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erbb2 inhibitor lapatinib  (MedChemExpress)


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    MedChemExpress erbb2 inhibitor lapatinib
    P61‐Sema3E produces a pro‐fibrotic effect through the activation of <t>ErbB2.</t> A) Western blot analysis of the levels of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 in primary human lung fibroblasts (PHLFs) after stimulation with different concentrations of P61‐Sema3E for 2 h. B) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 expression in PHLFs treated with PlexinD1 siRNA or Scrambled siRNA following P61‐Sema3E induction. C) Co‐immunoprecipitation analysis of Plexin D1 and ErbB2, FLAG‐tagged Plexin D1 plasmid were transfected into PHLFs. D) Co‐immunoprecipitation analysis of Plexin D1 and ErbB2, PHLFs were treated with P61‐Sema3E for 2 h. E) Western blot analysis of Fibronectin, Col1a1, and α‐SMA expression in PHLFs treated with the ErbB2 inhibitor Lapatinib or PBS following P61‐Sema3E stimulation for 48 h. Data are represented as the mean ± SEM of three independent experiments. Statistical analyses were performed using one‐way ANOVA test. * p < 0.05; ** p < 0.01; *** p < 0.001.
    Erbb2 Inhibitor Lapatinib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 84 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Semaphorin 3E–Plexin D1 Axis Drives Lung Fibrosis through ErbB2‐Mediated Fibroblast Activation"

    Article Title: Semaphorin 3E–Plexin D1 Axis Drives Lung Fibrosis through ErbB2‐Mediated Fibroblast Activation

    Journal: Advanced Science

    doi: 10.1002/advs.202415007

    P61‐Sema3E produces a pro‐fibrotic effect through the activation of ErbB2. A) Western blot analysis of the levels of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 in primary human lung fibroblasts (PHLFs) after stimulation with different concentrations of P61‐Sema3E for 2 h. B) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 expression in PHLFs treated with PlexinD1 siRNA or Scrambled siRNA following P61‐Sema3E induction. C) Co‐immunoprecipitation analysis of Plexin D1 and ErbB2, FLAG‐tagged Plexin D1 plasmid were transfected into PHLFs. D) Co‐immunoprecipitation analysis of Plexin D1 and ErbB2, PHLFs were treated with P61‐Sema3E for 2 h. E) Western blot analysis of Fibronectin, Col1a1, and α‐SMA expression in PHLFs treated with the ErbB2 inhibitor Lapatinib or PBS following P61‐Sema3E stimulation for 48 h. Data are represented as the mean ± SEM of three independent experiments. Statistical analyses were performed using one‐way ANOVA test. * p < 0.05; ** p < 0.01; *** p < 0.001.
    Figure Legend Snippet: P61‐Sema3E produces a pro‐fibrotic effect through the activation of ErbB2. A) Western blot analysis of the levels of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 in primary human lung fibroblasts (PHLFs) after stimulation with different concentrations of P61‐Sema3E for 2 h. B) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 expression in PHLFs treated with PlexinD1 siRNA or Scrambled siRNA following P61‐Sema3E induction. C) Co‐immunoprecipitation analysis of Plexin D1 and ErbB2, FLAG‐tagged Plexin D1 plasmid were transfected into PHLFs. D) Co‐immunoprecipitation analysis of Plexin D1 and ErbB2, PHLFs were treated with P61‐Sema3E for 2 h. E) Western blot analysis of Fibronectin, Col1a1, and α‐SMA expression in PHLFs treated with the ErbB2 inhibitor Lapatinib or PBS following P61‐Sema3E stimulation for 48 h. Data are represented as the mean ± SEM of three independent experiments. Statistical analyses were performed using one‐way ANOVA test. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Techniques Used: Activation Assay, Western Blot, Expressing, Immunoprecipitation, Plasmid Preparation, Transfection

