Review



antibody klf5  (Proteintech)


Bioz Verified Symbol Proteintech is a verified supplier  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94

    Structured Review

    Proteintech antibody klf5
    Antibody Klf5, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 76 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/klf5/KLF5+Antibody/pm41882103-112-7-11
    Average 94 stars, based on 76 article reviews
    antibody klf5 - by Bioz Stars, 2026-11
    94/100 stars

    Images

    Related Articles

    Blocking Assay:

    Article Title: Magnetic engineered bone mesenchymal stem cells-derived exosomes for targeted acute lung injury therapy.
    Article Snippet: .. After blocking with the 5% bovine serum albumin solution for 1 h, the membranes were incubated with appropriate primary antibodies against CD81, CD9, TSG101, Calnexin, GAPDH, KLF5 (Proteintech Group, Inc, Chicago, USA), Phospho-NF-κB p65 (Ser536, #3033, Cell Signaling Technology (CST), Beverly, MA, USA), NF-κB p65 (#8424, CST) at 4 °C overnight and with horseradish peroxidase-coupled secondary antibody at ambient temperature for 1 h. Immunoreactive bands were displayed in chemiluminescent systems (VILBER LOURMAT, Paris, France) with chemiluminescent reagents (Vazyme, Nanjing, China). .. The data are shown as the means ± standard deviation (SD) of at least three independent experiments and were analyzed using GraphPad Prism version 8.0 software (GraphPad Software, Inc., San Diego, CA, USA).

    Article Title: Magnetic engineered bone mesenchymal stem cells-derived exosomes for targeted acute lung injury therapy
    Article Snippet: .. After blocking with the 5% bovine serum albumin solution for 1 h, the membranes were incubated with appropriate primary antibodies against CD81, CD9, TSG101, Calnexin, GAPDH, KLF5 (Proteintech Group, Inc, Chicago, USA), Phospho-NF-κB p65 (Ser536, #3033, Cell Signaling Technology (CST), Beverly, MA, USA), NF-κB p65 (#8424, CST) at 4 °C overnight and with horseradish peroxidase-coupled secondary antibody at ambient temperature for 1 h. Immunoreactive bands were displayed in chemiluminescent systems (VILBER LOURMAT, Paris, France) with chemiluminescent reagents (Vazyme, Nanjing, China). .. The data are shown as the means ± standard deviation (SD) of at least three independent experiments and were analyzed using GraphPad Prism version 8.0 software (GraphPad Software, Inc., San Diego, CA, USA).

    Incubation:

    Article Title: Magnetic engineered bone mesenchymal stem cells-derived exosomes for targeted acute lung injury therapy.
    Article Snippet: .. After blocking with the 5% bovine serum albumin solution for 1 h, the membranes were incubated with appropriate primary antibodies against CD81, CD9, TSG101, Calnexin, GAPDH, KLF5 (Proteintech Group, Inc, Chicago, USA), Phospho-NF-κB p65 (Ser536, #3033, Cell Signaling Technology (CST), Beverly, MA, USA), NF-κB p65 (#8424, CST) at 4 °C overnight and with horseradish peroxidase-coupled secondary antibody at ambient temperature for 1 h. Immunoreactive bands were displayed in chemiluminescent systems (VILBER LOURMAT, Paris, France) with chemiluminescent reagents (Vazyme, Nanjing, China). .. The data are shown as the means ± standard deviation (SD) of at least three independent experiments and were analyzed using GraphPad Prism version 8.0 software (GraphPad Software, Inc., San Diego, CA, USA).

    Article Title: Magnetic engineered bone mesenchymal stem cells-derived exosomes for targeted acute lung injury therapy
    Article Snippet: .. After blocking with the 5% bovine serum albumin solution for 1 h, the membranes were incubated with appropriate primary antibodies against CD81, CD9, TSG101, Calnexin, GAPDH, KLF5 (Proteintech Group, Inc, Chicago, USA), Phospho-NF-κB p65 (Ser536, #3033, Cell Signaling Technology (CST), Beverly, MA, USA), NF-κB p65 (#8424, CST) at 4 °C overnight and with horseradish peroxidase-coupled secondary antibody at ambient temperature for 1 h. Immunoreactive bands were displayed in chemiluminescent systems (VILBER LOURMAT, Paris, France) with chemiluminescent reagents (Vazyme, Nanjing, China). .. The data are shown as the means ± standard deviation (SD) of at least three independent experiments and were analyzed using GraphPad Prism version 8.0 software (GraphPad Software, Inc., San Diego, CA, USA).

    Article Title: KLF5-regulated ZDHHC8 reduces chemosensitivity in high-grade serous ovarian cancer through β-catenin signaling
    Article Snippet: Equal amounts of protein (10 μg per sample) were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) on a 12% gel and transferred to PVDF membranes (Millipore, Germany). .. Membranes were blocked with 5% nonfat milk in TBST (Beyotime, Shanghai, China, Cat# P0231) for 1 h at room temperature, followed by overnight incubation at 4 °C with primary antibodies against ZDHHC8 (1:1000, Cat# 27179-1-AP), KLF5 (1:1000, Cat# 21017-1-AP), β-catenin (1:5000, Cat# 51067-2-AP), β-actin (1:5000, Cat# 81115-1-RR), and H3 (1:2000, Cat# 17168-1-AP) (Proteintech, USA). .. After washing, membranes were incubated with HRP-conjugated secondary antibodies (1:5000, ZSGB-Bio, Beijing, China, Cat# ZB-2301) for 2 h at room temperature.

    Article Title: Feed-forward loops by NR5A2 ensure robust gene activation during pre-implantation development
    Article Snippet: .. Embryos were incubated in antibody buffer [20 mM HEPES-NaOH, pH 7.5, 150 mM NaCl, 0.5 mM Spermidine, 0.1% BSA, 2 mM EDTA and 1× Protease inhibitor cocktail (Roche) with primary antibody [1:100; NR5A2 (R&D Systems, PP-H2325-00), KLF5 (Proteintech, 21017-1-AP), GATA6 (R&D Systems, AF1700), H3K27ac (Active motif, 39133)] overnight at 4°C on nutator. .. Embryos were washed three times through antibody buffer and further incubated with secondary antibody [1:100, guinea pig anti-rabbit H&L antibody (ABIN101961, Antibodies-Online) for anti-rabbit primary antibody, rabbit anti-mouse IgG H&L (ab46540, abcam) for anti-mouse primary antibody, and rabbit anti-goat IgG H&L (ab6697, abcam) for anti-goat primary antibody] for 1.5 h at room temperature.

