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Lsl trp53r172h

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The LSL-Trp53R172H is a genetically engineered mouse model that expresses the Trp53R172H mutation, a common mutation found in human cancers. The core function of this model is to provide a platform for studying the role of the Trp53 gene and its mutant variants in cancer biology and therapeutic research.

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Lab products found in correlation

Lsl krasg12d, by Jackson ImmunoResearch (8 mentions) Pdx1 cre mice, by Jackson ImmunoResearch (4 mentions) Pdx1 cre, by Jackson ImmunoResearch (3 mentions) Lsl krasg12d mice, by Jackson ImmunoResearch (1 mentions) Ptf1acre, by Jackson ImmunoResearch (1 mentions)

9 protocols using lsl trp53r172h

1

Genetically Engineered Mouse Models for Pancreatic Cancer

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Wild-type (Pdx-1-Cre), LSL-Trp53R172H, and LSL-KrasG12D mice were obtained from Jackson Laboratory. Double transgenic LSL-KrasG12D/+; LSL-Trp53R172/+ mice were generated by cross-mating LSL-Trp53R172H and LSL-KrasG12D mice. These mice were further bred with wild-type (Pdx-1-Cre) mice, resulting in different genotypes, including Pdx-1-Cre, LSL-Trp53R172H, LSL-KrasG12D, KC (LSL-KrasG12D/+; Pdx-1-Cre), PC (LSL-Trp53R172H/+; Pdx-1-Cre), and KPC (KrasG12D/+; LSL-Trp53R172H/+; Pdx-1-Cre). Genomic DNA was extracted from mouse tail samples for PCR amplification, and the genotypes of the mice were identified by running nucleic acid gel against the PCR products. We selected wild-type (Pdx-1-Cre), KC (LSL-KrasG12D/+; Pdx-1-Cre), and KPC (KrasG12D/+; LSL-Trp53R172H/+; Pdx-1-Cre) mice for use in the study. Primer sequences for genotyping are listed in Supplementary Table S2. Syngeneic C57BL/6 mice, aged 5–7 weeks, were purchased from Weitonglihua (Peking, China) and housed in specific pathogen-free conditions. All animal procedures and studies were conducted in accordance with the Institutional Animal Care and Use Committee of the Second Hospital of Shandong University.
Zhang S., Li P., Li J., Gao J., Qi Q., Dong G., Liu X., Jiao Q., Wang Y., Du L., Zhan H., Xu S, & Wang C. (2023). Chromatin accessibility uncovers KRAS-driven FOSL2 promoting pancreatic ductal adenocarcinoma progression through up-regulation of CCL28. British Journal of Cancer, 129(3), 426-443.
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2

Genetically Engineered Mouse Model of Pancreatic Cancer

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LSL-KrasG12D/+; LSL-Trp53R172H/+; Pdx-1-Cre mice were purchased from Jackson Laboratory (Bar Harbor, ME). GEM-KPC mice were generated by crossing LSL-KrasG12D/+ with LSL-Trp53R172H/+, and subsequently crossing with Pdx-1-Cre.
Turaga R.C., Sharma M., Mishra F., Krasinskas A., Yuan Y., Yang J.J., Wang S., Liu C., Li S, & Liu Z.R. (2020). Modulation of Cancer-Associated Fibrotic Stroma by An Integrin αvβ3 Targeting Protein for Pancreatic Cancer Treatment. Cellular and Molecular Gastroenterology and Hepatology, 11(1), 161-179.
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3

Genetic Mouse Models of Pancreatic Cancer

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All animal work and procedures were approved by the Northwestern University Institutional Animal Care and Use Committee. In addition, all animal experiments were performed in accordance with relevant guidelines and regulations. The following mice were used in the study: Pdx1-Cre mice (Jackson Laboratory #014647), Gna13 (kindly provided by Stefan Offermans, Max Planck Institute) (Moers et al., 2003 (link)), LSL-KRasG12D/+ (Jackson Laboratory #019104) LSL-Trp53R172H/+ (Jackson Laboratory 008652). All mice were bred on a C57/BL6 background, with ages ranging from 3–20 months and from both genders.
Animals were housed at 12h light/dark cycle in ventilated cages with controlled temperature and humidity. Water and standard mouse diet were provided ad libitum, and bedding changed regularly.
Shields M.A., Spaulding C., Metropulos A.E., Khalafalla M.G., Pharm T.N, & Munshi H.G. (2022). Gα13 loss in Kras/Tp53 mouse model of pancreatic tumorigenesis promotes tumors susceptible to rapamycin. Cell reports, 38(9), 110441.
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4

