erbb3 functions  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc erbb3 functions
    <t>ErbB3</t> interacts with erbB2 to activate signaling pathways leading to multi-drug resistance in breast cancer. Hetero-dimerization of erbB2 and erbB3 is able to induce activation of multiple downstream signaling pathways. In both luminal B and erbB2+ subtypes of human breast cancer, erbB2/erbB3 association may recruit IGF-1R to form a trimeric complex activating PI-3 K/Akt signaling and Src kinase and resulting in trastuzumab resistance. In erbB2+ breast cancer, interaction between erbB2 and erbB3 upregulates Survivin via a PI-3 K/Akt-dependent mechanism, and thereby confers paclitaxel resistance. In luminal B breast cancer, the erbB2/erbB3 hetero-dimers modulate ERα phosphorylation (activation) mainly through MEK/MAPK and/or PI-3 K/Akt signaling pathways, and subsequently alter tamoxifen sensitivity. These data support the hypothesis that targeting of erbB3 will significantly enhance the efficacy of those commonly used therapeutics in the treatment of erbB2+ breast cancer.
    Erbb3 Functions, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/erbb3 functions/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    erbb3 functions - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "Targeting of erbB3 receptor to overcome resistance in cancer treatment"

    Article Title: Targeting of erbB3 receptor to overcome resistance in cancer treatment

    Journal: Molecular Cancer

    doi: 10.1186/1476-4598-13-105

    ErbB3 interacts with erbB2 to activate signaling pathways leading to multi-drug resistance in breast cancer. Hetero-dimerization of erbB2 and erbB3 is able to induce activation of multiple downstream signaling pathways. In both luminal B and erbB2+ subtypes of human breast cancer, erbB2/erbB3 association may recruit IGF-1R to form a trimeric complex activating PI-3 K/Akt signaling and Src kinase and resulting in trastuzumab resistance. In erbB2+ breast cancer, interaction between erbB2 and erbB3 upregulates Survivin via a PI-3 K/Akt-dependent mechanism, and thereby confers paclitaxel resistance. In luminal B breast cancer, the erbB2/erbB3 hetero-dimers modulate ERα phosphorylation (activation) mainly through MEK/MAPK and/or PI-3 K/Akt signaling pathways, and subsequently alter tamoxifen sensitivity. These data support the hypothesis that targeting of erbB3 will significantly enhance the efficacy of those commonly used therapeutics in the treatment of erbB2+ breast cancer.
    Figure Legend Snippet: ErbB3 interacts with erbB2 to activate signaling pathways leading to multi-drug resistance in breast cancer. Hetero-dimerization of erbB2 and erbB3 is able to induce activation of multiple downstream signaling pathways. In both luminal B and erbB2+ subtypes of human breast cancer, erbB2/erbB3 association may recruit IGF-1R to form a trimeric complex activating PI-3 K/Akt signaling and Src kinase and resulting in trastuzumab resistance. In erbB2+ breast cancer, interaction between erbB2 and erbB3 upregulates Survivin via a PI-3 K/Akt-dependent mechanism, and thereby confers paclitaxel resistance. In luminal B breast cancer, the erbB2/erbB3 hetero-dimers modulate ERα phosphorylation (activation) mainly through MEK/MAPK and/or PI-3 K/Akt signaling pathways, and subsequently alter tamoxifen sensitivity. These data support the hypothesis that targeting of erbB3 will significantly enhance the efficacy of those commonly used therapeutics in the treatment of erbB2+ breast cancer.

