b6.129s4 ptentm1hwu j, by Jackson ImmunoResearch - Product details

1

Conditional Pten Knockout in Sensorimotor Cortex and Red Nucleus

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All procedures were approved by the Institutional Animals Care and Use Committee at UCSD or by the Animal Care Committee of the University of British Columbia in accordance with the guidelines of the Canadian Council for Animal Care. The Pten conditional allele (Pten^flox, or Pten^f) was obtained from the Jackson Laboratory (B6.129S4-Pten^tm1Hwu/J; Stock # 006440) (Lesche et al., 2002 (link)). AAV-Cre or control virus AAV-GFP was injected into the sensorimotor cortex of different age groups for the dorsal hemisection experimental groups and AAV-Cre-GFP or AAV-GFP control was injected into the red nucleus for the dorsolateral funiculus crush groups (see Supplemental Experimental Procedures for details).

Geoffroy C.G., Hilton B.J., Tetzlaff W, & Zheng B. (2016). Evidence for an age-dependent decline in axon regeneration in the adult mammalian central nervous system. Cell reports, 15(2), 238-246.

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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 Pten^fl/fl mice (006440, B6.129S4-Ptentm1Hwu/J) were purchased from Jackson Laboratory (Bar Harbor, ME). Alb-Cre mice were bred with Pten^fl/fl mice to ultimately generate Pten^fl/fl;Alb^cre 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, Pten^fl/fl;Alb^cre (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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Preclinical Mouse Models for Cancer

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Animal studies were approved by the Institutional Animal Care and Use Committee (IACUC) at The University of Pennsylvania and/or The University of Michigan. Animal use and care was in strict compliance with institutional guidelines and all experiments conformed to the relevant regulatory standards by the Universities. The maximal tumor size in our study models (mice) never exceeded 1 cm in diameter as allowed by the above ethics committee. NOD SCID or NCI SCID/NCr athymic nude mice were obtained from the Jackson Laboratory (strain code: 005557) and Charles River (strain code: 561). Prostate-specific Pten knockout mice were generated by crossing Pbsn-Cre male mice Tg (Pbsn-cre) 4Prb/J (Jackson laboratory, Strain: 026662) with Pten floxed mice (B6.129S4-Ptentm1Hwu/J, Strain: 006440). All mice were housed in a pathogen-free animal barrier facility and all in vivo experiments were initiated with male mice aged 5-8 weeks.
The maintenance of mice and the experimental procedures (immunizations) have been conducted according to the Austrian Animal Experiments Act and have been approved by the Austrian Federal Ministry of Science and Research BMWFW-66.009/0211-WF/V/3b/2015 and the animal experiments ethics committee of the Medical University of Vienna.

Rasool R.U., O’Connor C.M., Das C.K., Alhusayan M., Verma B.K., Islam S., Frohner I.E., Deng Q., Mitchell-Velasquez E., Sangodkar J., Ahmed A., Linauer S., Mudrak I., Rainey J., Zawacki K.P., Suhan T.K., Callahan C.G., Rebernick R., Natesan R., Siddiqui J., Sauter G., Thomas D., Wang S., Taylor D.J., Simon R., Cieslik M., Chinnaiyan A.M., Busino L., Ogris E., Narla G, & Asangani I.A. (2023). Loss of LCMT1 and biased protein phosphatase 2A heterotrimerization drive prostate cancer progression and therapy resistance. Nature Communications, 14, 5253.

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Genetically Engineered Mouse Models

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K19-Cre, wild-type C57, B6.129S4-PTEN ^tm1Hwu/J, pvillin-Cre and alb-Cre mice (Jackson Lab), Rosa26-lacZ reporter mice (Kindly presented by Prof. Zhi-hong Zheng, China Medical University), B6.Cg-Dkk3^t^m1 (Kindly presented by Prof. Hiromi Kumon, Okayama University), and B6.Cg-Becn1^tm1(Purchased from UCDAVIS KOMP Repository) mice were maintained in specific-pathogen-free room. We crossed K19-Cre and pvillin-Cre with Rosa26-lacZ reporter mice or B6.129S4-PTEN ^tm1Hwu/J to obtain the K19-Cre/Rosa, K19-Cre/PTEN ^Loxp/Loxp, pvillin-Cre/Rosa and pvillin-Cre/PTEN ^Loxp/Loxp. Every four mice were housed to a plastic cage with paper chips for bedding. All had access to standard rodent food (Beijing HFK Bioscience) and water, and were housed in a temperature-controlled animal room with a 12-h light/dark illumination cycle. Animal use procedures were in accordance with the Guide for the Care and Use of Laboratory Animals and approved by the Committee on Animal Experimentation of our hospital.