    Downregulation of Sema3E attenuates BLM‐induced pulmonary fibrosis. A,B) Histological analysis of lung fibrosis severity in mice following BLM induction. (A) Representative images of lung sections stained with H&E, Masson's trichrome, and Sirius red to assess fibrosis severity. (B) Bar graph showing the quantitative mean score of fibrosis severity. Samples include AAV9‐NC saline mice ( n = 5), AAV9‐ShSema3E saline mice ( n = 5), AAV9‐NC BLM mice ( n = 5), and AAV9‐ShSema3E BLM mice ( n = 5). C) Quantification of hydroxyproline contents in AAV9‐NC mice and AAV9‐ShSema3E mice after BLM challenge. D,E) Western blot and RT‐qPCR analysis of Fibronectin, Col1a1, and α‐SMA protein and mRNA expression in lung homogenates from the mentioned mouse groups. F) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 expression in lung homogenates from the mentioned mouse groups. Samples include AAV9‐NC saline mice ( n = 3), AAV9‐ShSema3E saline mice ( n = 3), AAV9‐NC BLM mice ( n = 3), and AAV9‐ShSema3E BLM mice ( n = 3). Data are represented as the mean ± SEM. Statistical analyses were performed using one‐way ANOVA tests. * p < 0.05; ** p < 0.01; *** p < 0.001.
    Figure Legend Snippet: Downregulation of Sema3E attenuates BLM‐induced pulmonary fibrosis. A,B) Histological analysis of lung fibrosis severity in mice following BLM induction. (A) Representative images of lung sections stained with H&E, Masson's trichrome, and Sirius red to assess fibrosis severity. (B) Bar graph showing the quantitative mean score of fibrosis severity. Samples include AAV9‐NC saline mice ( n = 5), AAV9‐ShSema3E saline mice ( n = 5), AAV9‐NC BLM mice ( n = 5), and AAV9‐ShSema3E BLM mice ( n = 5). C) Quantification of hydroxyproline contents in AAV9‐NC mice and AAV9‐ShSema3E mice after BLM challenge. D,E) Western blot and RT‐qPCR analysis of Fibronectin, Col1a1, and α‐SMA protein and mRNA expression in lung homogenates from the mentioned mouse groups. F) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 expression in lung homogenates from the mentioned mouse groups. Samples include AAV9‐NC saline mice ( n = 3), AAV9‐ShSema3E saline mice ( n = 3), AAV9‐NC BLM mice ( n = 3), and AAV9‐ShSema3E BLM mice ( n = 3). Data are represented as the mean ± SEM. Statistical analyses were performed using one‐way ANOVA tests. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Techniques Used: Staining, Saline, Western Blot, Quantitative RT-PCR, Expressing

    Sema3E deficiency in fibroblasts protects mice from BLM‐induced lung injury and fibrosis. A,B) Representative lung sections from Sema3E‐C and Sema3E‐CKO mice treated with saline or BLM, stained with H&E, Masson's Trichrome, and Sirius Red (Panel A, left). Panel B (right) shows quantitative fibrosis scores. Each group consisted of five mice ( n = 5). C) Quantification of hydroxyproline contents in Sema3E‐CKO and Sema3E‐C mice after BLM challenge. D,E) Western blot and RT‐qPCR analyses of Fibronectin, Col1a1, and α‐SMA protein and mRNA levels in lung homogenates from each group ( n = 5). F) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 in lung homogenates from the same groups of three mice( n = 3). Data are expressed as the mean ± SEM. Statistical significance was determined by one‐way ANOVA (* p < 0.05; ** p < 0.01; *** p < 0.001).
    Figure Legend Snippet: Sema3E deficiency in fibroblasts protects mice from BLM‐induced lung injury and fibrosis. A,B) Representative lung sections from Sema3E‐C and Sema3E‐CKO mice treated with saline or BLM, stained with H&E, Masson's Trichrome, and Sirius Red (Panel A, left). Panel B (right) shows quantitative fibrosis scores. Each group consisted of five mice ( n = 5). C) Quantification of hydroxyproline contents in Sema3E‐CKO and Sema3E‐C mice after BLM challenge. D,E) Western blot and RT‐qPCR analyses of Fibronectin, Col1a1, and α‐SMA protein and mRNA levels in lung homogenates from each group ( n = 5). F) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 in lung homogenates from the same groups of three mice( n = 3). Data are expressed as the mean ± SEM. Statistical significance was determined by one‐way ANOVA (* p < 0.05; ** p < 0.01; *** p < 0.001).

    Techniques Used: Saline, Staining, Western Blot, Quantitative RT-PCR



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    P61‐Sema3E produces a pro‐fibrotic effect through the activation of ErbB2. A) Western blot analysis of the levels of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 in primary human lung fibroblasts (PHLFs) after stimulation with different concentrations of P61‐Sema3E for 2 h. B) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 expression in PHLFs treated with PlexinD1 siRNA or Scrambled siRNA following P61‐Sema3E induction. C) Co‐immunoprecipitation analysis of Plexin D1 and ErbB2, FLAG‐tagged Plexin D1 plasmid were transfected into PHLFs. D) Co‐immunoprecipitation analysis of Plexin D1 and ErbB2, PHLFs were treated with P61‐Sema3E for 2 h. E) Western blot analysis of Fibronectin, Col1a1, and α‐SMA expression in PHLFs treated with the ErbB2 inhibitor Lapatinib or PBS following P61‐Sema3E stimulation for 48 h. Data are represented as the mean ± SEM of three independent experiments. Statistical analyses were performed using one‐way ANOVA test. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Journal: Advanced Science

