Pdx1 cre

Manufactured by Jackson ImmunoResearch

Sourced in Montenegro, United States

Pdx1-Cre is a transgenic mouse line that expresses Cre recombinase under the control of the pancreas-specific Pdx1 (Pancreatic and Duodenal Homeobox 1) promoter. Cre recombinase is a site-specific DNA recombinase that can be used to conditionally modify gene expression in the pancreas of genetically engineered mice.

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11 protocols using pdx1 cre

Characterizing Pdx1-Cre;Kras Pancreatic Tissue

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Pdx1^Cre and LSL-Kras^G12D mice were purchased from Jackson Laboratory (Bar Harbor, Maine).^{14 (link)} Pancreas tissue from Pdx1^Cre/+;LSL-Kras^G12D/+ mice (5–6 month of age) were used for fluorescence immunostaining and organoid formation. All animal experiments were performed in accordance with the National Institutes of Health guidelines under the protocol approved by the Institutional Animal Care and Use Committee at the University of Southern California.

Skrypek K., Balog S., Eriguchi Y, & Asahina K. (2021). Inhibition of Stearoyl-CoA Desaturase Induces the Unfolded Protein Response in Pancreatic Tumors and Suppresses Their Growth. Pancreas, 50(2), 219-226.

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Genetic Lineage Tracing in Mice

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Mouse strain Jag1^flox/flox (43 (link)) was kindly provided by Dr Freddy Radtke (Ecole Polytechnique Fédérale de Lausanne). Kras^LSL-G12D, Pdx1-Cre, Rosa^LSL-YFP, and Sox9-CreER mouse strains were purchased from the Jackson Laboratory. Mice were interbred and maintained on a mixed background. All mouse experiments were performed in accordance with a protocol approved by the Institutional Animal Care and Use Committee of the University of Mississippi Medical Center.

Chung W.C., Challagundla L., Zhou Y., Li M., Atfi A, & Xu K. (2020). Loss of Jag1 cooperates with oncogenic Kras to induce pancreatic cystic neoplasms. Life Science Alliance, 4(2), e201900503.

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Genetically Engineered Mouse Models

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Pdx1‐Cre, Trp53^fl/fl, and LSL‐Kras^G12D mice were obtained from Jackson Laboratory and Ppdpf^fl/fl was obtained from Nanjing University. Pdx1‐Cre; LSL‐Kras^G12D; Ppdpf^fl/fl was bred by crossing Pdx1‐Cre mice with LSL‐Kras^G12D; Ppdpf^f^l/fl mice. Pdx1‐Cre; LSL‐Kras^G12D; P53^fl/fl; Ppdpf^fl/fl was generated by crossing Pdx1‐Cre with Trp53^fl/fl; LSL‐Kras^G12D; Ppdpf^fl/fl. The sequences of primers used to identify the genotype of mice are listed in Table S3, Supporting Information. Six‐week‐old male BALB/c mice were housed under standard conditions. The animal protocols were complied with SIBS Guide for the Care and Use of Laboratory Animals and approved by Animal Care and Use Committee, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences.

Ni Q., Zhu B., Ji Y., Zheng Q., Liang X., Ma N., Jiang H., Zhang F., Shang Y., Wang Y., Xu S., Zhang E., Yuan Y., Chen T., Yin F., Cao H., Huang J., Xia J., Ding X., Qiu X., Ding K., Song C., Zhou W., Wu M., Wang K., Lui R., Lin Q., Chen W., Li Z., Cheng S., Wang X., Xie D, & Li J. (2022). PPDPF Promotes the Development of Mutant KRAS‐Driven Pancreatic Ductal Adenocarcinoma by Regulating the GEF Activity of SOS1. Advanced Science, 10(2), 2202448.

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Engineered Mouse Models for Pancreatic Cancer

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The generation and use of mouse strains of Villin-Cre⁺;Klf4^loxp/loxp and Villin-Cre⁺;Klf4^+/+ were described previously (32 (link)). For genetically engineered mouse model of PDA progression, Pdx1-Cre mice (Stock Number: 014647, Jackson Laboratory) were across bred with LSL-Kras^G12D/+ mice (Stock Number: 008180, Jackson Laboratory) to generate Pdx1-Cre;LSL-Kras^G12D/+ mice (34 (link)). The mice were euthanized to harvest pancreas and liver tissues when they became old (>12 months) or very sick.

YAN Y., LI Z., KONG X., JIA Z., ZUO X., GAGEA M., HUANG S., WEI D, & XIE K. (2016). KLF4-mediated Suppression of CD44 Signaling Negatively Impacts Pancreatic Cancer Stemness and Metastasis. Cancer research, 76(8), 2419-2431.