    Article Title: Feed-forward loops by NR5A2 ensure robust gene activation during pre-implantation development.
    Article Snippet: .. Embryos were incubated in antibody buffer (20 mM HEPES-NaOH (pH7.5), 150 mM NaCl, 0.5 mM Spermidine, 0.1% BSA, 2 mM EDTA and 1x Protease inhibitor cocktail (Roche) with primary antibody (1:100 dilution, NR5A2 (R&D Systems, PP-H2325-00), KLF5 (Proteintech, 21017-1-AP), GATA6 (R&D Systems, AF1700), H3K27ac (Active motif, 39133)) overnight at 4°C on nutator. .. Embryos were washed three times through antibody buffer and further incubated with secondary antibody (1:100 dilution, Guinea pig anti-rabbit H&L antibody (ABIN101961, AntibodiesOnline) for anti-rabbit primary antibody, rabbit anti-mouse IgG H&L (ab46540, abcam) for anti-mouse primary antibody, and Rabbit anti-goat IgG H&L (ab6697, abcam) for anti-goat primary antibody) for 1.5 hours at room temperature.

    Staining:

    Article Title: The role of FAK in renal collecting duct in the progression from acute kidney injury to chronic kidney disease.
    Article Snippet: AKI and CKD are major global health problem, which closely connected and promote each other.. The mechanism may be related to maladaptive repair after renal tubular injury.. FAK is a non-receptor tyrosine kinase located at the intersection of multiple cell signal transduction pathways.

    Protease Inhibitor:

    Article Title: Feed-forward loops by NR5A2 ensure robust gene activation during pre-implantation development
    Article Snippet: .. Embryos were incubated in antibody buffer [20 mM HEPES-NaOH, pH 7.5, 150 mM NaCl, 0.5 mM Spermidine, 0.1% BSA, 2 mM EDTA and 1× Protease inhibitor cocktail (Roche) with primary antibody [1:100; NR5A2 (R&D Systems, PP-H2325-00), KLF5 (Proteintech, 21017-1-AP), GATA6 (R&D Systems, AF1700), H3K27ac (Active motif, 39133)] overnight at 4°C on nutator. .. Embryos were washed three times through antibody buffer and further incubated with secondary antibody [1:100, guinea pig anti-rabbit H&L antibody (ABIN101961, Antibodies-Online) for anti-rabbit primary antibody, rabbit anti-mouse IgG H&L (ab46540, abcam) for anti-mouse primary antibody, and rabbit anti-goat IgG H&L (ab6697, abcam) for anti-goat primary antibody] for 1.5 h at room temperature.

    Article Title: Feed-forward loops by NR5A2 ensure robust gene activation during pre-implantation development.
    Article Snippet: .. Embryos were incubated in antibody buffer (20 mM HEPES-NaOH (pH7.5), 150 mM NaCl, 0.5 mM Spermidine, 0.1% BSA, 2 mM EDTA and 1x Protease inhibitor cocktail (Roche) with primary antibody (1:100 dilution, NR5A2 (R&D Systems, PP-H2325-00), KLF5 (Proteintech, 21017-1-AP), GATA6 (R&D Systems, AF1700), H3K27ac (Active motif, 39133)) overnight at 4°C on nutator. .. Embryos were washed three times through antibody buffer and further incubated with secondary antibody (1:100 dilution, Guinea pig anti-rabbit H&L antibody (ABIN101961, AntibodiesOnline) for anti-rabbit primary antibody, rabbit anti-mouse IgG H&L (ab46540, abcam) for anti-mouse primary antibody, and Rabbit anti-goat IgG H&L (ab6697, abcam) for anti-goat primary antibody) for 1.5 hours at room temperature.

    other:

    Article Title: HERVH-derived eRNA activates a super-enhancer–driven ALDH1A3/SAT1 axis to promote ferroptosis escape and pancreatic cancer development
    Article Snippet: Second antibodies for Western blot were as follows: goat anti-rabbit (LI-COR Biosciences, Lincoln, NE, USA, 926-3221; 1:10,000) and goat anti-mouse (LI-COR Biosciences, 926-68020; 1:10,000).



    Similar Products

    94
    Proteintech antibody klf5
    Antibody Klf5, supplied by Proteintech, 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/product/klf5/KLF5+Antibody/pm41882103-112-7-11
    Average 94 stars, based on 1 article reviews
    antibody klf5 - by Bioz Stars, 2026-11
    94/100 stars
      Buy from Supplier

    94
    ABclonal Biotechnology klf5
    Klf5, supplied by ABclonal Biotechnology, 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/product/klf5/KLF5+Rabbit+pAb/pm42242406-111-32-53
    Average 94 stars, based on 1 article reviews
    klf5 - by Bioz Stars, 2026-11
    94/100 stars
      Buy from Supplier

    94
    Proteintech 147 anti klf5
    147 Anti Klf5, supplied by Proteintech, 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/product/klf5/KLF5+Antibody/10__1016_slash_j__jpha__2026__101696-90-18-54
    Average 94 stars, based on 1 article reviews
    147 anti klf5 - by Bioz Stars, 2026-11
    94/100 stars
      Buy from Supplier

    94
    ABclonal Biotechnology western blotting
    Western Blotting, supplied by ABclonal Biotechnology, 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/product/klf5/KLF5+Rabbit+pAb/pm42092415-68-0-9
    Average 94 stars, based on 1 article reviews
    western blotting - by Bioz Stars, 2026-11
    94/100 stars
      Buy from Supplier

    88
    Thermo Fisher gene exp klf5 hs00156145 m1
    Gene Exp Klf5 Hs00156145 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/klf5/Gene+Exp%2E+KLF5%2C+Hs00156145_m1/pm41957847-355-23-7
    Average 88 stars, based on 1 article reviews
    gene exp klf5 hs00156145 m1 - by Bioz Stars, 2026-11
    88/100 stars
      Buy from Supplier

    94
    Proteintech anti klf5
    Anti Klf5, supplied by Proteintech, 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/product/klf5/KLF5+Antibody/pm41805193-367-61-62
    Average 94 stars, based on 1 article reviews
    anti klf5 - by Bioz Stars, 2026-11
    94/100 stars
      Buy from Supplier