    Techniques Used: Activation Assay

    Current and novel therapeutic strategies targeting of erbB2 and/or erbB3 receptors for cancer therapy. Several erbB2-targeted therapies (trastuzumab, pertuzumab, T-DM1, and lapatinib) have being used in clinic, whereas no erbB3-targeted therapy has been approved for cancer treatment. Blocking Abs, such as MM-121, MM-111, AMG 888/U3-1287, and MP-RM-1/EV20, are the only agents being tested in early clinical and/or preclinical investigations. Our recent data show that entinostat, a class I HDAC inhibitor selectively downregulates erbB2/erbB3 via induction of specific miRNAs, miR-125a, miR-125b, and miR-205 in erbB2+ breast cancer cells. Further characterization demonstrates that these “sister” miRNAs (share common targets) act in concert to inhibit erbB2/erbB3 protein translation. Thus, the novel strategy, like cooperative miRNA targeting of erbB2/erbB3 may represent a new approach for cancer therapy.
    Figure Legend Snippet: Current and novel therapeutic strategies targeting of erbB2 and/or erbB3 receptors for cancer therapy. Several erbB2-targeted therapies (trastuzumab, pertuzumab, T-DM1, and lapatinib) have being used in clinic, whereas no erbB3-targeted therapy has been approved for cancer treatment. Blocking Abs, such as MM-121, MM-111, AMG 888/U3-1287, and MP-RM-1/EV20, are the only agents being tested in early clinical and/or preclinical investigations. Our recent data show that entinostat, a class I HDAC inhibitor selectively downregulates erbB2/erbB3 via induction of specific miRNAs, miR-125a, miR-125b, and miR-205 in erbB2+ breast cancer cells. Further characterization demonstrates that these “sister” miRNAs (share common targets) act in concert to inhibit erbB2/erbB3 protein translation. Thus, the novel strategy, like cooperative miRNA targeting of erbB2/erbB3 may represent a new approach for cancer therapy.

    Techniques Used: Blocking Assay

    erbb3 functions  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc erbb3 functions
    <t>ErbB3</t> interacts with erbB2 to activate signaling pathways leading to multi-drug resistance in breast cancer. Hetero-dimerization of erbB2 and erbB3 is able to induce activation of multiple downstream signaling pathways. In both luminal B and erbB2+ subtypes of human breast cancer, erbB2/erbB3 association may recruit IGF-1R to form a trimeric complex activating PI-3 K/Akt signaling and Src kinase and resulting in trastuzumab resistance. In erbB2+ breast cancer, interaction between erbB2 and erbB3 upregulates Survivin via a PI-3 K/Akt-dependent mechanism, and thereby confers paclitaxel resistance. In luminal B breast cancer, the erbB2/erbB3 hetero-dimers modulate ERα phosphorylation (activation) mainly through MEK/MAPK and/or PI-3 K/Akt signaling pathways, and subsequently alter tamoxifen sensitivity. These data support the hypothesis that targeting of erbB3 will significantly enhance the efficacy of those commonly used therapeutics in the treatment of erbB2+ breast cancer.
    Erbb3 Functions, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/erbb3 functions/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    erbb3 functions - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "Targeting of erbB3 receptor to overcome resistance in cancer treatment"

    Article Title: Targeting of erbB3 receptor to overcome resistance in cancer treatment

    Journal: Molecular Cancer

    doi: 10.1186/1476-4598-13-105

    ErbB3 interacts with erbB2 to activate signaling pathways leading to multi-drug resistance in breast cancer. Hetero-dimerization of erbB2 and erbB3 is able to induce activation of multiple downstream signaling pathways. In both luminal B and erbB2+ subtypes of human breast cancer, erbB2/erbB3 association may recruit IGF-1R to form a trimeric complex activating PI-3 K/Akt signaling and Src kinase and resulting in trastuzumab resistance. In erbB2+ breast cancer, interaction between erbB2 and erbB3 upregulates Survivin via a PI-3 K/Akt-dependent mechanism, and thereby confers paclitaxel resistance. In luminal B breast cancer, the erbB2/erbB3 hetero-dimers modulate ERα phosphorylation (activation) mainly through MEK/MAPK and/or PI-3 K/Akt signaling pathways, and subsequently alter tamoxifen sensitivity. These data support the hypothesis that targeting of erbB3 will significantly enhance the efficacy of those commonly used therapeutics in the treatment of erbB2+ breast cancer.
    Figure Legend Snippet: ErbB3 interacts with erbB2 to activate signaling pathways leading to multi-drug resistance in breast cancer. Hetero-dimerization of erbB2 and erbB3 is able to induce activation of multiple downstream signaling pathways. In both luminal B and erbB2+ subtypes of human breast cancer, erbB2/erbB3 association may recruit IGF-1R to form a trimeric complex activating PI-3 K/Akt signaling and Src kinase and resulting in trastuzumab resistance. In erbB2+ breast cancer, interaction between erbB2 and erbB3 upregulates Survivin via a PI-3 K/Akt-dependent mechanism, and thereby confers paclitaxel resistance. In luminal B breast cancer, the erbB2/erbB3 hetero-dimers modulate ERα phosphorylation (activation) mainly through MEK/MAPK and/or PI-3 K/Akt signaling pathways, and subsequently alter tamoxifen sensitivity. These data support the hypothesis that targeting of erbB3 will significantly enhance the efficacy of those commonly used therapeutics in the treatment of erbB2+ breast cancer.

