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Pdx1 cre mice

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Pdx1-Cre mice are a genetically modified mouse model where the Cre recombinase enzyme is expressed under the control of the Pdx1 gene promoter. The Pdx1 gene is essential for the development of the pancreas. Pdx1-Cre mice can be used to induce Cre-mediated recombination in pancreatic cells.

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Lab products found in correlation

Lsl krasg12d, by Jackson ImmunoResearch (6 mentions) Lsl trp53r172h, by Jackson ImmunoResearch (4 mentions) Bio plex lysis buffer, by Bio-Rad (2 mentions) Factor 1, by Bio-Rad (2 mentions) Factor 2, by Bio-Rad (2 mentions) Dclk1, by Cell Signaling Technology (2 mentions) Kraslsl g12d, by Jackson ImmunoResearch (2 mentions) Tp53lsl r172h, by Jackson ImmunoResearch (2 mentions) Gapdh, by Cell Signaling Technology (2 mentions) Complete protease inhibitor cocktail, by Merck Group (2 mentions) Lsl krasg12d mice, by Jackson ImmunoResearch (2 mentions) Trp53flox, by Jackson ImmunoResearch (1 mentions) Pdx1 cre, by Jackson ImmunoResearch (1 mentions) C57bl 6j mice, by Charles River Laboratories (1 mentions) Trp53flox flox mice, by Jackson ImmunoResearch (1 mentions) Lox stop lox krasg12d, by Jackson ImmunoResearch (1 mentions)

15 protocols using pdx1 cre mice

1

Pancreatic Protein Extraction and Analysis

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Pancreases were harvested from 8-week-old mice and flash frozen in liquid N2 immediately upon dissection. Frozen tissue was lysed in Bio-Plex Lysis Buffer (Bio-Rad, #171304011) supplemented with Factor I (Bio-Rad, #171304011), Factor II (Bio-Rad, #171304011), and cOmplete protease inhibitor cocktail (Sigma-Aldrich) according to the manufacturer’s instructions. Lysates were clarified by centrifugation and immunoblotting was performed as previously described.55 (link) The following primary antibodies were employed in this study: DCLK1 (Cell Signaling, #62257) and GAPDH (Cell Signaling, #D16H11). Immunoglobulin G horseradish peroxidase linked secondary antibodies were employed as appropriate.
Animal studies for immunohistochemistry and immunoblotting (Supplementary Fig. 8a–b) were approved and performed in accordance with the IACUC at Beth Israel Deaconess Medical Center. All experiments were adherent to institutional standards and were performed in pathogen-free animal facilities. Pdx1-Cre mice were obtained from The Jackson Laboratory (#014647); K-RasLSL-G12D (#01XJ6) and Tp53LSL-R172H (#01XM2) mice were obtained from the NCI Mouse Repository.
Ferguson F.M., Nabet B., Raghavan S., Liu Y., Leggett A.L., Kuljanin M., Kalekar R.L., Yang A., He S., Wang J., Ng R.W., Sulahian R., Li L., Poulin E.J., Huang L., Koren J., Dieguez-Martinez N., Espinosa S., Zeng Z., Corona C.R., Vasta J.D., Ohi R., Sim T., Kim N.D., Harshbarger W., Lizcano J.M., Robers M.B., Muthaswamy S., Lin C.Y., Look A.T., Haigis K.M., Mancias J.D., Wolpin B.M., Aguirre A.J., Hahn W.C., Westover K.D, & Gray N.S. (2020). Discovery of a selective inhibitor of Doublecortin Like Kinase 1. Nature chemical biology, 16(6), 635-643.
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2

Kras, Trp53, and Pdx1 Driven Pancreatic Tumor Development

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Three individual strains of LSL-KrasG12D/+, Trp53flox/+, and Pdx-1-cre mice were obtained from Jackson Laboratory (Sacramento). We crossed and generated the LSL-KrasG12D/+;Trp53flox/+;Pdx-1-cre (KPCflox) mice in house. All animals were kept in specific pathogen-free housing with abundant food and water under guidelines approved by the Nihon University, School of Medical, Animal Care and Use Committee (AP15M001). At 3 months old, the mice were intraperitoneally injected with 40 mg/kg Indox or a vehicle (a mixture of DMSO/PEG400, 1:1 (v/v)) twice a week until the endpoint. The total pancreatic weight and tumor sizes were measured, and their volumes were calculated using the following formula: width x length x height. All samples were embedded in paraffin followed after fixing in 10% neutral buffered formalin.
Ichimaru Y., Sano M., Kajiwara I., Tobe T., Yoshioka H., Hayashi K., Ijichi H, & Miyairi S. (2019). Indirubin 3′-Oxime Inhibits Migration, Invasion, and Metastasis InVivo in Mice Bearing Spontaneously Occurring Pancreatic Cancer via Blocking the RAF/ERK, AKT, and SAPK/JNK Pathways. Translational Oncology, 12(12), 1574-1582.
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3