    93
    Santa Cruz Biotechnology klf5
    PKA signaling pathway aberrantly activated in PDAC (A) Heatmap showing mRNA expression levels of moderately and poorly differentiated PDAC from the GEO database ( GSE226307 ). PRKAR2B and <t>KLF5</t> were labeled. (B) KEGG pathway enrichment analysis of differentially expressed genes from RNA-seq in GEO database ( GSE226307 ). The “cAMP signaling pathway” is highlighted in red. (C) Volcano plot of RNA-seq data comparing PDAC tissue and normal pancreatic tissue ( GSE16515 ). Red dots represent upregulated mRNAs, blue dots represent downregulated mRNAs ( p < 0.05, log 2 foldchange >1 or < –1). PRKAR2B and KLF5 were labeled. (D–F) Colorimetric analysis of PKA activity (D) and ELISA analysis of pCREB and KLF5 levels (E–F) in pancreatic puncture fluid from patients with benign pancreatic diseases ( n = 3 independent samples), well or moderately differentiated PDAC ( n = 10 independent samples), or poorly differentiated PDAC ( n = 7 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05; ∗∗, p < 0.01. (G and H) Colorimetric analysis of PKA activity (G) and qPCR analysis of mRNA expression of KLF5 (H) in H6C7, Capan-2, and AsPC-1 cells ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01, ∗∗∗, p < 0.001. (I and J) mRNA expression profiles of KLF5 based on data from 182 PDAC patients and 4 normal controls in the TCGA database. ∗, p < 0.05. (K) Kaplan-Meier survival analysis of KLF5 expression using data from 182 PDAC patients in the TCGA database. ∗, p < 0.05.
    Klf5, supplied by Santa Cruz Biotechnology, 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/product/klf5/BTEB2+Antibody/pmc12907050-479-30-34
    Average 93 stars, based on 1 article reviews
    klf5 - by Bioz Stars, 2026-11
    93/100 stars
      Buy from Supplier

    86
    Genechem human klf5
    PKA signaling pathway aberrantly activated in PDAC (A) Heatmap showing mRNA expression levels of moderately and poorly differentiated PDAC from the GEO database ( GSE226307 ). PRKAR2B and <t>KLF5</t> were labeled. (B) KEGG pathway enrichment analysis of differentially expressed genes from RNA-seq in GEO database ( GSE226307 ). The “cAMP signaling pathway” is highlighted in red. (C) Volcano plot of RNA-seq data comparing PDAC tissue and normal pancreatic tissue ( GSE16515 ). Red dots represent upregulated mRNAs, blue dots represent downregulated mRNAs ( p < 0.05, log 2 foldchange >1 or < –1). PRKAR2B and KLF5 were labeled. (D–F) Colorimetric analysis of PKA activity (D) and ELISA analysis of pCREB and KLF5 levels (E–F) in pancreatic puncture fluid from patients with benign pancreatic diseases ( n = 3 independent samples), well or moderately differentiated PDAC ( n = 10 independent samples), or poorly differentiated PDAC ( n = 7 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05; ∗∗, p < 0.01. (G and H) Colorimetric analysis of PKA activity (G) and qPCR analysis of mRNA expression of KLF5 (H) in H6C7, Capan-2, and AsPC-1 cells ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01, ∗∗∗, p < 0.001. (I and J) mRNA expression profiles of KLF5 based on data from 182 PDAC patients and 4 normal controls in the TCGA database. ∗, p < 0.05. (K) Kaplan-Meier survival analysis of KLF5 expression using data from 182 PDAC patients in the TCGA database. ∗, p < 0.05.
    Human Klf5, supplied by Genechem, 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/klf5/klf5+shrna/10__1016_slash_j__jpha__2026__101575-89-30-40
    Average 86 stars, based on 1 article reviews
    human klf5 - by Bioz Stars, 2026-11
    86/100 stars
      Buy from Supplier

    94
    Proteintech rabbit anti klf5
    PKA signaling pathway aberrantly activated in PDAC (A) Heatmap showing mRNA expression levels of moderately and poorly differentiated PDAC from the GEO database ( GSE226307 ). PRKAR2B and <t>KLF5</t> were labeled. (B) KEGG pathway enrichment analysis of differentially expressed genes from RNA-seq in GEO database ( GSE226307 ). The “cAMP signaling pathway” is highlighted in red. (C) Volcano plot of RNA-seq data comparing PDAC tissue and normal pancreatic tissue ( GSE16515 ). Red dots represent upregulated mRNAs, blue dots represent downregulated mRNAs ( p < 0.05, log 2 foldchange >1 or < –1). PRKAR2B and KLF5 were labeled. (D–F) Colorimetric analysis of PKA activity (D) and ELISA analysis of pCREB and KLF5 levels (E–F) in pancreatic puncture fluid from patients with benign pancreatic diseases ( n = 3 independent samples), well or moderately differentiated PDAC ( n = 10 independent samples), or poorly differentiated PDAC ( n = 7 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05; ∗∗, p < 0.01. (G and H) Colorimetric analysis of PKA activity (G) and qPCR analysis of mRNA expression of KLF5 (H) in H6C7, Capan-2, and AsPC-1 cells ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01, ∗∗∗, p < 0.001. (I and J) mRNA expression profiles of KLF5 based on data from 182 PDAC patients and 4 normal controls in the TCGA database. ∗, p < 0.05. (K) Kaplan-Meier survival analysis of KLF5 expression using data from 182 PDAC patients in the TCGA database. ∗, p < 0.05.
    Rabbit Anti Klf5, supplied by Proteintech, 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/product/klf5/KLF5+Antibody/pm41617093-55-15-35
    Average 94 stars, based on 1 article reviews
    rabbit anti klf5 - by Bioz Stars, 2026-11
    94/100 stars
      Buy from Supplier

