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Angela I M Barth – One of the best experts on this subject based on the ideXlab platform.

  • neurite outgrowth involves Adenomatous Polyposis Coli protein and β catenin
    Journal of Cell Science, 2005
    Co-Authors: Violet Votin, James W Nelson, Angela I M Barth
    Abstract:

    Neuronal morphogenesis involves the initial formation of neurites and then differentiation of neurites into axons and dendrites. The mechanisms underlying neurite formation are poorly understood. A candidate protein for controlling neurite extension is the Adenomatous Polyposis Coli (APC) protein, which regulates membrane extensions, microtubules and β-catenin-mediated transcription downstream of Wnt signaling. APC is enriched at the tip of several neurites of unpolarized hippocampal neurons and the tip of only the long axon in polarized hippocampal neurons. Significantly, APC localized to the tip of only one neurite, marked by dephospho-tau as the future axon, before that neurite had grown considerably longer than other neurites. To determine whether neurite outgrowth was affected by β-catenin accumulation and signaling, a stabilized β-catenin mutant was expressed in PC12 cells, and neurite formation was measured. Stabilized β-catenin mutants accumulated in APC clusters and inhibited neurite formation and growth. Importantly, these effects were also observed was independently of the gene transcriptional activity of β-catenin. These results indicate that APC is involved in both early neurite outgrowth and increased growth of the future axon, and that β-catenin has a structural role in inhibiting APC function in neurite growth.

  • Neurite outgrowth involves Adenomatous Polyposis Coli protein and beta-catenin.
    Journal of cell science, 2005
    Co-Authors: Violet Votin, W James Nelson, Angela I M Barth
    Abstract:

    Neuronal morphogenesis involves the initial formation of neurites and then differentiation of neurites into axons and dendrites. The mechanisms underlying neurite formation are poorly understood. A candidate protein for controlling neurite extension is the Adenomatous Polyposis Coli (APC) protein, which regulates membrane extensions, microtubules and beta-catenin-mediated transcription downstream of Wnt signaling. APC is enriched at the tip of several neurites of unpolarized hippocampal neurons and the tip of only the long axon in polarized hippocampal neurons. Significantly, APC localized to the tip of only one neurite, marked by dephospho-tau as the future axon, before that neurite had grown considerably longer than other neurites. To determine whether neurite outgrowth was affected by beta-catenin accumulation and signaling, a stabilized beta-catenin mutant was expressed in PC12 cells, and neurite formation was measured. Stabilized beta-catenin mutants accumulated in APC clusters and inhibited neurite formation and growth. Importantly, these effects were also observed was independently of the gene transcriptional activity of beta-catenin. These results indicate that APC is involved in both early neurite outgrowth and increased growth of the future axon, and that beta-catenin has a structural role in inhibiting APC function in neurite growth.

  • What can humans learn from flies about Adenomatous Polyposis Coli
    BioEssays, 2002
    Co-Authors: Angela I M Barth, W James Nelson
    Abstract:

    Somatic or inherited mutations in the Adenomatous Polyposis Coli (APC) gene are a frequent cause of colorectal cancer in humans. APC protein has an important tumor suppression function to reduce cellular levels of the signaling protprotein β-catenin and, thereby, inhibit β-catenin and T-cell-factor-mediated gene expression. In addition, APC protein binds to microtubules in vertebrate cells and localizes to actin-rich adherens junctions in epithelial cells of the fruit fly Drosophila (Fig. 1). Very little is known, however, about the function of these cytoskeletal associations. Recently, Hamada and Bienz have described a potential role for Drosophila E-APC in cellular adhesion,1 which offers new clues to APC function in embryonic development, and potentially colorectal adenoma formation and tumor progression in humans. BioEssays 24:771–774, 2002. © 2002 Wiley Periodicals, Inc.

Inke S. Näthke – One of the best experts on this subject based on the ideXlab platform.

Violet Votin – One of the best experts on this subject based on the ideXlab platform.

