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ctgf  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ctgf
    <t>GM2-mediated</t> <t>ERK-target</t> gene expression is Egr1-dependent. A , screening of Egr1 KO clones from an array of Egr1 sgRNA transfected clones (CRISPR-Cas9) in HeLa cells. The panel depicting Egr1 expression in clones 1, 2, 3, 4, 6, and 7 in comparison to the HeLa wt, is also shown along with an array of total 17 clones selected as depicted in E . B , sequencing data depict 1 bp insertion in Egr1 KO3 clone ( B , top panel) and 52 bp deletion in Egr1 KO6 clone ( B , lower panel) resulting in complete Egr1 KO clones generation. Inserted and deleted bases are marked, and the boxed portion shows guide RNA targeted DNA sequence. RT-PCR data show diminished expression of GM2-induced ( C ) Tgfβ1 , ( D ) Pai-1 and ( E ) <t>Ctgf</t> genes in Egr1 KO clones in the presence or absence of exogenous GM2. All mRNA quantification data are normalized against 7SL and represented as relative fold changes with respect to untreated control. Data represents mean ± SEM of at least two independent experiments [Student's t test, two-tailed; unpaired ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001]. F , western blot show GM2-induced Ctgf protein expression in Egr1 KO clones 3 and 6 in the presence of exogenous GM2. G , bar diagram shows densitometric quantification data of Egr1 and Ctgf protein. Band intensities are quantified using ImageJ software and normalized to GAPDH (loading control). Data represent mean ± SEM of at least two independent experiments [Student's t test (one-tailed; unpaired); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ns = nonsignificant]. gRNA, guide RNA; wt, wild type; SFM, serum-free media, KO clone, knock out clone. ERK, extracellular signal-regulated kinase; Egr1, early growth response protein 1; Tgfβ1, transforming growth factor beta 1; Pai-1, plasminogen activator 1; CRISPR-Cas9, clustered regularly interspaced short palindromic repeats and CRISPR associated protein; RT-PCR, real-time PCR; Ctgf, connective tissue growth factor.
    Ctgf, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 96 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ctgf/product/Cell Signaling Technology Inc
    Average 95 stars, based on 96 article reviews
    ctgf - by Bioz Stars, 2026-06
    95/100 stars

    Images

    1) Product Images from "Ganglioside GM2 induces epithelial–mesenchymal transition (EMT) in cancer cells in a MEK/ERK/Egr1-dependent transcriptional program"

    Article Title: Ganglioside GM2 induces epithelial–mesenchymal transition (EMT) in cancer cells in a MEK/ERK/Egr1-dependent transcriptional program