    Image Search Results


    PKA signaling pathway aberrantly activated in PDAC (A) Heatmap showing mRNA expression levels of moderately and poorly differentiated PDAC from the GEO database ( GSE226307 ). PRKAR2B and KLF5 were labeled. (B) KEGG pathway enrichment analysis of differentially expressed genes from RNA-seq in GEO database ( GSE226307 ). The “cAMP signaling pathway” is highlighted in red. (C) Volcano plot of RNA-seq data comparing PDAC tissue and normal pancreatic tissue ( GSE16515 ). Red dots represent upregulated mRNAs, blue dots represent downregulated mRNAs ( p < 0.05, log 2 foldchange >1 or < –1). PRKAR2B and KLF5 were labeled. (D–F) Colorimetric analysis of PKA activity (D) and ELISA analysis of pCREB and KLF5 levels (E–F) in pancreatic puncture fluid from patients with benign pancreatic diseases ( n = 3 independent samples), well or moderately differentiated PDAC ( n = 10 independent samples), or poorly differentiated PDAC ( n = 7 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05; ∗∗, p < 0.01. (G and H) Colorimetric analysis of PKA activity (G) and qPCR analysis of mRNA expression of KLF5 (H) in H6C7, Capan-2, and AsPC-1 cells ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01, ∗∗∗, p < 0.001. (I and J) mRNA expression profiles of KLF5 based on data from 182 PDAC patients and 4 normal controls in the TCGA database. ∗, p < 0.05. (K) Kaplan-Meier survival analysis of KLF5 expression using data from 182 PDAC patients in the TCGA database. ∗, p < 0.05.

    Journal: iScience

    Article Title: HHEX-PRKAR2B axis-mediated PKA activation drives glucose metabolism-dependent progression of pancreatic ductal adenocarcinoma

    doi: 10.1016/j.isci.2026.114691

    Figure Lengend Snippet: PKA signaling pathway aberrantly activated in PDAC (A) Heatmap showing mRNA expression levels of moderately and poorly differentiated PDAC from the GEO database ( GSE226307 ). PRKAR2B and KLF5 were labeled. (B) KEGG pathway enrichment analysis of differentially expressed genes from RNA-seq in GEO database ( GSE226307 ). The “cAMP signaling pathway” is highlighted in red. (C) Volcano plot of RNA-seq data comparing PDAC tissue and normal pancreatic tissue ( GSE16515 ). Red dots represent upregulated mRNAs, blue dots represent downregulated mRNAs ( p < 0.05, log 2 foldchange >1 or < –1). PRKAR2B and KLF5 were labeled. (D–F) Colorimetric analysis of PKA activity (D) and ELISA analysis of pCREB and KLF5 levels (E–F) in pancreatic puncture fluid from patients with benign pancreatic diseases ( n = 3 independent samples), well or moderately differentiated PDAC ( n = 10 independent samples), or poorly differentiated PDAC ( n = 7 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05; ∗∗, p < 0.01. (G and H) Colorimetric analysis of PKA activity (G) and qPCR analysis of mRNA expression of KLF5 (H) in H6C7, Capan-2, and AsPC-1 cells ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01, ∗∗∗, p < 0.001. (I and J) mRNA expression profiles of KLF5 based on data from 182 PDAC patients and 4 normal controls in the TCGA database. ∗, p < 0.05. (K) Kaplan-Meier survival analysis of KLF5 expression using data from 182 PDAC patients in the TCGA database. ∗, p < 0.05.

    Article Snippet: The following primary antibodies were used: GAPDH (1:1000, cat. sc-137179, Santa Cruz Biotechnology), PRKAR2B (1:1000, cat. sc-376778, Santa Cruz Biotechnology), CREB (1:1000, cat. ab31515, Abcam), pCREB (1:1000, cat. ab32096, Abcam), KLF5 (1:1000, cat. sc-398014, Santa Cruz Biotechnology), and HK2 (1:1000, cat. sc-130358, Santa Cruz Biotechnology).

    Techniques: Expressing, Labeling, RNA Sequencing, Activity Assay, Enzyme-linked Immunosorbent Assay

    PRKAR2B downregulation activates PKA in PDAC (A) Volcano plot of RNA-seq data comparing PDAC tissue and normal pancreatic tissue ( GSE226307 ). Red dots represent upregulated mRNAs, blue dots represent downregulated mRNAs ( p < 0.05, log 2 foldchange >1 or < -1). KLF5, PRKAR1A, PRKAR1B, PRKAR2A, PRKAR2B, PRKACA, and PRKACB were labeled. (B) mRNA expression levels of PRKAR2B based on data from 182 PDAC patients and 4 normal controls in the TCGA database. ∗, p < 0.05. (C) Protein expression levels of PRKAR2B based on data from 137 PDAC patients and 74 normal controls in the CPTAC database. ∗∗∗∗, p < 0.0001. (D) Kaplan-Meier survival analysis of PRKAR2B expression using data from 182 PDAC patients in the TCGA database. ∗, p < 0.05. (E) mRNA expression levels of indicated genes in AsPC-1 cells with or without siRNA ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗, p < 0.01, ∗∗∗, p < 0.001, ∗∗∗∗, p < 0.0001. (F) Colorimetric analysis of PKA activity in AsPC-1 cells transfected with siRNA targeting EPHA2 , SEMA4B , PYGB , or PRKAR2B ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01; NS, no significance. (G) Schematic diagram of PKA activation and inactivation. RS, regulatory subunit; CS, catalytic subunit. (H) Immunoblot analysis of PRKAR2B in H6C7, Capan-2, and AsPC-1 cells. (I) Immunoblot analysis of PRKAR2B in AsPC-1 cells with PRKAR2B knockout or overexpression. (J) Colorimetric analysis of PKA activity in AsPC-1 cells with PRKAR2B knockout or overexpression ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05. (K) Immunoblot analysis of CREB, pCREB, and KLF5 in AsPC-1 cells with PRKAR2B knockout or overexpression. (L) Correlation between PRKAR2B and KLF5 expression based on data from 182 PDAC patients in the TCGA database. ∗∗∗∗, p < 0.0001.