Genetically Engineered Mouse Models for Pancreatic Cancer

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Pdx1:Cre, LSL-KrasG12D and LSL-Trp53R172H mice (Jackson Laboratories) were bred to generate KC Pdx1 and KPCPdx1 mice. Mist1:CreERT2; LSL-KrasG12D and LSL-tdTomato mice were bred to generate KCMist1tdT mice. KCMist1tdT mice were injected with Tamoxifen and treated with cerulein as described previously (14 (link)). Animal studies were approved by the Animal Care and Use Committees of Johns Hopkins University School of Medicine, Memorial Sloan Kettering Cancer Center and Cold Spring Harbor Laboratory.
Sinha S., Fu Y.Y., Grimont A., Ketcham M., Lafaro K., Saglimbeni J.A., Askan G., Bailey J.M., Melchor J.P., Zhong Y., Joo M.G., Grbovic-Huezo O., Yang I.H., Basturk O., Baker L., Park Y., Kurtz R.C., Tuveson D., Leach S.D, & Pasricha P.J. (2017). PanIN neuroendocrine cells promote tumorigenesis via neuronal crosstalk. Cancer research, 77(8), 1868-1879.
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5

Genetic Mouse Models of Pancreatic Cancer

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All animal work and procedures were approved by the Northwestern University Institutional Animal Care and Use Committee. In addition, all animal experiments were performed in accordance with relevant guidelines and regulations. The following mice were used in the study: Pdx1-Cre mice (Jackson Laboratory #014647), Gna13 (kindly provided by Stefan Offermans, Max Planck Institute) (Moers et al., 2003 (link)), LSL-KRasG12D/+ (Jackson Laboratory #019104) LSL-Trp53R172H/+ (Jackson Laboratory 008652). All mice were bred on a C57/BL6 background, with ages ranging from 3–20 months and from both genders.
Animals were housed at 12h light/dark cycle in ventilated cages with controlled temperature and humidity. Water and standard mouse diet were provided ad libitum, and bedding changed regularly.
Shields M.A., Spaulding C., Metropulos A.E., Khalafalla M.G., Pharm T.N, & Munshi H.G. (2022). Gα13 loss in Kras/Tp53 mouse model of pancreatic tumorigenesis promotes tumors susceptible to rapamycin. Cell reports, 38(9), 110441.
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6

Conditional Knockout of Gα13 in Pancreas

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Mice with loss of Gα13 in the pancreas were generated by crossing Pdx1-Cre mice (Jackson Laboratory #014647) to mice expressing the floxed allele of Gna13 (kindly provided by Stefan Offermans, Max Planck Institute) (Moers et al., 2003 (link)), to generate CGα13fl/+ and CGα13fl/fl mice. The bigenic mice were further crossed with mice expressing an LSL-KRasG12D/+ (Jackson Laboratory #019104) mutant allele to generate KCGα13fl/+ (KCGfl/+) or KCGα13fl/fl (KCGfl/fl) mice. These mice were further crossed with mice expressing LSL-Trp53R172H/+ (Jackson Laboratory 008652) to generate KPCGfl/+ and KPCGfl/fl mice. For survival studies, mice were aged singly or in groups of 2–5. Some mice developed anogenital or facial papillomas that were surgically removed before compromising health. Mice that developed extra-pancreatic diseases such as thymoma, prolapse, or inoperable papillomas were excluded from the study. All mice were bred on a C57/BL6 background, and both genders were used in the studies.
Shields M.A., Spaulding C., Metropulos A.E., Khalafalla M.G., Pharm T.N, & Munshi H.G. (2022). Gα13 loss in Kras/Tp53 mouse model of pancreatic tumorigenesis promotes tumors susceptible to rapamycin. Cell reports, 38(9), 110441.
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7