    Techniques Used: Activation Assay

    Current and novel therapeutic strategies targeting of erbB2 and/or erbB3 receptors for cancer therapy. Several erbB2-targeted therapies (trastuzumab, pertuzumab, T-DM1, and lapatinib) have being used in clinic, whereas no erbB3-targeted therapy has been approved for cancer treatment. Blocking Abs, such as MM-121, MM-111, AMG 888/U3-1287, and MP-RM-1/EV20, are the only agents being tested in early clinical and/or preclinical investigations. Our recent data show that entinostat, a class I HDAC inhibitor selectively downregulates erbB2/erbB3 via induction of specific miRNAs, miR-125a, miR-125b, and miR-205 in erbB2+ breast cancer cells. Further characterization demonstrates that these “sister” miRNAs (share common targets) act in concert to inhibit erbB2/erbB3 protein translation. Thus, the novel strategy, like cooperative miRNA targeting of erbB2/erbB3 may represent a new approach for cancer therapy.
    Figure Legend Snippet: Current and novel therapeutic strategies targeting of erbB2 and/or erbB3 receptors for cancer therapy. Several erbB2-targeted therapies (trastuzumab, pertuzumab, T-DM1, and lapatinib) have being used in clinic, whereas no erbB3-targeted therapy has been approved for cancer treatment. Blocking Abs, such as MM-121, MM-111, AMG 888/U3-1287, and MP-RM-1/EV20, are the only agents being tested in early clinical and/or preclinical investigations. Our recent data show that entinostat, a class I HDAC inhibitor selectively downregulates erbB2/erbB3 via induction of specific miRNAs, miR-125a, miR-125b, and miR-205 in erbB2+ breast cancer cells. Further characterization demonstrates that these “sister” miRNAs (share common targets) act in concert to inhibit erbB2/erbB3 protein translation. Thus, the novel strategy, like cooperative miRNA targeting of erbB2/erbB3 may represent a new approach for cancer therapy.

    Techniques Used: Blocking Assay

    her3 immunoreactivity  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc her3 immunoreactivity
    (A) Panel of <t>HER3</t> negative cases (0–1+) and HER3 positive cases (2–3+). For HER3 staining, the guidelines from CAP HER2 scoring guidelines were used to generate an ad-hoc HER2 like score. (B) Kaplan–Meier curve of HER3 positive versus HER3 negative cases. (C) ERBB3 gene copy number and HER3 immunohistochemistry.
    Her3 Immunoreactivity, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/her3 immunoreactivity/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    94/100 stars

    Images

    1) Product Images from "HER3 expression and MEK activation in non-small-cell lung carcinoma"

    Article Title: HER3 expression and MEK activation in non-small-cell lung carcinoma

    Journal: Lung Cancer Management

    doi: 10.2217/lmt-2020-0031

    (A) Panel of HER3 negative cases (0–1+) and HER3 positive cases (2–3+). For HER3 staining, the guidelines from CAP HER2 scoring guidelines were used to generate an ad-hoc HER2 like score. (B) Kaplan–Meier curve of HER3 positive versus HER3 negative cases. (C) ERBB3 gene copy number and HER3 immunohistochemistry.
    Figure Legend Snippet: (A) Panel of HER3 negative cases (0–1+) and HER3 positive cases (2–3+). For HER3 staining, the guidelines from CAP HER2 scoring guidelines were used to generate an ad-hoc HER2 like score. (B) Kaplan–Meier curve of HER3 positive versus HER3 negative cases. (C) ERBB3 gene copy number and HER3 immunohistochemistry.

    Techniques Used: Staining, Immunohistochemistry

    Membranous  HER3  and HER2 protein expression by immunohistochemistry.
    Figure Legend Snippet: Membranous HER3 and HER2 protein expression by immunohistochemistry.

    Techniques Used: Expressing, Immunohistochemistry, Staining

    Clinical characteristics for  HER3  positive and  HER3  negative patients.
    Figure Legend Snippet: Clinical characteristics for HER3 positive and HER3 negative patients.

