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Ptenfl fl mice

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The Ptenfl/fl mice are a genetically engineered mouse strain with a conditional knockout of the Pten gene. The Pten gene is involved in the regulation of cell growth and proliferation. These mice can be used as a model to study the effects of Pten deficiency in various biological processes.

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Lab products found in correlation

B6.129s4 ptentm1hwu j, by Jackson ImmunoResearch (1 mentions) B6 cg tg alb cre 21mgn j, by Jackson ImmunoResearch (1 mentions) Lysm cre mice, by Jackson ImmunoResearch (1 mentions) C57bl 6j, by Jackson ImmunoResearch (1 mentions)

4 protocols using ptenfl fl mice

1

Liver Tumor Model in Pten-Deficient Mice

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All animal work was conducted in accordance with national guidelines and was approved by the Institutional Animal Care and Use Committee (IACUC) at the University of Washington, Seattle. 8 week old male albumin (Alb)-Cre mice (003574, B6.Cg-Tg(Alb-cre)21Mgn/J) and 8-week old female Ptenfl/fl mice (006440, B6.129S4-Ptentm1Hwu/J) were purchased from Jackson Laboratory (Bar Harbor, ME). Alb-Cre mice were bred with Ptenfl/fl mice to ultimately generate Ptenfl/fl;Albcre experimental mice. Genotyping protocols and primers were obtained from Jackson Laboratory, and PCR was performed to confirm the correct genotype. At 40 weeks of age, Ptenfl/fl;Albcre (Pten-null) mice develop tumors that are physiologically similar to human HCCs and ICCs (intrahepatic cholangiocarcinoma) (Horie et al., 2004 (link); Kenerson et al., 2011 (link)). Moreover, the mice develop hepatic steatosis, resulting in livers that are abnormally large preceding tumorigenesis. Tumor progression was monitored through weekly ultrasound scans with an L15-7io imaging probe on a Philips iU22 (Philips Medical Systems, Bothell, WA) starting at 36 weeks of age. Mice (20 male and 18 female) were treated once tumors were 1 cm in diameter.
Keller S.B., Suo D., Wang Y.N., Kenerson H., Yeung R.S, & Averkiou M.A. (2020). Image-Guided Treatment of Primary Liver Cancer in Mice Leads to Vascular Disruption and Increased Drug Penetration. Frontiers in Pharmacology, 11, 584344.
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2

Conditional Activation of NFAT-PTEN Signaling

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All animal studies were approved by the Washington University Animal Studies Committee and have been conducted according to relevant NIH guidelines. The PBCre4-Cre (PCre/+), ROSArtTA (RT), TetO-NFATc1Nuc (TN) strains and the genotyping methods were described previously.17 (link), 21 (link)–23 (link) For NFATc1Nuc, the substitution of the serines targeted for phosphorylation and dephosphorylation with alanines renders the modified NFATc1 proteins constitutively nuclear and active. For studying interactions between NFAT and PTEN, PCre mice were crossed with Ptenfl/fl mice (The Jackson Laboratory, Bar Harbor, ME, USA) to generate PCre/+;Ptenfl/+ males. These PCre/+;Ptenfl/+ mice were then crossed to RT/RT;TN/+;Ptenfl/fl mice to generate controls and PCre/+;RT/+;TN/+;Ptenfl/fl mutants. Dox was given through drinking water provided ad libitum at 2 mg/ml, starting at P21. Drastic morphological differences makes blinding of specimens from different genotype groups ineffective in this study.
Manda K.R., Tripathi P., Hsi A.C., Ning J., Ruzinova M.B., Liapis H., Bailey M., Zhang H., Maher C.A., Humphrey P.A., Andriole G.L., Ding L., You Z, & Chen F. (2015). NFATc1 Promotes Prostate Tumorigenesis and Overcomes PTEN Loss-Induced Senescence. Oncogene, 35(25), 3282-3292.
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3

Conditional Activation of NFAT-PTEN Signaling

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All animal studies were approved by the Washington University Animal Studies Committee and have been conducted according to relevant NIH guidelines. The PBCre4-Cre (PCre/+), ROSArtTA (RT), TetO-NFATc1Nuc (TN) strains and the genotyping methods were described previously.17 (link), 21 (link)–23 (link) For NFATc1Nuc, the substitution of the serines targeted for phosphorylation and dephosphorylation with alanines renders the modified NFATc1 proteins constitutively nuclear and active. For studying interactions between NFAT and PTEN, PCre mice were crossed with Ptenfl/fl mice (The Jackson Laboratory, Bar Harbor, ME, USA) to generate PCre/+;Ptenfl/+ males. These PCre/+;Ptenfl/+ mice were then crossed to RT/RT;TN/+;Ptenfl/fl mice to generate controls and PCre/+;RT/+;TN/+;Ptenfl/fl mutants. Dox was given through drinking water provided ad libitum at 2 mg/ml, starting at P21. Drastic morphological differences makes blinding of specimens from different genotype groups ineffective in this study.
Manda K.R., Tripathi P., Hsi A.C., Ning J., Ruzinova M.B., Liapis H., Bailey M., Zhang H., Maher C.A., Humphrey P.A., Andriole G.L., Ding L., You Z, & Chen F. (2015). NFATc1 Promotes Prostate Tumorigenesis and Overcomes PTEN Loss-Induced Senescence. Oncogene, 35(25), 3282-3292.
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4

Generation of Conditional Knockout Mice

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Animal experiments were carried out in strict accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. All protocols were reviewed and approved by the Institutional Animal Care and Use Committee at the University of Washington (Protocol 4410–01). Animals were group-housed in University of Washington Department of Comparative Medicine facilities under specific pathogen-free conditions. 6 week old wildtype (#000664) and Tlr2–/– (#004650) female C57BL/6J mice were purchased from The Jackson Laboratory for isolating BMDMs. To generate Pten conditional knockout mice, male LysM-Cre+/+ mice (#004781) and female Ptenfl/fl mice (#006440) were purchased from The Jackson Laboratory and bred to produce double heterozygotes. Female heterozygotes were bred back to male LysM-Cre+/+ mice to generate LysM-Cre+/+Ptenfl/wt breeders, which were then bred together to produce LysM-Cre+/+Ptenfl/fl knockout mice (PTENM-KO) and LysM-Cre+/+Ptenwt/wt controls (PTENM-WT). Genotyping was performed by isolating gDNA from ear biopsies and following PCR protocols provided by The Jackson Laboratory. 8–10 week old male and female mice were used for infection studies. Animals were assigned to experimental groups by age-, sex-, and littermate-matching and groups were co-housed when possible.
Glover R.C., Schwardt N.H., Leano S.K., Sanchez M.E., Thomason M.K., Olive A.J, & Reniere M.L. (2023). A genome-wide screen in macrophages identifies PTEN as required for myeloid restriction of Listeria monocytogenes infection. PLOS Pathogens, 19(5), e1011058.
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