    Journal: iScience

    Article Title: HHEX-PRKAR2B axis-mediated PKA activation drives glucose metabolism-dependent progression of pancreatic ductal adenocarcinoma

    doi: 10.1016/j.isci.2026.114691

    Figure Lengend Snippet: PRKAR2B downregulation activates PKA in PDAC (A) Volcano plot of RNA-seq data comparing PDAC tissue and normal pancreatic tissue ( GSE226307 ). Red dots represent upregulated mRNAs, blue dots represent downregulated mRNAs ( p < 0.05, log 2 foldchange >1 or < -1). KLF5, PRKAR1A, PRKAR1B, PRKAR2A, PRKAR2B, PRKACA, and PRKACB were labeled. (B) mRNA expression levels of PRKAR2B based on data from 182 PDAC patients and 4 normal controls in the TCGA database. ∗, p < 0.05. (C) Protein expression levels of PRKAR2B based on data from 137 PDAC patients and 74 normal controls in the CPTAC database. ∗∗∗∗, p < 0.0001. (D) Kaplan-Meier survival analysis of PRKAR2B expression using data from 182 PDAC patients in the TCGA database. ∗, p < 0.05. (E) mRNA expression levels of indicated genes in AsPC-1 cells with or without siRNA ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗, p < 0.01, ∗∗∗, p < 0.001, ∗∗∗∗, p < 0.0001. (F) Colorimetric analysis of PKA activity in AsPC-1 cells transfected with siRNA targeting EPHA2 , SEMA4B , PYGB , or PRKAR2B ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01; NS, no significance. (G) Schematic diagram of PKA activation and inactivation. RS, regulatory subunit; CS, catalytic subunit. (H) Immunoblot analysis of PRKAR2B in H6C7, Capan-2, and AsPC-1 cells. (I) Immunoblot analysis of PRKAR2B in AsPC-1 cells with PRKAR2B knockout or overexpression. (J) Colorimetric analysis of PKA activity in AsPC-1 cells with PRKAR2B knockout or overexpression ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05. (K) Immunoblot analysis of CREB, pCREB, and KLF5 in AsPC-1 cells with PRKAR2B knockout or overexpression. (L) Correlation between PRKAR2B and KLF5 expression based on data from 182 PDAC patients in the TCGA database. ∗∗∗∗, p < 0.0001.

    Article Snippet: The following primary antibodies were used: GAPDH (1:1000, cat. sc-137179, Santa Cruz Biotechnology), PRKAR2B (1:1000, cat. sc-376778, Santa Cruz Biotechnology), CREB (1:1000, cat. ab31515, Abcam), pCREB (1:1000, cat. ab32096, Abcam), KLF5 (1:1000, cat. sc-398014, Santa Cruz Biotechnology), and HK2 (1:1000, cat. sc-130358, Santa Cruz Biotechnology).

    Techniques: RNA Sequencing, Labeling, Expressing, Activity Assay, Transfection, Activation Assay, Western Blot, Knock-Out, Over Expression

    HHEX downregulation represses PRKAR2B transcription (A) Enrichment of H3K27me3 at the PRKAR2B gene in AsPC-1 cells. Chromatin immunoprecipitation was performed using an antibody against H3K27me3 or a control IgG antibody. The enriched DNA was quantified by qPCR and is presented as % of Input. Values are shown as mean ± SD ( n = 3 independent repeats). NS, no significance. (B and C) Overlap of the upregulated (B) and downregulated (C) genes in moderate and poor differentiation PDAC compared with normal pancreatic tissue with known transcription factor. (D) mRNA expression profile of HHEX using 182 PDAC patient data and 4 normal controls from TCGA database. ∗∗, p < 0.01. (E) Kaplan-Meier survival analysis of HHEX expression using data from 182 PDAC patients in the TCGA database. ∗∗, p < 0.01. (F) Correlation between PRKAR2B and HHEX expression based on data from 182 PDAC patients in the TCGA database. ∗∗∗, p < 0.001. (G) Enrichment of HHEX at the PRKAR2B gene in AsPC-1 cells. Chromatin immunoprecipitation was performed using an antibody against HHEX or a control IgG antibody. The enriched DNA was quantified by qPCR and is presented as % of input. Values are shown as mean ± SD ( n = 3 independent repeats). ∗∗∗∗, p < 0.0001. (H and I) mRNA levels of HHEX (H) or PRKAR2B (I) in AsPC-1 cells with HHEX knockdown or overexpression ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01, ∗∗∗, p < 0.001. (J) mRNA levels of HHEX in AsPC-1 cells with PRKAR2B knockout or overexpression ( n = 3 independent repeats). Data were expressed as mean ± SD. NS, no significance. (K–L) Colorimetric analysis of PKA activity (K) and qPCR analysis of KLF5 mRNA levels (L) in AsPC-1 cells with or without PRKAR2B knockout followed by HHEX knockdown ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗, p < 0.01, ∗∗∗∗, p < 0.0001; NS, no significance.

    Journal: iScience

    Article Title: HHEX-PRKAR2B axis-mediated PKA activation drives glucose metabolism-dependent progression of pancreatic ductal adenocarcinoma

    doi: 10.1016/j.isci.2026.114691

    Figure Lengend Snippet: HHEX downregulation represses PRKAR2B transcription (A) Enrichment of H3K27me3 at the PRKAR2B gene in AsPC-1 cells. Chromatin immunoprecipitation was performed using an antibody against H3K27me3 or a control IgG antibody. The enriched DNA was quantified by qPCR and is presented as % of Input. Values are shown as mean ± SD ( n = 3 independent repeats). NS, no significance. (B and C) Overlap of the upregulated (B) and downregulated (C) genes in moderate and poor differentiation PDAC compared with normal pancreatic tissue with known transcription factor. (D) mRNA expression profile of HHEX using 182 PDAC patient data and 4 normal controls from TCGA database. ∗∗, p < 0.01. (E) Kaplan-Meier survival analysis of HHEX expression using data from 182 PDAC patients in the TCGA database. ∗∗, p < 0.01. (F) Correlation between PRKAR2B and HHEX expression based on data from 182 PDAC patients in the TCGA database. ∗∗∗, p < 0.001. (G) Enrichment of HHEX at the PRKAR2B gene in AsPC-1 cells. Chromatin immunoprecipitation was performed using an antibody against HHEX or a control IgG antibody. The enriched DNA was quantified by qPCR and is presented as % of input. Values are shown as mean ± SD ( n = 3 independent repeats). ∗∗∗∗, p < 0.0001. (H and I) mRNA levels of HHEX (H) or PRKAR2B (I) in AsPC-1 cells with HHEX knockdown or overexpression ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01, ∗∗∗, p < 0.001. (J) mRNA levels of HHEX in AsPC-1 cells with PRKAR2B knockout or overexpression ( n = 3 independent repeats). Data were expressed as mean ± SD. NS, no significance. (K–L) Colorimetric analysis of PKA activity (K) and qPCR analysis of KLF5 mRNA levels (L) in AsPC-1 cells with or without PRKAR2B knockout followed by HHEX knockdown ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗, p < 0.01, ∗∗∗∗, p < 0.0001; NS, no significance.