  • neurite outgrowth involves Adenomatous Polyposis Coli protein and β catenin
    Journal of Cell Science, 2005
    Co-Authors: Violet Votin, James W Nelson, Angela I M Barth
    Abstract:

    Neuronal morphogenesis involves the initial formation of neurites and then differentiation of neurites into axons and dendrites. The mechanisms underlying neurite formation are poorly understood. A candidate protein for controlling neurite extension is the Adenomatous Polyposis Coli (APC) protein, which regulates membrane extensions, microtubules and β-catenin-mediated transcription downstream of Wnt signaling. APC is enriched at the tip of several neurites of unpolarized hippocampal neurons and the tip of only the long axon in polarized hippocampal neurons. Significantly, APC localized to the tip of only one neurite, marked by dephospho-tau as the future axon, before that neurite had grown considerably longer than other neurites. To determine whether neurite outgrowth was affected by β-catenin accumulation and signaling, a stabilized β-catenin mutant was expressed in PC12 cells, and neurite formation was measured. Stabilized β-catenin mutants accumulated in APC clusters and inhibited neurite formation and growth. Importantly, these effects were also observed was independently of the gene transcriptional activity of β-catenin. These results indicate that APC is involved in both early neurite outgrowth and increased growth of the future axon, and that β-catenin has a structural role in inhibiting APC function in neurite growth.

  • Neurite outgrowth involves Adenomatous Polyposis Coli protein and beta-catenin.
    Journal of cell science, 2005
    Co-Authors: Violet Votin, W James Nelson, Angela I M Barth
    Abstract:

    Neuronal morphogenesis involves the initial formation of neurites and then differentiation of neurites into axons and dendrites. The mechanisms underlying neurite formation are poorly understood. A candidate protein for controlling neurite extension is the Adenomatous Polyposis Coli (APC) protein, which regulates membrane extensions, microtubules and beta-catenin-mediated transcription downstream of Wnt signaling. APC is enriched at the tip of several neurites of unpolarized hippocampal neurons and the tip of only the long axon in polarized hippocampal neurons. Significantly, APC localized to the tip of only one neurite, marked by dephospho-tau as the future axon, before that neurite had grown considerably longer than other neurites. To determine whether neurite outgrowth was affected by beta-catenin accumulation and signaling, a stabilized beta-catenin mutant was expressed in PC12 cells, and neurite formation was measured. Stabilized beta-catenin mutants accumulated in APC clusters and inhibited neurite formation and growth. Importantly, these effects were also observed was independently of the gene transcriptional activity of beta-catenin. These results indicate that APC is involved in both early neurite outgrowth and increased growth of the future axon, and that beta-catenin has a structural role in inhibiting APC function in neurite growth.

Satya Narayan – One of the best experts on this subject based on the ideXlab platform.

W James Nelson – One of the best experts on this subject based on the ideXlab platform.

  • Neurite outgrowth involves Adenomatous Polyposis Coli protein and beta-catenin.
    Journal of cell science, 2005
    Co-Authors: Violet Votin, W James Nelson, Angela I M Barth
    Abstract:

    Neuronal morphogenesis involves the initial formation of neurites and then differentiation of neurites into axons and dendrites. The mechanisms underlying neurite formation are poorly understood. A candidate protein for controlling neurite extension is the Adenomatous Polyposis Coli (APC) protein, which regulates membrane extensions, microtubules and beta-catenin-mediated transcription downstream of Wnt signaling. APC is enriched at the tip of several neurites of unpolarized hippocampal neurons and the tip of only the long axon in polarized hippocampal neurons. Significantly, APC localized to the tip of only one neurite, marked by dephospho-tau as the future axon, before that neurite had grown considerably longer than other neurites. To determine whether neurite outgrowth was affected by beta-catenin accumulation and signaling, a stabilized beta-catenin mutant was expressed in PC12 cells, and neurite formation was measured. Stabilized beta-catenin mutants accumulated in APC clusters and inhibited neurite formation and growth. Importantly, these effects were also observed was independently of the gene transcriptional activity of beta-catenin. These results indicate that APC is involved in both early neurite outgrowth and increased growth of the future axon, and that beta-catenin has a structural role in inhibiting APC function in neurite growth.

  • What can humans learn from flies about Adenomatous Polyposis Coli
    BioEssays, 2002
    Co-Authors: Angela I M Barth, W James Nelson
    Abstract:

    Somatic or inherited mutations in the Adenomatous Polyposis Coli (APC) gene are a frequent cause of colorectal cancer in humans. APC protein has an important tumor suppression function to reduce cellular levels of the signaling protein β-catenin and, thereby, inhibit β-catenin and T-cell-factor-mediated gene expression. In addition, APC protein binds to microtubules in vertebrate cells and localizes to actin-rich adherens junctions in epithelial cells of the fruit fly Drosophila (Fig. 1). Very little is known, however, about the function of these cytoskeletal associations. Recently, Hamada and Bienz have described a potential role for Drosophila E-APC in cellular adhesion,1 which offers new clues to APC function in embryonic development, and potentially colorectal adenoma formation and tumor progression in humans. BioEssays 24:771–774, 2002. © 2002 Wiley Periodicals, Inc.