    Journal: The Journal of Biological Chemistry

    doi: 10.1016/j.jbc.2026.111306

    GM2-mediated ERK-target gene expression is Egr1-dependent. A , screening of Egr1 KO clones from an array of Egr1 sgRNA transfected clones (CRISPR-Cas9) in HeLa cells. The panel depicting Egr1 expression in clones 1, 2, 3, 4, 6, and 7 in comparison to the HeLa wt, is also shown along with an array of total 17 clones selected as depicted in E . B , sequencing data depict 1 bp insertion in Egr1 KO3 clone ( B , top panel) and 52 bp deletion in Egr1 KO6 clone ( B , lower panel) resulting in complete Egr1 KO clones generation. Inserted and deleted bases are marked, and the boxed portion shows guide RNA targeted DNA sequence. RT-PCR data show diminished expression of GM2-induced ( C ) Tgfβ1 , ( D ) Pai-1 and ( E ) Ctgf genes in Egr1 KO clones in the presence or absence of exogenous GM2. All mRNA quantification data are normalized against 7SL and represented as relative fold changes with respect to untreated control. Data represents mean ± SEM of at least two independent experiments [Student's t test, two-tailed; unpaired ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001]. F , western blot show GM2-induced Ctgf protein expression in Egr1 KO clones 3 and 6 in the presence of exogenous GM2. G , bar diagram shows densitometric quantification data of Egr1 and Ctgf protein. Band intensities are quantified using ImageJ software and normalized to GAPDH (loading control). Data represent mean ± SEM of at least two independent experiments [Student's t test (one-tailed; unpaired); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ns = nonsignificant]. gRNA, guide RNA; wt, wild type; SFM, serum-free media, KO clone, knock out clone. ERK, extracellular signal-regulated kinase; Egr1, early growth response protein 1; Tgfβ1, transforming growth factor beta 1; Pai-1, plasminogen activator 1; CRISPR-Cas9, clustered regularly interspaced short palindromic repeats and CRISPR associated protein; RT-PCR, real-time PCR; Ctgf, connective tissue growth factor.
    Figure Legend Snippet: GM2-mediated ERK-target gene expression is Egr1-dependent. A , screening of Egr1 KO clones from an array of Egr1 sgRNA transfected clones (CRISPR-Cas9) in HeLa cells. The panel depicting Egr1 expression in clones 1, 2, 3, 4, 6, and 7 in comparison to the HeLa wt, is also shown along with an array of total 17 clones selected as depicted in E . B , sequencing data depict 1 bp insertion in Egr1 KO3 clone ( B , top panel) and 52 bp deletion in Egr1 KO6 clone ( B , lower panel) resulting in complete Egr1 KO clones generation. Inserted and deleted bases are marked, and the boxed portion shows guide RNA targeted DNA sequence. RT-PCR data show diminished expression of GM2-induced ( C ) Tgfβ1 , ( D ) Pai-1 and ( E ) Ctgf genes in Egr1 KO clones in the presence or absence of exogenous GM2. All mRNA quantification data are normalized against 7SL and represented as relative fold changes with respect to untreated control. Data represents mean ± SEM of at least two independent experiments [Student's t test, two-tailed; unpaired ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001]. F , western blot show GM2-induced Ctgf protein expression in Egr1 KO clones 3 and 6 in the presence of exogenous GM2. G , bar diagram shows densitometric quantification data of Egr1 and Ctgf protein. Band intensities are quantified using ImageJ software and normalized to GAPDH (loading control). Data represent mean ± SEM of at least two independent experiments [Student's t test (one-tailed; unpaired); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ns = nonsignificant]. gRNA, guide RNA; wt, wild type; SFM, serum-free media, KO clone, knock out clone. ERK, extracellular signal-regulated kinase; Egr1, early growth response protein 1; Tgfβ1, transforming growth factor beta 1; Pai-1, plasminogen activator 1; CRISPR-Cas9, clustered regularly interspaced short palindromic repeats and CRISPR associated protein; RT-PCR, real-time PCR; Ctgf, connective tissue growth factor.

    Techniques Used: Targeted Gene Expression, Clone Assay, Transfection, CRISPR, Expressing, Comparison, Sequencing, Reverse Transcription Polymerase Chain Reaction, Control, Two Tailed Test, Western Blot, Software, One-tailed Test, Knock-Out, Real-time Polymerase Chain Reaction

    Schematic diagram of the role of MEK-ERK-Egr1 axis GM2-mediated EMT process. In summary, ganglioside GM2 interacts with membrane bound integrin receptor and induces MEK activation which in turn phosphorylates and activates ERK. Activated ERK then activates immediate early genes like Egr1 which further activates the transcription of its downstream gene like Ctgf that may play a critical role in GM2-mediated tumor cell migration, invasion and EMT process. The figure was made by BioRender. ERK, extracellular signal-regulated kinase; Egr1, early growth response protein 1; EMT, epithelial–mesenchymal transition; Ctgf, connective tissue growth factor.
    Figure Legend Snippet: Schematic diagram of the role of MEK-ERK-Egr1 axis GM2-mediated EMT process. In summary, ganglioside GM2 interacts with membrane bound integrin receptor and induces MEK activation which in turn phosphorylates and activates ERK. Activated ERK then activates immediate early genes like Egr1 which further activates the transcription of its downstream gene like Ctgf that may play a critical role in GM2-mediated tumor cell migration, invasion and EMT process. The figure was made by BioRender. ERK, extracellular signal-regulated kinase; Egr1, early growth response protein 1; EMT, epithelial–mesenchymal transition; Ctgf, connective tissue growth factor.