    Article Snippet: The following primary antibodies were used: GAPDH (1:1000, cat. sc-137179, Santa Cruz Biotechnology), PRKAR2B (1:1000, cat. sc-376778, Santa Cruz Biotechnology), CREB (1:1000, cat. ab31515, Abcam), pCREB (1:1000, cat. ab32096, Abcam), KLF5 (1:1000, cat. sc-398014, Santa Cruz Biotechnology), and HK2 (1:1000, cat. sc-130358, Santa Cruz Biotechnology).

    Techniques: Chromatin Immunoprecipitation, Control, Expressing, Knockdown, Over Expression, Knock-Out, Activity Assay

    PKA activation promotes PDAC progression through metabolic reprogramming (A and B) Colorimetric analysis of PKA activity (A) and qPCR analysis of KLF5 mRNA levels (B) in AsPC-1 cells treated with or without KT5720 (5 μM, 48 h) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗∗, p < 0.001. (C) Immunoblot analysis of CREB, pCREB, and KLF5 in AsPC-1 cells following PRKAR2B knockout or overexpression, with or without KT5720 treatment (5 μM, 48 h). (D) Cell viability was measured by CCK-8 assay in AsPC-1 cells subjected to PRKAR2B knockout or HHEX knockdown, in the presence or absence of treatment with KT5720 (5 μM, 48 h) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗∗, p < 0.001; NS, no significance. (E) Cell death analysis by PI staining and flow cytometry in AsPC-1 cells subjected to PRKAR2B knockout or HHEX knockdown, in the presence or absence of treatment with KT5720 (5 μM, 48 h) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01; NS, no significance. (F) Cell invasion assays in AsPC-1 cells following PRKAR2B knockout or HHEX knockdown, with or without KT5720 treatment (5 μM, 48 h). Scale bars, 80 μm (G) KEGG pathway enrichment analysis of differentially expressed genes identified in GEO database ( GSE134618 ). (H) Cell viability measured by CCK-8 assay in AsPC-1 cells under low FBS (2%) or low glucose (1,000 mg/L) conditions, with or without KT5720 treatment (5 μM, 48 h, n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01; ∗∗∗∗, p < 0.0001; NS, no significance. (I) Cell death analysis by PI staining and flow cytometry in AsPC-1 cells under low FBS (2%) or low glucose (1,000 mg/L) conditions, with or without KT5720 treatment (5 μM, 48 h, n = 3 independent repeats). Data were expressed as mean ± SD. NS, no significance. (J) Cell invasion assays in AsPC-1 cells treated with low FBS (2%), low glucose (1,000 mg/L), or KT5720 (5 μM, 48 h). Scale bars, 80 μm (K) Relative lactate levels in pancreatic puncture fluid from patients with benign pancreatic diseases ( n = 3 independent samples), well or moderately differentiated PDAC ( n = 10 independent samples), or poorly differentiated PDAC ( n = 7 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05; ∗∗, p < 0.01. (L) Relative lactate levels in the supernatant of H6C7, Capan-2, and AsPC-1 cells ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05. (M) Intracellular and extracellular glucose levels in H6C7, Capan-2, and AsPC-1 cells ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01.

    Journal: iScience

    Article Title: HHEX-PRKAR2B axis-mediated PKA activation drives glucose metabolism-dependent progression of pancreatic ductal adenocarcinoma

    doi: 10.1016/j.isci.2026.114691

    Figure Lengend Snippet: PKA activation promotes PDAC progression through metabolic reprogramming (A and B) Colorimetric analysis of PKA activity (A) and qPCR analysis of KLF5 mRNA levels (B) in AsPC-1 cells treated with or without KT5720 (5 μM, 48 h) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗∗, p < 0.001. (C) Immunoblot analysis of CREB, pCREB, and KLF5 in AsPC-1 cells following PRKAR2B knockout or overexpression, with or without KT5720 treatment (5 μM, 48 h). (D) Cell viability was measured by CCK-8 assay in AsPC-1 cells subjected to PRKAR2B knockout or HHEX knockdown, in the presence or absence of treatment with KT5720 (5 μM, 48 h) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗∗, p < 0.001; NS, no significance. (E) Cell death analysis by PI staining and flow cytometry in AsPC-1 cells subjected to PRKAR2B knockout or HHEX knockdown, in the presence or absence of treatment with KT5720 (5 μM, 48 h) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01; NS, no significance. (F) Cell invasion assays in AsPC-1 cells following PRKAR2B knockout or HHEX knockdown, with or without KT5720 treatment (5 μM, 48 h). Scale bars, 80 μm (G) KEGG pathway enrichment analysis of differentially expressed genes identified in GEO database ( GSE134618 ). (H) Cell viability measured by CCK-8 assay in AsPC-1 cells under low FBS (2%) or low glucose (1,000 mg/L) conditions, with or without KT5720 treatment (5 μM, 48 h, n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01; ∗∗∗∗, p < 0.0001; NS, no significance. (I) Cell death analysis by PI staining and flow cytometry in AsPC-1 cells under low FBS (2%) or low glucose (1,000 mg/L) conditions, with or without KT5720 treatment (5 μM, 48 h, n = 3 independent repeats). Data were expressed as mean ± SD. NS, no significance. (J) Cell invasion assays in AsPC-1 cells treated with low FBS (2%), low glucose (1,000 mg/L), or KT5720 (5 μM, 48 h). Scale bars, 80 μm (K) Relative lactate levels in pancreatic puncture fluid from patients with benign pancreatic diseases ( n = 3 independent samples), well or moderately differentiated PDAC ( n = 10 independent samples), or poorly differentiated PDAC ( n = 7 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05; ∗∗, p < 0.01. (L) Relative lactate levels in the supernatant of H6C7, Capan-2, and AsPC-1 cells ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05. (M) Intracellular and extracellular glucose levels in H6C7, Capan-2, and AsPC-1 cells ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01.