    Techniques Used:

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    Cell Signaling Technology Inc erbb3 functions
    <t>ErbB3</t> interacts with erbB2 to activate signaling pathways leading to multi-drug resistance in breast cancer. Hetero-dimerization of erbB2 and erbB3 is able to induce activation of multiple downstream signaling pathways. In both luminal B and erbB2+ subtypes of human breast cancer, erbB2/erbB3 association may recruit IGF-1R to form a trimeric complex activating PI-3 K/Akt signaling and Src kinase and resulting in trastuzumab resistance. In erbB2+ breast cancer, interaction between erbB2 and erbB3 upregulates Survivin via a PI-3 K/Akt-dependent mechanism, and thereby confers paclitaxel resistance. In luminal B breast cancer, the erbB2/erbB3 hetero-dimers modulate ERα phosphorylation (activation) mainly through MEK/MAPK and/or PI-3 K/Akt signaling pathways, and subsequently alter tamoxifen sensitivity. These data support the hypothesis that targeting of erbB3 will significantly enhance the efficacy of those commonly used therapeutics in the treatment of erbB2+ breast cancer.
    Erbb3 Functions, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/erbb3 functions/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    erbb3 functions - by Bioz Stars, 2023-02
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    Cell Signaling Technology Inc her3 immunoreactivity
    (A) Panel of <t>HER3</t> negative cases (0–1+) and HER3 positive cases (2–3+). For HER3 staining, the guidelines from CAP HER2 scoring guidelines were used to generate an ad-hoc HER2 like score. (B) Kaplan–Meier curve of HER3 positive versus HER3 negative cases. (C) ERBB3 gene copy number and HER3 immunohistochemistry.
    Her3 Immunoreactivity, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/her3 immunoreactivity/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    her3 immunoreactivity - by Bioz Stars, 2023-02
    94/100 stars
      Buy from Supplier

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    ErbB3 interacts with erbB2 to activate signaling pathways leading to multi-drug resistance in breast cancer. Hetero-dimerization of erbB2 and erbB3 is able to induce activation of multiple downstream signaling pathways. In both luminal B and erbB2+ subtypes of human breast cancer, erbB2/erbB3 association may recruit IGF-1R to form a trimeric complex activating PI-3 K/Akt signaling and Src kinase and resulting in trastuzumab resistance. In erbB2+ breast cancer, interaction between erbB2 and erbB3 upregulates Survivin via a PI-3 K/Akt-dependent mechanism, and thereby confers paclitaxel resistance. In luminal B breast cancer, the erbB2/erbB3 hetero-dimers modulate ERα phosphorylation (activation) mainly through MEK/MAPK and/or PI-3 K/Akt signaling pathways, and subsequently alter tamoxifen sensitivity. These data support the hypothesis that targeting of erbB3 will significantly enhance the efficacy of those commonly used therapeutics in the treatment of erbB2+ breast cancer.

    Journal: Molecular Cancer

    Article Title: Targeting of erbB3 receptor to overcome resistance in cancer treatment

    doi: 10.1186/1476-4598-13-105

    Figure Lengend Snippet: ErbB3 interacts with erbB2 to activate signaling pathways leading to multi-drug resistance in breast cancer. Hetero-dimerization of erbB2 and erbB3 is able to induce activation of multiple downstream signaling pathways. In both luminal B and erbB2+ subtypes of human breast cancer, erbB2/erbB3 association may recruit IGF-1R to form a trimeric complex activating PI-3 K/Akt signaling and Src kinase and resulting in trastuzumab resistance. In erbB2+ breast cancer, interaction between erbB2 and erbB3 upregulates Survivin via a PI-3 K/Akt-dependent mechanism, and thereby confers paclitaxel resistance. In luminal B breast cancer, the erbB2/erbB3 hetero-dimers modulate ERα phosphorylation (activation) mainly through MEK/MAPK and/or PI-3 K/Akt signaling pathways, and subsequently alter tamoxifen sensitivity. These data support the hypothesis that targeting of erbB3 will significantly enhance the efficacy of those commonly used therapeutics in the treatment of erbB2+ breast cancer.

    Article Snippet: It has been reported that erbB3 functions primarily to drive erbB2-mediated cell signaling [ , ].