    Techniques Used: Membrane, Activation Assay, Migration



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    <t>GM2-mediated</t> <t>ERK-target</t> gene expression is Egr1-dependent. A , screening of Egr1 KO clones from an array of Egr1 sgRNA transfected clones (CRISPR-Cas9) in HeLa cells. The panel depicting Egr1 expression in clones 1, 2, 3, 4, 6, and 7 in comparison to the HeLa wt, is also shown along with an array of total 17 clones selected as depicted in E . B , sequencing data depict 1 bp insertion in Egr1 KO3 clone ( B , top panel) and 52 bp deletion in Egr1 KO6 clone ( B , lower panel) resulting in complete Egr1 KO clones generation. Inserted and deleted bases are marked, and the boxed portion shows guide RNA targeted DNA sequence. RT-PCR data show diminished expression of GM2-induced ( C ) Tgfβ1 , ( D ) Pai-1 and ( E ) <t>Ctgf</t> genes in Egr1 KO clones in the presence or absence of exogenous GM2. All mRNA quantification data are normalized against 7SL and represented as relative fold changes with respect to untreated control. Data represents mean ± SEM of at least two independent experiments [Student's t test, two-tailed; unpaired ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001]. F , western blot show GM2-induced Ctgf protein expression in Egr1 KO clones 3 and 6 in the presence of exogenous GM2. G , bar diagram shows densitometric quantification data of Egr1 and Ctgf protein. Band intensities are quantified using ImageJ software and normalized to GAPDH (loading control). Data represent mean ± SEM of at least two independent experiments [Student's t test (one-tailed; unpaired); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ns = nonsignificant]. gRNA, guide RNA; wt, wild type; SFM, serum-free media, KO clone, knock out clone. ERK, extracellular signal-regulated kinase; Egr1, early growth response protein 1; Tgfβ1, transforming growth factor beta 1; Pai-1, plasminogen activator 1; CRISPR-Cas9, clustered regularly interspaced short palindromic repeats and CRISPR associated protein; RT-PCR, real-time PCR; Ctgf, connective tissue growth factor.
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    <t>GM2-mediated</t> <t>ERK-target</t> gene expression is Egr1-dependent. A , screening of Egr1 KO clones from an array of Egr1 sgRNA transfected clones (CRISPR-Cas9) in HeLa cells. The panel depicting Egr1 expression in clones 1, 2, 3, 4, 6, and 7 in comparison to the HeLa wt, is also shown along with an array of total 17 clones selected as depicted in E . B , sequencing data depict 1 bp insertion in Egr1 KO3 clone ( B , top panel) and 52 bp deletion in Egr1 KO6 clone ( B , lower panel) resulting in complete Egr1 KO clones generation. Inserted and deleted bases are marked, and the boxed portion shows guide RNA targeted DNA sequence. RT-PCR data show diminished expression of GM2-induced ( C ) Tgfβ1 , ( D ) Pai-1 and ( E ) <t>Ctgf</t> genes in Egr1 KO clones in the presence or absence of exogenous GM2. All mRNA quantification data are normalized against 7SL and represented as relative fold changes with respect to untreated control. Data represents mean ± SEM of at least two independent experiments [Student's t test, two-tailed; unpaired ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001]. F , western blot show GM2-induced Ctgf protein expression in Egr1 KO clones 3 and 6 in the presence of exogenous GM2. G , bar diagram shows densitometric quantification data of Egr1 and Ctgf protein. Band intensities are quantified using ImageJ software and normalized to GAPDH (loading control). Data represent mean ± SEM of at least two independent experiments [Student's t test (one-tailed; unpaired); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ns = nonsignificant]. gRNA, guide RNA; wt, wild type; SFM, serum-free media, KO clone, knock out clone. ERK, extracellular signal-regulated kinase; Egr1, early growth response protein 1; Tgfβ1, transforming growth factor beta 1; Pai-1, plasminogen activator 1; CRISPR-Cas9, clustered regularly interspaced short palindromic repeats and CRISPR associated protein; RT-PCR, real-time PCR; Ctgf, connective tissue growth factor.
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    Image Search Results


    GM2-mediated ERK-target gene expression is Egr1-dependent. A , screening of Egr1 KO clones from an array of Egr1 sgRNA transfected clones (CRISPR-Cas9) in HeLa cells. The panel depicting Egr1 expression in clones 1, 2, 3, 4, 6, and 7 in comparison to the HeLa wt, is also shown along with an array of total 17 clones selected as depicted in E . B , sequencing data depict 1 bp insertion in Egr1 KO3 clone ( B , top panel) and 52 bp deletion in Egr1 KO6 clone ( B , lower panel) resulting in complete Egr1 KO clones generation. Inserted and deleted bases are marked, and the boxed portion shows guide RNA targeted DNA sequence. RT-PCR data show diminished expression of GM2-induced ( C ) Tgfβ1 , ( D ) Pai-1 and ( E ) Ctgf genes in Egr1 KO clones in the presence or absence of exogenous GM2. All mRNA quantification data are normalized against 7SL and represented as relative fold changes with respect to untreated control. Data represents mean ± SEM of at least two independent experiments [Student's t test, two-tailed; unpaired ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001]. F , western blot show GM2-induced Ctgf protein expression in Egr1 KO clones 3 and 6 in the presence of exogenous GM2. G , bar diagram shows densitometric quantification data of Egr1 and Ctgf protein. Band intensities are quantified using ImageJ software and normalized to GAPDH (loading control). Data represent mean ± SEM of at least two independent experiments [Student's t test (one-tailed; unpaired); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ns = nonsignificant]. gRNA, guide RNA; wt, wild type; SFM, serum-free media, KO clone, knock out clone. ERK, extracellular signal-regulated kinase; Egr1, early growth response protein 1; Tgfβ1, transforming growth factor beta 1; Pai-1, plasminogen activator 1; CRISPR-Cas9, clustered regularly interspaced short palindromic repeats and CRISPR associated protein; RT-PCR, real-time PCR; Ctgf, connective tissue growth factor.

    Journal: The Journal of Biological Chemistry

    Article Title: Ganglioside GM2 induces epithelial–mesenchymal transition (EMT) in cancer cells in a MEK/ERK/Egr1-dependent transcriptional program