    Article Snippet: The following primary antibodies were used: GAPDH (1:1000, cat. sc-137179, Santa Cruz Biotechnology), PRKAR2B (1:1000, cat. sc-376778, Santa Cruz Biotechnology), CREB (1:1000, cat. ab31515, Abcam), pCREB (1:1000, cat. ab32096, Abcam), KLF5 (1:1000, cat. sc-398014, Santa Cruz Biotechnology), and HK2 (1:1000, cat. sc-130358, Santa Cruz Biotechnology).

    Techniques: Activation Assay, Activity Assay, Western Blot, Knock-Out, Over Expression, CCK-8 Assay, Knockdown, Staining, Flow Cytometry

    Glucose-activated PKA promotes PDAC progression via HK2-driven glycolysis (A) Colorimetric analysis of PKA activity in AsPC-1 cells treated with high glucose (4,500 mg/L) or low glucose (1,000 mg/L) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05. (B) Immunoblot analysis of CREB, pCREB, and KLF5 in AsPC-1 cells treated with high glucose (4,500 mg/L) or low glucose (1,000 mg/L). (C–E) mRNA expression of KLF5 (C), intracellular cAMP levels (D), and relative ATP levels (E) in AsPC-1 cells treated with high glucose (4,500 mg/L) or low glucose (1,000 mg/L) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗, p < 0.01. (F) Schematic diagram of carbohydrate metabolism. TCA, tricarboxylic acid; PPP, pentose phosphate pathway. (G) Intracellular and extracellular glucose levels in AsPC-1 cells with or without PRKAR2B knockout ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗∗, p < 0.001. (H) Relative lactate levels in the supernatant of AsPC-1 cultures with or without PRKAR2B knockout ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01. (I–J) NADP + /NADPH ratio (I) and relative ATP levels (J) in AsPC-1 cells with or without PRKAR2B knockout ( n = 3 independent repeats). Data were expressed as mean ± SD. NS, no significance. (K) Schematic diagram of the 19 core genes identified in the network analysis of C. (L) mRNA expression levels of HK2 based on data from 182 PDAC patients and 4 normal controls in the TCGA database. ∗∗∗∗, p < 0.0001. (M) Protein expression levels of HK2 based on data from 137 PDAC patients and 74 normal controls in the CPTAC database. ∗∗∗∗, p < 0.0001. (N–O) Correlation analysis among HK2 , KLF5 , and PRKAR2B expression using transcriptomic data from 182 PDAC patients in TCGA. ∗∗∗, p < 0.001, ∗∗∗∗, p < 0.0001. (P) HK2 mRNA expression in AsPC-1 cells following PRKAR2B knockout or treatment with dbcAMP (0.2 mM, 24 h) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01. (Q) HK2 mRNA expression in AsPC-1 cells with or without HK2 knockdown ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05. (R) Cell viability measured by CCK-8 assay in AsPC-1 cells after HK2 knockdown or treatment with 2-DG (4 mM, 24 h) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01; NS, no significance. (S) Cell invasion assays in AsPC-1 cells after HK2 knockdown or treatment with 2-DG (4 mM, 24 h). Data were expressed as mean ± SD. Scale bars, 80 μm.

    Journal: iScience

    Article Title: HHEX-PRKAR2B axis-mediated PKA activation drives glucose metabolism-dependent progression of pancreatic ductal adenocarcinoma

    doi: 10.1016/j.isci.2026.114691

    Figure Lengend Snippet: Glucose-activated PKA promotes PDAC progression via HK2-driven glycolysis (A) Colorimetric analysis of PKA activity in AsPC-1 cells treated with high glucose (4,500 mg/L) or low glucose (1,000 mg/L) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05. (B) Immunoblot analysis of CREB, pCREB, and KLF5 in AsPC-1 cells treated with high glucose (4,500 mg/L) or low glucose (1,000 mg/L). (C–E) mRNA expression of KLF5 (C), intracellular cAMP levels (D), and relative ATP levels (E) in AsPC-1 cells treated with high glucose (4,500 mg/L) or low glucose (1,000 mg/L) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗, p < 0.01. (F) Schematic diagram of carbohydrate metabolism. TCA, tricarboxylic acid; PPP, pentose phosphate pathway. (G) Intracellular and extracellular glucose levels in AsPC-1 cells with or without PRKAR2B knockout ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗∗, p < 0.001. (H) Relative lactate levels in the supernatant of AsPC-1 cultures with or without PRKAR2B knockout ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01. (I–J) NADP + /NADPH ratio (I) and relative ATP levels (J) in AsPC-1 cells with or without PRKAR2B knockout ( n = 3 independent repeats). Data were expressed as mean ± SD. NS, no significance. (K) Schematic diagram of the 19 core genes identified in the network analysis of C. (L) mRNA expression levels of HK2 based on data from 182 PDAC patients and 4 normal controls in the TCGA database. ∗∗∗∗, p < 0.0001. (M) Protein expression levels of HK2 based on data from 137 PDAC patients and 74 normal controls in the CPTAC database. ∗∗∗∗, p < 0.0001. (N–O) Correlation analysis among HK2 , KLF5 , and PRKAR2B expression using transcriptomic data from 182 PDAC patients in TCGA. ∗∗∗, p < 0.001, ∗∗∗∗, p < 0.0001. (P) HK2 mRNA expression in AsPC-1 cells following PRKAR2B knockout or treatment with dbcAMP (0.2 mM, 24 h) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01. (Q) HK2 mRNA expression in AsPC-1 cells with or without HK2 knockdown ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗, p < 0.05. (R) Cell viability measured by CCK-8 assay in AsPC-1 cells after HK2 knockdown or treatment with 2-DG (4 mM, 24 h) ( n = 3 independent repeats). Data were expressed as mean ± SD. ∗∗, p < 0.01; NS, no significance. (S) Cell invasion assays in AsPC-1 cells after HK2 knockdown or treatment with 2-DG (4 mM, 24 h). Data were expressed as mean ± SD. Scale bars, 80 μm.

    Article Snippet: The following primary antibodies were used: GAPDH (1:1000, cat. sc-137179, Santa Cruz Biotechnology), PRKAR2B (1:1000, cat. sc-376778, Santa Cruz Biotechnology), CREB (1:1000, cat. ab31515, Abcam), pCREB (1:1000, cat. ab32096, Abcam), KLF5 (1:1000, cat. sc-398014, Santa Cruz Biotechnology), and HK2 (1:1000, cat. sc-130358, Santa Cruz Biotechnology).

