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Sino Biological lifr
Lifr, supplied by Sino Biological, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress lif receptor lifr inhibitor
Cancer cell intrinsic CREB transcriptionally regulates <t>LIF</t> expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with <t>EC359</t> <t>(LIFR</t> blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR and ELISA in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).
Lif Receptor Lifr Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/lif receptor lifr inhibitor/product/MedChemExpress
Average 94 stars, based on 1 article reviews
lif receptor lifr inhibitor - by Bioz Stars, 2026-02
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Sino Biological lif receptor
Cancer cell intrinsic CREB transcriptionally regulates <t>LIF</t> expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with <t>EC359</t> <t>(LIFR</t> blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR and ELISA in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).
Lif Receptor, supplied by Sino Biological, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/lif receptor/product/Sino Biological
Average 94 stars, based on 1 article reviews
lif receptor - by Bioz Stars, 2026-02
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Proteintech anti lifr
Cancer cell intrinsic CREB transcriptionally regulates <t>LIF</t> expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with <t>EC359</t> <t>(LIFR</t> blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR and ELISA in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).
Anti Lifr, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech lifr
Cancer cell intrinsic CREB transcriptionally regulates <t>LIF</t> expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with <t>EC359</t> <t>(LIFR</t> blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR and ELISA in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).
Lifr, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/lifr/product/Proteintech
Average 93 stars, based on 1 article reviews
lifr - by Bioz Stars, 2026-02
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Proteintech lifr proteintech 22779 1 ap 4 e cdherin abcam ab11512
Cancer cell intrinsic CREB transcriptionally regulates <t>LIF</t> expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with <t>EC359</t> <t>(LIFR</t> blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR and ELISA in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).
Lifr Proteintech 22779 1 Ap 4 E Cdherin Abcam Ab11512, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/lifr proteintech 22779 1 ap 4 e cdherin abcam ab11512/product/Proteintech
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lifr proteintech 22779 1 ap 4 e cdherin abcam ab11512 - by Bioz Stars, 2026-02
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Cancer cell intrinsic CREB transcriptionally regulates LIF expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with EC359 (LIFR blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR and ELISA in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).

Journal: bioRxiv

Article Title: Targeting CREB remodels the immune microenvironment to enhance immunotherapy responses in pancreatic cancer

doi: 10.64898/2025.12.04.691935

Figure Lengend Snippet: Cancer cell intrinsic CREB transcriptionally regulates LIF expression, driving macrophage-modulatory signaling in PDAC. (A) Experimental schematic demonstrating RNA sequencing (RNA-seq) analysis conducted in KPC mouse CREB WT and CREB KO tumor cells. (B) Bubble plot visualizing differentially regulated pathways (using molecular signature databases) in CREB KO transcriptomics compared with CREB WT tumor cells (n=3). (C) Ridge plot showing normalized enrichment scores for the hallmark JAK–STAT3 signaling pathway across different cellular constituents in the human HTAN pancreatic cancer dataset from treatment-naïve patients. (D) Western blot image depicting pSTAT3 activation, along with tSTAT3, vinculin and vimentin in mouse RAW macrophage 264.7 cell line treated with either recombinant (r) LIF alone (1 µg/mL) or in combination with EC359 (LIFR blockade, 0.2µM). (E) Chromatin Immunoprecipitation sequencing (ChIP-seq) peak signals visualized as heat maps which depict CREB binding sites across genomic regions in KPC mouse pancreatic tumor cells. The adjacent call out boxes with the heat maps showing essential genes regulated via CREB as its downstream mediators. (F) Integrative Genome Viewer (IGV) plot visualizing occupancy of CREB binding peaks in ChIP-seq data at the site of mouse Lif promoter gene regulatory sequences. (G-H) Violin dot plots showing downregulation of LIF expression via qPCR and ELISA in bulk tumor lysates of CREB KO KPC orthotopic PDAC tumors as compared to CREB WT with n=3-7 mice per group. (I) Representative photomicrographs of whole pancreas along with its corresponding quantification depicting significantly reduced LIF expression via IHC in age matched KPC C -/- as compared to KPC mice. Individual data points with mean ± SEM are shown and compared by two-tailed unpaired t test. *p<0.05; **p<0.01; ns non-significant (p>0.05).

Article Snippet: Under specific experimental conditions, bone marrow derived macrophages (BMDMs) were treated with murine recombinant LIF (Biotechne, 1 μg/mL), with or without pretreatment using an LIF receptor (LIFR) inhibitor (0.2 μM EC359, HY-120142, MedChem Express) at 37°C for 30 minutes.

Techniques: Expressing, RNA Sequencing, Western Blot, Activation Assay, Recombinant, ChIP-sequencing, Binding Assay, Enzyme-linked Immunosorbent Assay, Two Tailed Test