Bae S.C. (2023). Runx3 Restoration Regresses K-Ras-Activated Mouse Lung Cancers and Inhibits Recurrence. Cells, 12(20), 2438.

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Targeted Cardiac Proteomic Analysis

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Animals were housed in pathogen‐free animal facility at the University of Pittsburgh with ad libitum access to food and water. The Mybpc3^−/− mice used in the present study were generated previously.⁴ (link) Briefly, mice with a knockout first tm1a allele of the Mybpc3 gene (Mybpc3^tm1a) in C57BL/6J background were crossed with an ACTB:Flp deleter line to create a conditional Mybpc3 allele (Mybpc3^tm1c) and then crossed with a CMV:Cre line to generate the germline null allele of Mybpc3^−/−. Cardiomyocyte deletion of p53 was accomplished by crossing Mybpc3^−/− with p53^flox (Jackson 008462) and Myh6Cre^+/− (Jackson 011038) to generate Mybpc3^−/−/p53 ^fl/flMyh6Cre^+/− animals. The transgenic mouse lines expressing human wild‐type troponin T2, cardiac type (TNNT2^WT), or mutant cardiac troponin T (TNNT2^I79N)⁹ (link) (kindly provided by Bjorn Knollmann, Vanderbilt University) were crossed into a C57BL/6J genetic background for a minimum of 6 generations before analysis. Investigators were blinded to animal genotyping and/or treatment at time of data collection, and no animals were excluded from analysis. The sample size (n) included per group was stated in each figure legend.

Pal S., Nixon B.R., Glennon M.S., Shridhar P., Satterfield S.L., Su Y.R, & Becker J.R. (2021). Replication Stress Response Modifies Sarcomeric Cardiomyopathy Remodeling. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 10(15), e021768.

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