    Techniques: Activity Assay, Western Blot, Expressing, Knock-Out, Knockdown, CCK-8 Assay

    In vivo demonstration of glucose-activated PKA promoting glycolysis-dependent progression A. Immunoblot analysis of PRKAR2B in KPC cells with or without PRKAR2B knockout. (B–D) Representative images of colony formation by KPC cells, with or without PRKAR2B knockout, cultured in normal or low-glucose medium (B). Colony size (C) and number of colonies (D) were graphed ( n = 3 independent repeats). Data were expressed as mean ± SD. Scale bars, 50 μm ∗, p < 0.05, ∗∗, p < 0.01, NS, no significance. (E) Representative H&E-stained pancreatic sections from mice with tamoxifen-inducible, pancreas-specific KRAS expression, harvested 3 weeks after tamoxifen or vehicle injection. Scale bars, 1 mm (F–H) PKA activity (F), pyruvic acid level (G), and lactate level (H) in pancreatic tissues from mice, harvested 3 weeks after tamoxifen or vehicle injection, assessing the effect of tamoxifen-inducible, pancreas-specific KRAS expression ( n = 4 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05; ∗∗, p < 0.01. (I) Colorimetric analysis of PKA activity in wild-type and diabetic mice ( n = 4 independent samples). Data were expressed as mean ± SD. ∗∗, p < 0.01. (J) Representative immunoblot of CREB, pCREB, and KLF5 in wild-type and diabetic mice ( n = 4 independent samples; see F for all replicates). (K) mRNA expression level of HK2 in wild-type and diabetic mice ( n = 4 independent samples). Data were expressed as mean ± SD. ∗∗, p < 0.01. (L) Schematic diagram of the experimental design in mice. Pan02 cells with or without PRKAR2B knockout was injected into wild type or diabetic mouse through the tail vein ( n = 4 independent samples). (M) Changes in mouse body weight following tail vein injection of PRKAR2B -knockout or wild-type Pan02 cells ( n = 4 independent samples). Data were expressed as mean ± SD. ∗∗, p < 0.01. (N) Colorimetric analysis of PKA activity in tumor allografts from wild-type and diabetic mice with or without PRKAR2B knockout ( n = 4 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗, p < 0.01. (O) Representative image of Ki67 IHC staining in Pan02-control and Pan02- PRKAR2B -sg allografts from wild-type or diabetic mice ( n = 4 independent samples). Scale bars, 150 μm (P) Representative H&E-stained lung sections at the experimental endpoint. Scale bars, 3 mm (Q–R) Quantification of metastatic lesion number (Q) and total metastatic burden (R) at the experimental endpoint across the indicated treatment groups ( n = 4 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05; NS, no significance.

    Journal: iScience

    Article Title: HHEX-PRKAR2B axis-mediated PKA activation drives glucose metabolism-dependent progression of pancreatic ductal adenocarcinoma

    doi: 10.1016/j.isci.2026.114691

    Figure Lengend Snippet: In vivo demonstration of glucose-activated PKA promoting glycolysis-dependent progression A. Immunoblot analysis of PRKAR2B in KPC cells with or without PRKAR2B knockout. (B–D) Representative images of colony formation by KPC cells, with or without PRKAR2B knockout, cultured in normal or low-glucose medium (B). Colony size (C) and number of colonies (D) were graphed ( n = 3 independent repeats). Data were expressed as mean ± SD. Scale bars, 50 μm ∗, p < 0.05, ∗∗, p < 0.01, NS, no significance. (E) Representative H&E-stained pancreatic sections from mice with tamoxifen-inducible, pancreas-specific KRAS expression, harvested 3 weeks after tamoxifen or vehicle injection. Scale bars, 1 mm (F–H) PKA activity (F), pyruvic acid level (G), and lactate level (H) in pancreatic tissues from mice, harvested 3 weeks after tamoxifen or vehicle injection, assessing the effect of tamoxifen-inducible, pancreas-specific KRAS expression ( n = 4 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05; ∗∗, p < 0.01. (I) Colorimetric analysis of PKA activity in wild-type and diabetic mice ( n = 4 independent samples). Data were expressed as mean ± SD. ∗∗, p < 0.01. (J) Representative immunoblot of CREB, pCREB, and KLF5 in wild-type and diabetic mice ( n = 4 independent samples; see F for all replicates). (K) mRNA expression level of HK2 in wild-type and diabetic mice ( n = 4 independent samples). Data were expressed as mean ± SD. ∗∗, p < 0.01. (L) Schematic diagram of the experimental design in mice. Pan02 cells with or without PRKAR2B knockout was injected into wild type or diabetic mouse through the tail vein ( n = 4 independent samples). (M) Changes in mouse body weight following tail vein injection of PRKAR2B -knockout or wild-type Pan02 cells ( n = 4 independent samples). Data were expressed as mean ± SD. ∗∗, p < 0.01. (N) Colorimetric analysis of PKA activity in tumor allografts from wild-type and diabetic mice with or without PRKAR2B knockout ( n = 4 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05, ∗∗, p < 0.01. (O) Representative image of Ki67 IHC staining in Pan02-control and Pan02- PRKAR2B -sg allografts from wild-type or diabetic mice ( n = 4 independent samples). Scale bars, 150 μm (P) Representative H&E-stained lung sections at the experimental endpoint. Scale bars, 3 mm (Q–R) Quantification of metastatic lesion number (Q) and total metastatic burden (R) at the experimental endpoint across the indicated treatment groups ( n = 4 independent samples). Data were expressed as mean ± SD. ∗, p < 0.05; NS, no significance.

    Article Snippet: The following primary antibodies were used: GAPDH (1:1000, cat. sc-137179, Santa Cruz Biotechnology), PRKAR2B (1:1000, cat. sc-376778, Santa Cruz Biotechnology), CREB (1:1000, cat. ab31515, Abcam), pCREB (1:1000, cat. ab32096, Abcam), KLF5 (1:1000, cat. sc-398014, Santa Cruz Biotechnology), and HK2 (1:1000, cat. sc-130358, Santa Cruz Biotechnology).

    Techniques: In Vivo, Western Blot, Knock-Out, Cell Culture, Staining, Expressing, Injection, Activity Assay, Immunohistochemistry, Control