Zhao G.F., Zhao S., Liu J.J., Wu J.C., He H.Y., Ding X.Q., Yu X.W., Huang K.Q., Li Z.J, & Zheng H.C. (2017). Cytokeratin 19 promoter directs the expression of Cre recombinase in various epithelia of transgenic mice. Oncotarget, 8(11), 18303-18311.

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Genetically Engineered Mice for Cancer Study

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Animal experiments were carried out according to protocols approved by the Institutional Committee of Animal Care and Use (ICACU) of the Albany Medical College and the ICACU of Georgia Regents University. ATF3 knockout (ATF3^−/−) mice (in C57BL/6 background) were described previously ^{24 (link),50 (link)}, and we obtained B6.129S4-Pten^tm1Hwu/J (Pten^loxP/loxP, or Pten^L/L) and PB-Cre4 (Cre⁺) mice from the Jackson Laboratory and the NCI Mouse Repository, respectively. To generate compound mutants, ATF3^−/− mice were first crossed with Pten^L/Land Cre⁺ mice, yielding Pten^L/L; ATF3^−/− and ATF3^−/−; Cre⁺ mice, respectively. The cross of the latter two strains generated male Pten^L/+; ATF3^−/−; Cre⁺ mice, which were further bred with female Pten^L/L; ATF3^−/− mice to generate male Pten^L/L; ATF3^−/−; Cre⁺ (ΔATF3ΔPten) and Pten^L/L; ATF3^−/−(ΔATF3) for histolopathological examinations. Male Pten^L/L; ATF3^+/+; Cre⁺ (ΔPten) and Pten^L/L; ATF3^+/+(WT) mice were generated similarly. For genotyping, mouse tails were lysed in PBND buffer supplemented with 0.2 μg/ml Proteinase K at 55°C overnight, and lysates were directly subjected to PCR following the protocols provided by the Jackson Laboratory. For castration, testes of 7-week-old male mice were surgically removed, and the mice were sacrificed at 12 week of age for histopathological examinations.

Wang Z., Xu D., Ding H.F., Kim J., Zhang J., Hai T, & Yan C. (2014). Loss of ATF3 Promotes Akt Activation and Prostate Cancer Development in a Pten Knockout Mouse Model. Oncogene, 34(38), 4975-4984.

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6

Genetically Engineered Mice for Cancer Study

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Animal experiments were carried out according to protocols approved by the Institutional Committee of Animal Care and Use (ICACU) of the Albany Medical College and the ICACU of Georgia Regents University. ATF3 knockout (ATF3^−/−) mice (in C57BL/6 background) were described previously ^{24 (link),50 (link)}, and we obtained B6.129S4-Pten^tm1Hwu/J (Pten^loxP/loxP, or Pten^L/L) and PB-Cre4 (Cre⁺) mice from the Jackson Laboratory and the NCI Mouse Repository, respectively. To generate compound mutants, ATF3^−/− mice were first crossed with Pten^L/Land Cre⁺ mice, yielding Pten^L/L; ATF3^−/− and ATF3^−/−; Cre⁺ mice, respectively. The cross of the latter two strains generated male Pten^L/+; ATF3^−/−; Cre⁺ mice, which were further bred with female Pten^L/L; ATF3^−/− mice to generate male Pten^L/L; ATF3^−/−; Cre⁺ (ΔATF3ΔPten) and Pten^L/L; ATF3^−/−(ΔATF3) for histolopathological examinations. Male Pten^L/L; ATF3^+/+; Cre⁺ (ΔPten) and Pten^L/L; ATF3^+/+(WT) mice were generated similarly. For genotyping, mouse tails were lysed in PBND buffer supplemented with 0.2 μg/ml Proteinase K at 55°C overnight, and lysates were directly subjected to PCR following the protocols provided by the Jackson Laboratory. For castration, testes of 7-week-old male mice were surgically removed, and the mice were sacrificed at 12 week of age for histopathological examinations.