    Techniques: Activation Assay

    Current and novel therapeutic strategies targeting of erbB2 and/or erbB3 receptors for cancer therapy. Several erbB2-targeted therapies (trastuzumab, pertuzumab, T-DM1, and lapatinib) have being used in clinic, whereas no erbB3-targeted therapy has been approved for cancer treatment. Blocking Abs, such as MM-121, MM-111, AMG 888/U3-1287, and MP-RM-1/EV20, are the only agents being tested in early clinical and/or preclinical investigations. Our recent data show that entinostat, a class I HDAC inhibitor selectively downregulates erbB2/erbB3 via induction of specific miRNAs, miR-125a, miR-125b, and miR-205 in erbB2+ breast cancer cells. Further characterization demonstrates that these “sister” miRNAs (share common targets) act in concert to inhibit erbB2/erbB3 protein translation. Thus, the novel strategy, like cooperative miRNA targeting of erbB2/erbB3 may represent a new approach for cancer therapy.

    Journal: Molecular Cancer

    Article Title: Targeting of erbB3 receptor to overcome resistance in cancer treatment

    doi: 10.1186/1476-4598-13-105

    Figure Lengend Snippet: Current and novel therapeutic strategies targeting of erbB2 and/or erbB3 receptors for cancer therapy. Several erbB2-targeted therapies (trastuzumab, pertuzumab, T-DM1, and lapatinib) have being used in clinic, whereas no erbB3-targeted therapy has been approved for cancer treatment. Blocking Abs, such as MM-121, MM-111, AMG 888/U3-1287, and MP-RM-1/EV20, are the only agents being tested in early clinical and/or preclinical investigations. Our recent data show that entinostat, a class I HDAC inhibitor selectively downregulates erbB2/erbB3 via induction of specific miRNAs, miR-125a, miR-125b, and miR-205 in erbB2+ breast cancer cells. Further characterization demonstrates that these “sister” miRNAs (share common targets) act in concert to inhibit erbB2/erbB3 protein translation. Thus, the novel strategy, like cooperative miRNA targeting of erbB2/erbB3 may represent a new approach for cancer therapy.

    Article Snippet: It has been reported that erbB3 functions primarily to drive erbB2-mediated cell signaling [ , ].

    Techniques: Blocking Assay

    (A) Panel of HER3 negative cases (0–1+) and HER3 positive cases (2–3+). For HER3 staining, the guidelines from CAP HER2 scoring guidelines were used to generate an ad-hoc HER2 like score. (B) Kaplan–Meier curve of HER3 positive versus HER3 negative cases. (C) ERBB3 gene copy number and HER3 immunohistochemistry.

    Journal: Lung Cancer Management

    Article Title: HER3 expression and MEK activation in non-small-cell lung carcinoma

    doi: 10.2217/lmt-2020-0031

    Figure Lengend Snippet: (A) Panel of HER3 negative cases (0–1+) and HER3 positive cases (2–3+). For HER3 staining, the guidelines from CAP HER2 scoring guidelines were used to generate an ad-hoc HER2 like score. (B) Kaplan–Meier curve of HER3 positive versus HER3 negative cases. (C) ERBB3 gene copy number and HER3 immunohistochemistry.

    Article Snippet: Briefly, HER3 immunoreactivity was investigated using the rabbit monoclonal anti-HER3 antibody clone D22C5 (#12708, Cell Signaling Technology, London, UK).

    Techniques: Staining, Immunohistochemistry

    Membranous  HER3  and HER2 protein expression by immunohistochemistry.

    Journal: Lung Cancer Management

    Article Title: HER3 expression and MEK activation in non-small-cell lung carcinoma

    doi: 10.2217/lmt-2020-0031

    Figure Lengend Snippet: Membranous HER3 and HER2 protein expression by immunohistochemistry.

    Article Snippet: Briefly, HER3 immunoreactivity was investigated using the rabbit monoclonal anti-HER3 antibody clone D22C5 (#12708, Cell Signaling Technology, London, UK).

    Techniques: Expressing, Immunohistochemistry, Staining

    Clinical characteristics for  HER3  positive and  HER3  negative patients.

    Journal: Lung Cancer Management

    Article Title: HER3 expression and MEK activation in non-small-cell lung carcinoma

    doi: 10.2217/lmt-2020-0031

    Figure Lengend Snippet: Clinical characteristics for HER3 positive and HER3 negative patients.

    Article Snippet: Briefly, HER3 immunoreactivity was investigated using the rabbit monoclonal anti-HER3 antibody clone D22C5 (#12708, Cell Signaling Technology, London, UK).

    Techniques: