pdx1 cre kpc mice kpc mt4 (Cold Spring Harbor Laboratory Meetings)
86
Structured Review
Cold Spring Harbor Laboratory Meetings
pdx1 cre kpc mice kpc mt4
Pdx1 Cre Kpc Mice Kpc Mt4, supplied by Cold Spring Harbor Laboratory Meetings, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/kpc+mice/bl6+c57+cancer+cell+derived+derivedtb32048+from+kpc+line+murine+pancreatic+pdxcretg+%C3%BE/pmc12856980-28-24-32
Average 86 stars, based on 1 article reviews
Pdx1 Cre Kpc Mice Kpc Mt4, supplied by Cold Spring Harbor Laboratory Meetings, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/kpc+mice/bl6+c57+cancer+cell+derived+derivedtb32048+from+kpc+line+murine+pancreatic+pdxcretg+%C3%BE/pmc12856980-28-24-32
Average 86 stars, based on 1 article reviews
pdx1 cre kpc mice kpc mt4 - by Bioz Stars,
2026-10
86/100 stars
Images
1) Product Images from "The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma"
Article Title: The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
Journal: Cancer Research Communications
doi: 10.1158/2767-9764.CRC-25-0278
Figure Legend Snippet: CRISPR-mediated KDM4C deletion attenuates PDAC growth in vitro and in vivo . A, Western blot showing KDM4C depletion in selected AsPC1 and KPC-mT4 KDM4C -null clones. B, Colony formation assay (CFA): representative wells comparing AsPC1 cells to KDM4C KO isogenic cells show reduced colony formation ability in the absence of KDM4C. C, Quantification of CFA by ImageJ shows a significant reduction in the number of colonies in KDM4C KO cells compared with KDM4C WT cells; P value was determined by one-way ANOVA test; *, P ≤ 0.05; **, P ≤ 0.01. D, Proliferation assay measured through % confluence over time by the Incucyte Live Imaging system shows decreased proliferation in the absence of KDM4C, P value determined by one-way ANOVA test. E, Kaplan–Meier survival plot showing increased survival of B6 mice orthotopically transplanted with KDM4C KO KPC-mT4 cells compared with those transplanted with KDM4C WT KPC-mT4 ( n = 6 per arm).
Techniques Used: CRISPR, In Vitro, In Vivo, Western Blot, Clone Assay, Colony Assay, Proliferation Assay, Imaging
Figure Legend Snippet: KDM4C expression correlates with ERK activity. A, Top enriched IPA pathways from RNA-seq data from KDM4C KO vs. WT AsPC1 are cell-cycle arrest, inhibition of MEK/ERK, protein synthesis inhibition, and increased oxidative phosphorylation and apoptosis, whereas ATF4, MYC, and ERK1/2 are among the top downregulated networks. B, GSEA plot from RNA-seq data showing downregulated KRAS and MYC signatures in KDM4C -depleted cells. C, RPPA data demonstrate downregulation of the ERK pathway in two different KDM4C -null clones. D, Western blot validating downregulation of ERK phosphorylation in human PDAC cell line AsPC1 and in mouse PDAC cell line (KPC-mT4) KDM4C KO clones. E, Representative micrographs of pERK expression by IHC in PDAC tumors harvested at day 30 from mice injected with PDAC cell line KPC-mT4 demonstrates downregulation of pERK in the KDM4C KO clones compared with untreated KPC-mT4 (Scale bar, 100 μm).