    doi: 10.1016/j.jbc.2026.111306

    Figure Lengend Snippet: GM2-mediated ERK-target gene expression is Egr1-dependent. A , screening of Egr1 KO clones from an array of Egr1 sgRNA transfected clones (CRISPR-Cas9) in HeLa cells. The panel depicting Egr1 expression in clones 1, 2, 3, 4, 6, and 7 in comparison to the HeLa wt, is also shown along with an array of total 17 clones selected as depicted in E . B , sequencing data depict 1 bp insertion in Egr1 KO3 clone ( B , top panel) and 52 bp deletion in Egr1 KO6 clone ( B , lower panel) resulting in complete Egr1 KO clones generation. Inserted and deleted bases are marked, and the boxed portion shows guide RNA targeted DNA sequence. RT-PCR data show diminished expression of GM2-induced ( C ) Tgfβ1 , ( D ) Pai-1 and ( E ) Ctgf genes in Egr1 KO clones in the presence or absence of exogenous GM2. All mRNA quantification data are normalized against 7SL and represented as relative fold changes with respect to untreated control. Data represents mean ± SEM of at least two independent experiments [Student's t test, two-tailed; unpaired ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001]. F , western blot show GM2-induced Ctgf protein expression in Egr1 KO clones 3 and 6 in the presence of exogenous GM2. G , bar diagram shows densitometric quantification data of Egr1 and Ctgf protein. Band intensities are quantified using ImageJ software and normalized to GAPDH (loading control). Data represent mean ± SEM of at least two independent experiments [Student's t test (one-tailed; unpaired); ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ns = nonsignificant]. gRNA, guide RNA; wt, wild type; SFM, serum-free media, KO clone, knock out clone. ERK, extracellular signal-regulated kinase; Egr1, early growth response protein 1; Tgfβ1, transforming growth factor beta 1; Pai-1, plasminogen activator 1; CRISPR-Cas9, clustered regularly interspaced short palindromic repeats and CRISPR associated protein; RT-PCR, real-time PCR; Ctgf, connective tissue growth factor.

    Article Snippet: FosB (#2251), Ctgf (#86641S), total ERK (#4695S), GAPDH (#97166) pMEK (#9154), N-cadherin (#14215), and Vimentin (#5741) were purchased from Cell Signaling Technology and Hsp90 (#BB-AB012), β-actin (#BB-AB0024) from BioBharati Life Science Pvt Ltd. Adam10 (#ab124695) primary antibody was purchased from Abcam.

    Techniques: Targeted Gene Expression, Clone Assay, Transfection, CRISPR, Expressing, Comparison, Sequencing, Reverse Transcription Polymerase Chain Reaction, Control, Two Tailed Test, Western Blot, Software, One-tailed Test, Knock-Out, Real-time Polymerase Chain Reaction

    Schematic diagram of the role of MEK-ERK-Egr1 axis GM2-mediated EMT process. In summary, ganglioside GM2 interacts with membrane bound integrin receptor and induces MEK activation which in turn phosphorylates and activates ERK. Activated ERK then activates immediate early genes like Egr1 which further activates the transcription of its downstream gene like Ctgf that may play a critical role in GM2-mediated tumor cell migration, invasion and EMT process. The figure was made by BioRender. ERK, extracellular signal-regulated kinase; Egr1, early growth response protein 1; EMT, epithelial–mesenchymal transition; Ctgf, connective tissue growth factor.

    Journal: The Journal of Biological Chemistry

    Article Title: Ganglioside GM2 induces epithelial–mesenchymal transition (EMT) in cancer cells in a MEK/ERK/Egr1-dependent transcriptional program

    doi: 10.1016/j.jbc.2026.111306

    Figure Lengend Snippet: Schematic diagram of the role of MEK-ERK-Egr1 axis GM2-mediated EMT process. In summary, ganglioside GM2 interacts with membrane bound integrin receptor and induces MEK activation which in turn phosphorylates and activates ERK. Activated ERK then activates immediate early genes like Egr1 which further activates the transcription of its downstream gene like Ctgf that may play a critical role in GM2-mediated tumor cell migration, invasion and EMT process. The figure was made by BioRender. ERK, extracellular signal-regulated kinase; Egr1, early growth response protein 1; EMT, epithelial–mesenchymal transition; Ctgf, connective tissue growth factor.

    Article Snippet: FosB (#2251), Ctgf (#86641S), total ERK (#4695S), GAPDH (#97166) pMEK (#9154), N-cadherin (#14215), and Vimentin (#5741) were purchased from Cell Signaling Technology and Hsp90 (#BB-AB012), β-actin (#BB-AB0024) from BioBharati Life Science Pvt Ltd. Adam10 (#ab124695) primary antibody was purchased from Abcam.