Generation and Characterization of Transgenic Pancreatic Cancer Murine Models

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Pdx1-Cre mice (generated by Dr. Lowy, University of Cincinnati) were purchased from the Jackson laboratory (Bar Harbor, Maine). LSL-Trp53R172H and LSL-KrasG12D/+ mice were obtained from MMHCC, NCI/NIH. All of these genetically engineered mice were bred and genotyped for the presence of Kras, p53, and Cre [54 (link), 60 (link), 61 (link)]. Six-week-old breeding pairs of genetically engineered mice, including transgenic Pdx1-Cre, LSLTrp53 R172H, and LSL-KrasG12D mice were used for breeding. To produce compound transgenic Pankras/p53 mice, the double transgenic LSLKrasG12D/+-LSL-Trp53R172/+ mice were first generated, and then further mated with heterozygous Pdx1-Cre transgenic mice [61 (link)]. Pancreatic CSCs were isolated from the Pankras/p53 mice as we described elsewhere [54 (link)].
Sharma N., Nanta R., Sharma J., Gunewardena S., Singh K.P., Shankar S, & Srivastava R.K. (2015). PI3K/AKT/mTOR and sonic hedgehog pathways cooperate together to inhibit human pancreatic cancer stem cell characteristics and tumor growth. Oncotarget, 6(31), 32039-32060.
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4

Mouse Models for IL-37 and GSDMD Studies

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Male C57BL/6 mice (6–8 weeks old, 20–25 g weight) and male ICR mice (6–8 weeks old, 25–30 g weight) were purchased from the Model Animal Research Center of Nanjing University (Nanjing, China), where all animals were housed under specific pathogen–free (SPF) conditions. The IL37tg mice on a C57BL/6 background were from Cyagen Biosciences Inc. Briefly, human IL-37 cDNA (NM_014439.3) was cloned and then inserted downstream of the CMV promoter in pRP [Exp] vector (VB150824-10008) (20 (link), 24 (link)). Besides, Pdx1cre mice (International Mouse Strain Resource [IMSR] catalog JAX:014647, RRID: IMSR_JAX:014647, The Jackson Laboratory) and Gsdmdfl/fl (Model Animal Research Center of Nanjing University, Nanjing, China) were intercrossed to generate pancreatic GSDMD-specific knockout (Pdx1cre Gsdmdfl/fl, GsdmdΔPan) (8 (link)).
All animal experiments were conducted in accordance with the Principles of Laboratory Animal Care, and were approved by the Experimental Animal Ethics Committee of Jinling Hospital, affiliated with Nanjing University.
Ma N., Yuan C., Shi J., Zhu Q., Liu Y., Ma X., Li B., Gong W., Xue J., Lu G., Li W, & Li J. (2022). Interleukin-37 protects against acinar cell pyroptosis in acute pancreatitis. JCI Insight, 7(21), e161244.
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5

Engineered Mouse Models for Pancreatic Cancer

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The generation and use of mouse strains of Villin-Cre+;Klf4loxp/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-KrasG12D/+ mice (Stock Number: 008180, Jackson Laboratory) to generate Pdx1-Cre;LSL-KrasG12D/+ 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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6