Techniques Used: Expressing, Activity Assay, RNA Sequencing, Inhibition, Phospho-proteomics, Clone Assay, Western Blot, Injection
Figure Legend Snippet: Compensatory upregulation of KDM4A restores cell-intrinsic ERK signaling in KDM4C -null cells but not immune surveillance. A, Western blot panel shows that late-passage KDM4C KO clones of both AsPC1 and KPC-mT4 (KO-late) restored pERK levels. B–D, ERK reactivation rescues the reduction in colony formation and proliferation in both AsPC1 and KPC-mT4 KO cells observed in earlier passages. Bar plots show number of colonies calculated by ImageJ. For each sample, two wells have been analyzed, and the statistical significance is calculated using one-way ANOVA. For both AsPC1 and KPC-mT4 cells, the difference between parental and adapted KDM4C KO clones was not significant. E, Lentiviral shRNA knockdown of KDM4C recapitulates the adaptation to KDM4C depletion in adapted cells. Western blot panel compares early-passage (day 7 after transduction) and late-passage (day 40 after transduction) in AsPC1 cells. Late-passage KDM4C knockdown cells have adapted to the loss of KDM4C and restored ERK activation. F, Western blot validating KDM4A upregulation in adapted KPC-mT4 KDM4C KO clones. G, RNA-seq results from AsPC1 early-passage KDM4C KO cells correlate with the ERK inhibitor (ERKi) transcriptome signature, whereas late-passage adapted cells are inversely correlated. H and I, Bar graphs showing significant reduction in the tumor growth of adapted KPC-mT4 KDM4C KO cells when transplanted into the immunocompetent B6 mice compared with KDM4C WT control ( n = 5), whereas the reverse is observed when the same cells are transplanted into immune-compromised athymic mice ( n = 8), significance determined by unpaired t test; *, P ≤ 0.05.
Techniques Used: Western Blot, Clone Assay, shRNA, Knockdown, Transduction, Activation Assay, RNA Sequencing, Control
Figure Legend Snippet: Pan-KDM4 Inhibitor TACH107 reduces proliferation and colony formation in PDAC cell lines in vitro and increases survival in vivo . A, MTT assay shows reduced proliferation in PDAC cell lines following TACH107 treatment, significance determined by one-way ANOVA. B, Reduced colony formation ability of human and mouse PDAC cell lines upon treatment with varying doses of TACH107 and ( C ) Quantification of the number of colonies, one-way ANOVA was used to assess significance. D, Survival plot showing B6 mice transplanted with PDAC cell line KPC-mT4 and treated with TACH107 survive longer than those treated with vehicle only ( n = 3). E, Results from CETSA show increased heat stability of KDM4 proteins when treated with TACH107 vs. DMSO. F, Representative IF images showing increased H3K9me3 signal after TACH107 treatment compared with control cells. G, Normalized fluorescence intensity of H3K9me3 signal calculated by the corrected total cell fluorescence method using ImageJ, significance determined via unpaired Student t test. For all plots; * is P ≤ 0.05; ** is P ≤ 0.01; *** is P ≤ 0.001; and **** is P ≤ 0.0001. H, Representative micrographs showing H3K9me3 levels by IHC in PDAC tumors harvested on day 30 from mice injected with PDAC cell line KPC-mT4 demonstrate increased H3K9me3 mark in the TACH107 treated mice compared with vehicle control mice. Scale bar, 100 μm. I, Quantification of the area of positive staining in H using ImageJ color deconvolution plugin for IHC DAB staining, the difference between vehicle-treated and TACH107-treated samples is statistically significant.
Techniques Used: In Vitro, In Vivo, MTT Assay, Control, Fluorescence, Injection, Staining
Related Articles
In Vivo:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Transplantation Assay:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Isolation:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Animal Model:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Staining:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Expressing:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Injection:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Activity Assay:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Derivative Assay:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at TRAP Assay:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Negative Control:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Western Blot:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Immunohistochemistry:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Generated:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Control:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Drug discovery:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at In Vivo Imaging:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Imaging:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Two Tailed Test:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at Clinical Proteomics:Article Title: GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Article Snippet: Article Title: Cetylpyridinium chloride triggers paraptosis to suppress pancreatic tumor growth via the ERN1-MAP3K5-p38 pathway Article Snippet: KPC mice were obtained and bred following the protocol established by Dr. David Tuveson at |