    Techniques: Membrane, Activation Assay, Migration

    In vivo quantitative reverse transcription PCR analysis of the anti-fibrotic effects of compound 3k in a mouse UIRI model . A , quantitative reverse transcription PCR analysis of total RNA extracted from whole kidney tissues 7 and 14 days after UIRI. The genes analyzed include collagen type 1α, fibronectin EIIIA, cellular communication network factor 2 ( Ccn2 ), and ( B ) TEA domain transcription factors 1 to 4 ( Tead1–4 ). C , dose-dependent effects of 3k treatment. The therapeutic effect of compound 3k (1, 3, and 5 mg/kg) was evaluated by measuring the mRNA levels of extracellular matrix components (Collagen type Iα and Fibronectin EIIIA isoform) and Ccn2 in mouse kidneys. The results were analyzed using the Steel test. ∗indicates statistical significance ( p < 0.05) compared with the vehicle-treated group at 14 days (Day 14 vehicle). Individual data points represent the median and IQR (N = 6). UIRI, unilateral ischemia–reperfusion injury.

    Journal: The Journal of Biological Chemistry

    Article Title: PKM2 inhibitor suppresses kidney fibrogenesis by disrupting YAP-TEAD-CCN2 transcriptional signaling following ischemia–reperfusion injury

    doi: 10.1016/j.jbc.2025.111029

    Figure Lengend Snippet: In vivo quantitative reverse transcription PCR analysis of the anti-fibrotic effects of compound 3k in a mouse UIRI model . A , quantitative reverse transcription PCR analysis of total RNA extracted from whole kidney tissues 7 and 14 days after UIRI. The genes analyzed include collagen type 1α, fibronectin EIIIA, cellular communication network factor 2 ( Ccn2 ), and ( B ) TEA domain transcription factors 1 to 4 ( Tead1–4 ). C , dose-dependent effects of 3k treatment. The therapeutic effect of compound 3k (1, 3, and 5 mg/kg) was evaluated by measuring the mRNA levels of extracellular matrix components (Collagen type Iα and Fibronectin EIIIA isoform) and Ccn2 in mouse kidneys. The results were analyzed using the Steel test. ∗indicates statistical significance ( p < 0.05) compared with the vehicle-treated group at 14 days (Day 14 vehicle). Individual data points represent the median and IQR (N = 6). UIRI, unilateral ischemia–reperfusion injury.

    Article Snippet: Primary antibodies against the following proteins were used: CCN2 (CTGF) (D8Z8U) (#86641; CST), phosphorylated YAP (Tyr357) (#ab62751; Abcam), YAP1 (#13584-1-AP; Proteintech), PKM2 (#15822-1-AP; Proteintech), Pan-TEAD (D3F7L) (#13295; CST), PKM1 (#15821-1-AP; Proteintech), β-catenin (D10A8) (#8480; CST), lamin B1 (#PM064MS; MBL), GAPDH (D16H11) (#5174; CST), Smad2/3 (D7G7) (#8685; CST), Phospho-Smad3 (Ser423/425) (#GT1207; GTX), and TEAD2 (#21159-1-AP; Proteintech).

    Techniques: In Vivo, Reverse Transcription

    In vitro analysis of 3k treatment and siPKM2 transfection in a human renal tubular epithelial (HK-2) cell injury model . A , time course analysis of the effects of oxygen–glucose deprivation and reoxygenation (OGD/R) and 3k treatment. mRNA expression analysis of PKM2 , TEAD2 , and CCN2 in ( B ) 3k-treated and ( C ) siPKM2-transfected cells, from 24 to 72 h. Statistical comparisons between the control or the mock and treatment groups at each time point were performed using the Wilcoxon test. ∗ indicates statistical significance ( p < 0.05). Individual data points represent the median and IQR (N = 6).