Wang Z., Xu D., Ding H.F., Kim J., Zhang J., Hai T, & Yan C. (2014). Loss of ATF3 Promotes Akt Activation and Prostate Cancer Development in a Pten Knockout Mouse Model. Oncogene, 34(38), 4975-4984.

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7

Mouse Strain Characterization for Immunology Research

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C57BL/6 and B6D2F1/J mice were purchased from Charles River Laboratories at the age of seven weeks and housed in our facility for at least one week before being used in experiments. B6.129S(C)-Batf3^tm1Kmm/J, B6(Cg)-Irf8^tm1.1Hm/J, B6.129S4-Pten^tm1Hwu/J, B6.129P2(C)-Ccr7^tm1Rfer/J, B6.129S7-Ifng^tm1Ts/J, B6.129S7-Ifngr1^tm1Agt/J, B6(Cg)-Ifnar1^tm1.2Ees/J, B6.129S7-Il1r1^tm1lmx/J, B6.129P2(SJL)-Myd88^tm1.1Befr/J, B6.129S7-Rag1^tm1Mom/J and C57BL/6J-Ticam1^Lps2/J mice were purchased from Jackson Laboratories and bred in our facility or used for experiments after at least one week of housing in our facility. Cd207-Cre mice were provided by B. Clausen^{21 (link)}. JEDI mice were provided by B. Brown. Axl^−/− and Axl^−/−Mertk^−/− bone marrow were provided by C. Rothlin and S. Ghosh. Asc^−/− mice were provided by Millenium.
Floxed mice were crossed to Cd207-Cre mice in our facility. Mice were maintained at specified pathogen-free (SPF) health status in individually ventilated cages at 21–22 °C and 39–50% humidity. Male mice at the age of 8–12 weeks were used for experiments. All animal procedures were approved by the Institutional Animal Care and Use Committees (IACUCs) of the respective institutions.

Maier B., Leader A.M., Chen S.T., Tung N., Chang C., LeBerichel J., Chudnovskiy A., Maskey S., Walker L., Finnigan J.P., Kirkling M.E., Reizis B., Ghosh S., D’Amore N.R., Bhardwaj N., Rothlin C.V., Wolf A., Flores R., Marron T., Rahman A.H., Kenigsberg E., Brown B.D, & Merad M. (2020). A conserved dendritic-cell regulatory program limits antitumour immunity. Nature, 580(7802), 257-262.

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8

Prostate-specific Pten Knockout Mice

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To generate the prostate-specific Pten knockout mice, we crossed Pbsn-Cre male mice Tg (Pbsn-cre) 4Prb/J (Jackson laboratory, Strain: 026662) with Pten floxed mice (B6.129S4-Ptentm1Hwu/J, Strain: 006440). The genotype of the mice was confirmed using the primers provided in the Supplementary Data 1.

Rasool R.U., O’Connor C.M., Das C.K., Alhusayan M., Verma B.K., Islam S., Frohner I.E., Deng Q., Mitchell-Velasquez E., Sangodkar J., Ahmed A., Linauer S., Mudrak I., Rainey J., Zawacki K.P., Suhan T.K., Callahan C.G., Rebernick R., Natesan R., Siddiqui J., Sauter G., Thomas D., Wang S., Taylor D.J., Simon R., Cieslik M., Chinnaiyan A.M., Busino L., Ogris E., Narla G, & Asangani I.A. (2023). Loss of LCMT1 and biased protein phosphatase 2A heterotrimerization drive prostate cancer progression and therapy resistance. Nature Communications, 14, 5253.

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B6.129s4 ptentm1hwu j

Lab products found in correlation

8 protocols using b6.129s4 ptentm1hwu j

Conditional Pten Knockout in Sensorimotor Cortex and Red Nucleus

Liver Tumor Model in Pten-Deficient Mice

Preclinical Mouse Models for Cancer

Genetically Engineered Mouse Models

Genetically Engineered Mice for Cancer Study

Genetically Engineered Mice for Cancer Study

Mouse Strain Characterization for Immunology Research

Prostate-specific Pten Knockout Mice

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