Pancreatic Protein Extraction and Analysis

Cited 1 time
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Pancreases were harvested from 8-week-old mice and flash frozen in liquid N2 immediately upon dissection. Frozen tissue was lysed in Bio-Plex Lysis Buffer (Bio-Rad, #171304011) supplemented with Factor I (Bio-Rad, #171304011), Factor II (Bio-Rad, #171304011), and cOmplete protease inhibitor cocktail (Sigma-Aldrich) according to the manufacturer’s instructions. Lysates were clarified by centrifugation and immunoblotting was performed as previously described.55 (link) The following primary antibodies were employed in this study: DCLK1 (Cell Signaling, #62257) and GAPDH (Cell Signaling, #D16H11). Immunoglobulin G horseradish peroxidase linked secondary antibodies were employed as appropriate.
Animal studies for immunohistochemistry and immunoblotting (Supplementary Fig. 8a–b) were approved and performed in accordance with the IACUC at Beth Israel Deaconess Medical Center. All experiments were adherent to institutional standards and were performed in pathogen-free animal facilities. Pdx1-Cre mice were obtained from The Jackson Laboratory (#014647); K-RasLSL-G12D (#01XJ6) and Tp53LSL-R172H (#01XM2) mice were obtained from the NCI Mouse Repository.
Ferguson F.M., Nabet B., Raghavan S., Liu Y., Leggett A.L., Kuljanin M., Kalekar R.L., Yang A., He S., Wang J., Ng R.W., Sulahian R., Li L., Poulin E.J., Huang L., Koren J., Dieguez-Martinez N., Espinosa S., Zeng Z., Corona C.R., Vasta J.D., Ohi R., Sim T., Kim N.D., Harshbarger W., Lizcano J.M., Robers M.B., Muthaswamy S., Lin C.Y., Look A.T., Haigis K.M., Mancias J.D., Wolpin B.M., Aguirre A.J., Hahn W.C., Westover K.D, & Gray N.S. (2020). Discovery of a selective inhibitor of Doublecortin Like Kinase 1. Nature chemical biology, 16(6), 635-643.
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7

Pdx1-cre;LSL-KrasG12D Pancreatic Cancer Model

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The 4-week old of LSL(lox-STOP-lox) KrasG12D mice on C57BL/6 background crossed with Pdx1-cre mice to generate the Pdx1-cre; LSL-KrasG12D mice. The KrasG12D mice are a G12D mutation that is introduced in exon 1 of the mice Kras allele and contains a STOP cassette flanked by loxP sites (lox-STOP-lox ; LSL) which can be removed by cre-recombinase to allow the expression of the mutated Kras allele. Pdx1-cre mice express cre-recombinase in pancreas under the control of pancreas specific pdx1 promoter. To generated the Pdx1-cre; LSL-KrasG12D mice, we used the LSL-KrasG12D mice crossed with Pdx1-cre transgenic mice. Both LSL-KrasG12D and Pdx1-cre mice were purchased from Jackson laboratory. The experimental protocols of this study were reviewed and approved by the Institutional Animal Care and Use Committee (IACUC) of NHRI (approval number: NHRI-IACUC-102082-A).
Arundhathi A., Chuang W.H., Chen J.K., Wang S.E., Shyr Y.M., Chen J.Y., Liao W.N., Chen H.W., Teng Y.M., Pai C.C, & Wang C.H. (2016). Prorenin receptor acts as a potential molecular target for pancreatic ductal adenocarcinoma diagnosis. Oncotarget, 7(34), 55437-55448.
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8

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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9

Generating Orai1-Deficient Mouse Models

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Six- to eight-week-old weighing 20–22 g C57BL6/J mice were purchased from the Beijing Vital River Laboratory Animal Technology Co., Ltd (Beijing, China). Orai1f/f mice were kindly gifted by Professor Bo Xiao from the State Key Laboratory of Biotherapy, Sichuan University. MRP8-Cre and Pdx1-Cre mice were purchased from the Jackson Laboratories (Bar Harbor, USA). To generate neutrophil-specific Orai1-deficient mice, MRP8-Cre mice were crossed with Orai1f/f mice, respectively. To generate pancreas-specific Orai1-deficient mice, Pdx1-Cre mouse line was crossed with Orai1f/f mice. All the control mice are the littermates of each strain. Mice were housed at 22°C with a 12-h light-dark cycle and maintained on a standard laboratory chow diet with free access to food and water in the Shanghai Model Organisms Center (Shanghai, China). All mice were allocated into each experimental group in a completely randomized manner using a randomized table (n = 6–8 per group).
Niu M., Zhang X., Wu Z., Li B., Bao J., Dai J., Yang Z., Zeng Y., Li L., Pandol S., Sutton R, & Wen L. (2023). Neutrophil-specific ORAI1 Calcium Channel Inhibition Reduces Pancreatitis-associated Acute Lung Injury. Function, 5(1), zqad061.
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10

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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