    Journal: The Journal of Biological Chemistry

    Article Title: PKM2 inhibitor suppresses kidney fibrogenesis by disrupting YAP-TEAD-CCN2 transcriptional signaling following ischemia–reperfusion injury

    doi: 10.1016/j.jbc.2025.111029

    Figure Lengend Snippet: In vitro analysis of 3k treatment and siPKM2 transfection in a human renal tubular epithelial (HK-2) cell injury model . A , time course analysis of the effects of oxygen–glucose deprivation and reoxygenation (OGD/R) and 3k treatment. mRNA expression analysis of PKM2 , TEAD2 , and CCN2 in ( B ) 3k-treated and ( C ) siPKM2-transfected cells, from 24 to 72 h. Statistical comparisons between the control or the mock and treatment groups at each time point were performed using the Wilcoxon test. ∗ indicates statistical significance ( p < 0.05). Individual data points represent the median and IQR (N = 6).

    Article Snippet: Primary antibodies against the following proteins were used: CCN2 (CTGF) (D8Z8U) (#86641; CST), phosphorylated YAP (Tyr357) (#ab62751; Abcam), YAP1 (#13584-1-AP; Proteintech), PKM2 (#15822-1-AP; Proteintech), Pan-TEAD (D3F7L) (#13295; CST), PKM1 (#15821-1-AP; Proteintech), β-catenin (D10A8) (#8480; CST), lamin B1 (#PM064MS; MBL), GAPDH (D16H11) (#5174; CST), Smad2/3 (D7G7) (#8685; CST), Phospho-Smad3 (Ser423/425) (#GT1207; GTX), and TEAD2 (#21159-1-AP; Proteintech).

    Techniques: In Vitro, Transfection, Expressing, Control

    Western blot analysis of cross-linked protein expression and Co-IP analysis in HK-2 cells . A , western blot analysis of cross-linked proteins extracted from 3k-treated HK-2 cells. B and C , Co-IP analysis of the interaction between YAP1, β-catenin, and PKM2 in HK-2 cells. IP was performed using protein samples from HK-2 cells overexpressing CCN2. Co-IP with an anti-PKM2 antibody confirmed that both β-catenin and YAP1 co-precipitated with PKM2 (N = 6), ( D ) as illustrated in the schematic diagram. CCN2, cellular communication network factor 2.

    Journal: The Journal of Biological Chemistry

    Article Title: PKM2 inhibitor suppresses kidney fibrogenesis by disrupting YAP-TEAD-CCN2 transcriptional signaling following ischemia–reperfusion injury

    doi: 10.1016/j.jbc.2025.111029

    Figure Lengend Snippet: Western blot analysis of cross-linked protein expression and Co-IP analysis in HK-2 cells . A , western blot analysis of cross-linked proteins extracted from 3k-treated HK-2 cells. B and C , Co-IP analysis of the interaction between YAP1, β-catenin, and PKM2 in HK-2 cells. IP was performed using protein samples from HK-2 cells overexpressing CCN2. Co-IP with an anti-PKM2 antibody confirmed that both β-catenin and YAP1 co-precipitated with PKM2 (N = 6), ( D ) as illustrated in the schematic diagram. CCN2, cellular communication network factor 2.

    Article Snippet: Primary antibodies against the following proteins were used: CCN2 (CTGF) (D8Z8U) (#86641; CST), phosphorylated YAP (Tyr357) (#ab62751; Abcam), YAP1 (#13584-1-AP; Proteintech), PKM2 (#15822-1-AP; Proteintech), Pan-TEAD (D3F7L) (#13295; CST), PKM1 (#15821-1-AP; Proteintech), β-catenin (D10A8) (#8480; CST), lamin B1 (#PM064MS; MBL), GAPDH (D16H11) (#5174; CST), Smad2/3 (D7G7) (#8685; CST), Phospho-Smad3 (Ser423/425) (#GT1207; GTX), and TEAD2 (#21159-1-AP; Proteintech).

    Techniques: Western Blot, Expressing, Co-Immunoprecipitation Assay