    Article Title: Semaphorin 3E–Plexin D1 Axis Drives Lung Fibrosis through ErbB2‐Mediated Fibroblast Activation

    doi: 10.1002/advs.202415007

    Figure Lengend Snippet: P61‐Sema3E produces a pro‐fibrotic effect through the activation of ErbB2. A) Western blot analysis of the levels of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 in primary human lung fibroblasts (PHLFs) after stimulation with different concentrations of P61‐Sema3E for 2 h. B) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 expression in PHLFs treated with PlexinD1 siRNA or Scrambled siRNA following P61‐Sema3E induction. C) Co‐immunoprecipitation analysis of Plexin D1 and ErbB2, FLAG‐tagged Plexin D1 plasmid were transfected into PHLFs. D) Co‐immunoprecipitation analysis of Plexin D1 and ErbB2, PHLFs were treated with P61‐Sema3E for 2 h. E) Western blot analysis of Fibronectin, Col1a1, and α‐SMA expression in PHLFs treated with the ErbB2 inhibitor Lapatinib or PBS following P61‐Sema3E stimulation for 48 h. Data are represented as the mean ± SEM of three independent experiments. Statistical analyses were performed using one‐way ANOVA test. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Article Snippet: The ErbB2 inhibitor Lapatinib, was obtained from MedChemExpress (CM00323).

    Techniques: Activation Assay, Western Blot, Expressing, Immunoprecipitation, Plasmid Preparation, Transfection

    Downregulation of Sema3E attenuates BLM‐induced pulmonary fibrosis. A,B) Histological analysis of lung fibrosis severity in mice following BLM induction. (A) Representative images of lung sections stained with H&E, Masson's trichrome, and Sirius red to assess fibrosis severity. (B) Bar graph showing the quantitative mean score of fibrosis severity. Samples include AAV9‐NC saline mice ( n = 5), AAV9‐ShSema3E saline mice ( n = 5), AAV9‐NC BLM mice ( n = 5), and AAV9‐ShSema3E BLM mice ( n = 5). C) Quantification of hydroxyproline contents in AAV9‐NC mice and AAV9‐ShSema3E mice after BLM challenge. D,E) Western blot and RT‐qPCR analysis of Fibronectin, Col1a1, and α‐SMA protein and mRNA expression in lung homogenates from the mentioned mouse groups. F) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 expression in lung homogenates from the mentioned mouse groups. Samples include AAV9‐NC saline mice ( n = 3), AAV9‐ShSema3E saline mice ( n = 3), AAV9‐NC BLM mice ( n = 3), and AAV9‐ShSema3E BLM mice ( n = 3). Data are represented as the mean ± SEM. Statistical analyses were performed using one‐way ANOVA tests. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Journal: Advanced Science

    Article Title: Semaphorin 3E–Plexin D1 Axis Drives Lung Fibrosis through ErbB2‐Mediated Fibroblast Activation

    doi: 10.1002/advs.202415007

    Figure Lengend Snippet: Downregulation of Sema3E attenuates BLM‐induced pulmonary fibrosis. A,B) Histological analysis of lung fibrosis severity in mice following BLM induction. (A) Representative images of lung sections stained with H&E, Masson's trichrome, and Sirius red to assess fibrosis severity. (B) Bar graph showing the quantitative mean score of fibrosis severity. Samples include AAV9‐NC saline mice ( n = 5), AAV9‐ShSema3E saline mice ( n = 5), AAV9‐NC BLM mice ( n = 5), and AAV9‐ShSema3E BLM mice ( n = 5). C) Quantification of hydroxyproline contents in AAV9‐NC mice and AAV9‐ShSema3E mice after BLM challenge. D,E) Western blot and RT‐qPCR analysis of Fibronectin, Col1a1, and α‐SMA protein and mRNA expression in lung homogenates from the mentioned mouse groups. F) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 expression in lung homogenates from the mentioned mouse groups. Samples include AAV9‐NC saline mice ( n = 3), AAV9‐ShSema3E saline mice ( n = 3), AAV9‐NC BLM mice ( n = 3), and AAV9‐ShSema3E BLM mice ( n = 3). Data are represented as the mean ± SEM. Statistical analyses were performed using one‐way ANOVA tests. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Article Snippet: The ErbB2 inhibitor Lapatinib, was obtained from MedChemExpress (CM00323).