Genetically Engineered Mouse Models of Pancreatic Cancer

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KPC (Pdx1-Cre; LSL-KrasG12D/+; LSL-Trp53R172H/+) and PKT (Ptf1a-Cre; LSL-KrasG12D/+; Tgfbr2loxP/loxP) mouse models alleles were purchased from Jackson Laboratory. B6.FVB-Tg(Pdx1-Cre)6Tuv/J (RRID:IMSR_JAX:014647); B6.129S4-Krastm4Tyj/J (RRID:IMSR_JAX:008179); 129S-Trp53tm2Tyj/J (RRID:IMSR_JAX:008652); Ptf1atm1(Cre)Hnak/RschJ (RRID:IMSR_JAX:023329); B6;129-Tgfbr2tm1Karl/J (RRID:IMSR_JAX:012603).
Rab27aash/ash allele was kindly provided by Doctor Miguel Seabra, CEDOC, NOVA Medical School, Lisbon, Portugal [18 (link)].
PKT Ashen (Ptf1a-Cre; LSL-KrasG12D/+; Tgfbr2loxP/loxP; Rab27aash/ash) developed PDAC in a spontaneous manner in a similar way to the PKT mouse model.
Regarding the KPC mouse model, a cross-sectional study was performed. Mice were euthanized at different timepoints of disease progression (8 weeks, 16 weeks and HEP - humane end point). PKT and PKT Ashen mice were euthanized when presented severe symptoms.
All mice were housed under standard housing conditions at the i3S animal facility.
Bastos N., Castaldo S.A., Adem B., Machado J.C., Melo C.A, & Melo S.A. (2023). SMC3 epigenetic silencing regulates Rab27a expression and drives pancreatic cancer progression. Journal of Translational Medicine, 21, 578.
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8

Conditional Knockout of Gα13 in Pancreas

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Mice with loss of Gα13 in the pancreas were generated by crossing Pdx1-Cre mice (Jackson Laboratory #014647) to mice expressing the floxed allele of Gna13 (kindly provided by Stefan Offermans, Max Planck Institute) (Moers et al., 2003 (link)), to generate CGα13fl/+ and CGα13fl/fl mice. The bigenic mice were further crossed with mice expressing an LSL-KRasG12D/+ (Jackson Laboratory #019104) mutant allele to generate KCGα13fl/+ (KCGfl/+) or KCGα13fl/fl (KCGfl/fl) mice. These mice were further crossed with mice expressing LSL-Trp53R172H/+ (Jackson Laboratory 008652) to generate KPCGfl/+ and KPCGfl/fl mice. For survival studies, mice were aged singly or in groups of 2–5. Some mice developed anogenital or facial papillomas that were surgically removed before compromising health. Mice that developed extra-pancreatic diseases such as thymoma, prolapse, or inoperable papillomas were excluded from the study. All mice were bred on a C57/BL6 background, and both genders were used in the studies.
Shields M.A., Spaulding C., Metropulos A.E., Khalafalla M.G., Pharm T.N, & Munshi H.G. (2022). Gα13 loss in Kras/Tp53 mouse model of pancreatic tumorigenesis promotes tumors susceptible to rapamycin. Cell reports, 38(9), 110441.
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9

Generating Spontaneous Pancreatic Cancer in Mice

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LSL-Kras G12D/+ , LSL-Trp53 R172H/+ , and Pdx1-Cre mice were obtained from the Jackson Laboratory (Bar Harbor, ME, USA). To produce triple transgenic Kras G12D ;Trp53 R172 ;Pdx-1-Cre mice (KPC mice), double transgenic LSL-Kras G12D/+ ;LSL-Trp53 R172/+ mice were first generated by cross-mating LSL-Kras G12D/+ and LSL-Trp53 R172/+ mice, and then LSL-Kras G12D/+ ; LSL-Trp53 R172/+ mice were further mated with transgenic Pdx-1-Cre mice (Figure 1). All mice were genotyped in our laboratory following the protocols provided by Jackson lab. Ten KPC mice were used to generate spontaneous PDAC and monitored using high-resolution MRI approaches.
The subjects were housed under clean conditions in the facilities of Laboratory Animal Services at the Northwestern University.
Hu S., Pan L., Shangguan J., Figini M., Eresen A., Sun C., Wang B., Ma Q., Hu C., Yaghmai V., Velichko Y., Yang J, & Zhang Z. (2019). Non-invasive dynamic monitoring initiation and growth of pancreatic tumor in the LSL-KrasG12D/+;LSL-Trp53R172H/+;Pdx-1-Cre (KPC) transgenic mouse model. Journal of immunological methods, 465.
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