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Genetically Engineered Mouse Models for Pancreatic Cancer

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The Pdx1-Cre and LSL-Trp53^R172H/+ mice were all obtained from The Jackson Laboratory (https://www.jax.org) (LSL: Lox/Stop/Lox). The LSL-Kras^G12D/+ mice were a generous gift from Professor Xiu-Feng Pang (Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University). The Pdx1-Cre, LSL-Kras^G12D/+, and LSL-Trp53^R172H/+ mice were raised in our laboratory. The KP mice were generated by hybridizing the LSL-Kras^G12D/+ mice and LSL-Trp53^R172H/+ mice. The KPC mice were generated by hybridizing the LSL-Kras^G12D/+ mice, LSL-Trp53^R172H/+ mice and Pdx1-Cre mice. All animal experiments were undertaken in accordance with the NIH Guide for the Care and Use of Laboratory Animals.

Nie H., Huang P.Q., Jiang S.H., Yang Q., Hu L.P., Yang X.M., Li J., Wang Y.H., Li Q., Zhang Y.F., Zhu L., Zhang Y.L., Yu Y., Xiao G.G., Sun Y.W., Ji J, & Zhang Z.G. (2021). The short isoform of PRLR suppresses the pentose phosphate pathway and nucleotide synthesis through the NEK9-Hippo axis in pancreatic cancer. Theranostics, 11(8), 3898-3915.

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Genetically Modified Mouse Strains for Research

Cited 1 time

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Kras^LSL-G12D, Pdx1-Cre, Rosa^LSL-lacZ, and Rosa^LSL-YFP mouse strains were obtained from the Jackson Laboratory and have been previously described [12] (link), [13] (link), [14] (link), [15] (link). Jag1^flox strain was provided by Dr. Radtke and described previously [16] (link). Generation of Notch3^β-Geo strain was described previously [17] (link). All mouse experiments were performed in accordance with a protocol approved by the Institutional Animal Care and Use Committee of UMMC.

Chung W.C., Zhou Y., Atfi A, & Xu K. (2019). Downregulation of Notch Signaling in Kras-Induced Gastric Metaplasia. Neoplasia (New York, N.Y.), 21(8), 810-821.

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Genetically Engineered Mouse Model of Pancreatic Cancer

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LSL-Kras^G12D/+; LSL-Trp53^R172H/+; Pdx-1-Cre mice were purchased from Jackson Laboratory (Bar Harbor, ME). GEM-KPC mice were generated by crossing LSL-Kras^G12D/+ with LSL-Trp53^R172H/+, 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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Genetically Engineered Mouse Models

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Kras^LSL-G12D/+, Rosa^LSL-lacZ/+ and Pdx1-Cre mouse strains were obtained from the Jackson Laboratory and have been previously described [18 (link)–20 (link)]. Jag1^flox strain was provided by Dr. Radtke and described previously [21 (link)]. Mouse experiments were performed in accordance with a protocol approved by the Institutional Animal Care and Use Committee of the University of Mississippi Medical Center.

Chung W.C., Wang J., Zhou Y, & Xu K. (2017). KrasG12D upregulates Notch signaling to induce gallbladder tumorigenesis in mice. Oncoscience, 4(9-10), 131-138.

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Mouse Strains for Pancreatic Research

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The following mice strains were used: Ptf1a^Cre, Ptf1a^CreERTM, and Pdx1^f/f (Gannon et al. 2008 (link); Roy and Hebrok 2015 (link)); Kras^LSL-G12D, PDX1-Cre, and Trp53^R172H (gifts of David Tuveson, Cold Spring Harbor Laboratory); and Trp53^f/f, R26R^LSL-YFP, and NOD scidγ (purchased from the Jackson Laboratory). Mice were crossed on a mixed background. The University of California at San Francisco and University of Michigan Institutional Care and Use of Animals Committees (IACUCs) approved all of the mouse experiments.

Roy N., Takeuchi K.K., Ruggeri J.M., Bailey P., Chang D., Li J., Leonhardt L., Puri S., Hoffman M.T., Gao S., Halbrook C.J., Song Y., Ljungman M., Malik S., Wright C.V., Dawson D.W., Biankin A.V., Hebrok M, & Crawford H.C. (2016). PDX1 dynamically regulates pancreatic ductal adenocarcinoma initiation and maintenance. Genes & Development, 30(24), 2669-2683.

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Genetically Engineered Mouse Models of Pancreatic Cancer

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KPC (Pdx1-Cre; LSL-Kras^G12D/+; LSL-Trp53^R172H/+) and PKT (Ptf1a-Cre; LSL-Kras^G12D/+; Tgfbr2^loxP/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).
Rab27a^ash/ash allele was kindly provided by Doctor Miguel Seabra, CEDOC, NOVA Medical School, Lisbon, Portugal [18 (link)].
PKT Ashen (Ptf1a-Cre; LSL-Kras^G12D/+; Tgfbr2^loxP/loxP; Rab27a^ash/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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