    Techniques: Staining, Saline, Western Blot, Quantitative RT-PCR, Expressing

    Sema3E deficiency in fibroblasts protects mice from BLM‐induced lung injury and fibrosis. A,B) Representative lung sections from Sema3E‐C and Sema3E‐CKO mice treated with saline or BLM, stained with H&E, Masson's Trichrome, and Sirius Red (Panel A, left). Panel B (right) shows quantitative fibrosis scores. Each group consisted of five mice ( n = 5). C) Quantification of hydroxyproline contents in Sema3E‐CKO and Sema3E‐C mice after BLM challenge. D,E) Western blot and RT‐qPCR analyses of Fibronectin, Col1a1, and α‐SMA protein and mRNA levels in lung homogenates from each group ( n = 5). F) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 in lung homogenates from the same groups of three mice( n = 3). Data are expressed as the mean ± SEM. Statistical significance was determined by one‐way ANOVA (* p < 0.05; ** p < 0.01; *** p < 0.001).

    Journal: Advanced Science

    Article Title: Semaphorin 3E–Plexin D1 Axis Drives Lung Fibrosis through ErbB2‐Mediated Fibroblast Activation

    doi: 10.1002/advs.202415007

    Figure Lengend Snippet: Sema3E deficiency in fibroblasts protects mice from BLM‐induced lung injury and fibrosis. A,B) Representative lung sections from Sema3E‐C and Sema3E‐CKO mice treated with saline or BLM, stained with H&E, Masson's Trichrome, and Sirius Red (Panel A, left). Panel B (right) shows quantitative fibrosis scores. Each group consisted of five mice ( n = 5). C) Quantification of hydroxyproline contents in Sema3E‐CKO and Sema3E‐C mice after BLM challenge. D,E) Western blot and RT‐qPCR analyses of Fibronectin, Col1a1, and α‐SMA protein and mRNA levels in lung homogenates from each group ( n = 5). F) Western blot analysis of ErbB2, P‐ErbB2, AKT, P‐AKT, ERK1/2, and P‐ERK1/2 in lung homogenates from the same groups of three mice( n = 3). Data are expressed as the mean ± SEM. Statistical significance was determined by one‐way ANOVA (* p < 0.05; ** p < 0.01; *** p < 0.001).

    Article Snippet: The ErbB2 inhibitor Lapatinib, was obtained from MedChemExpress (CM00323).

    Techniques: Saline, Staining, Western Blot, Quantitative RT-PCR

    Figure 6. Single-cell and spatial profiling revealed cellular interactions within CSC niche. A) The circle plot depicts global interaction strength among cellular components within the CSC niche by scRNA-seq. Color intensity indicates the strength of the interactions. B) The heatmap illustrates the involvement of WNT (left) and EGF (right) signaling pathways in the interactions between CSCs and their niche by scRNA-seq. C) The ligand-receptor pairs mediating interactions between CSCs and their principal CAF niche by scRNA-seq. D) Spatial distribution of CSCs and iCAFs in three GC samples by spatial transcriptomic sequencing (10x Genomics Visium). E) The correlation of spatial distribution of iCAFs and CSCs in three GC samples by 10x Genomics Visium. F) The co-expression of AREG and ERBB2 in three GC samples by 10x Genomics Visium.

    Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    Article Title: Dissecting the Spatial and Single-Cell Transcriptomic Architecture of Cancer Stem Cell Niche Driving Tumor Progression in Gastric Cancer.

    doi: 10.1002/advs.202413019

    Figure Lengend Snippet: Figure 6. Single-cell and spatial profiling revealed cellular interactions within CSC niche. A) The circle plot depicts global interaction strength among cellular components within the CSC niche by scRNA-seq. Color intensity indicates the strength of the interactions. B) The heatmap illustrates the involvement of WNT (left) and EGF (right) signaling pathways in the interactions between CSCs and their niche by scRNA-seq. C) The ligand-receptor pairs mediating interactions between CSCs and their principal CAF niche by scRNA-seq. D) Spatial distribution of CSCs and iCAFs in three GC samples by spatial transcriptomic sequencing (10x Genomics Visium). E) The correlation of spatial distribution of iCAFs and CSCs in three GC samples by 10x Genomics Visium. F) The co-expression of AREG and ERBB2 in three GC samples by 10x Genomics Visium.

    Article Snippet: GC cells were treated with 10 μM ErbB2 inhibitor, Lapatinib (S2111, Selleck) or DMSO as control.

    Techniques: Protein-Protein interactions, Sequencing, Expressing