The Experts below are selected from a list of 15096 Experts worldwide ranked by ideXlab platform
Angela I M Barth - One of the best experts on this subject based on the ideXlab platform.
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neurite outgrowth involves Adenomatous Polyposis Coli protein and β catenin
Journal of Cell Science, 2005Co-Authors: Violet Votin, James W Nelson, Angela I M BarthAbstract: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.
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Neurite outgrowth involves Adenomatous Polyposis Coli protein and beta-catenin.
Journal of cell science, 2005Co-Authors: Violet Votin, W James Nelson, Angela I M BarthAbstract: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.
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What can humans learn from flies about Adenomatous Polyposis Coli
BioEssays, 2002Co-Authors: Angela I M Barth, W James NelsonAbstract: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.
Inke S. Näthke - One of the best experts on this subject based on the ideXlab platform.
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Interactions and functions of the Adenomatous Polyposis Coli (APC) protein at a glance.
Journal of Cell Science, 2013Co-Authors: Scott M. Nelson, Inke S. NäthkeAbstract:Since its discovery as the major tumour suppressor in colorectal cancer, the Adenomatous Polyposis Coli (APC) protein has emerged as a multi-functional protein that directly or indirectly regulates the cellular processes that govern epithelial tissues ([McCartney and Nathke, 2008][1]). Today, the
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THE Adenomatous Polyposis Coli PROTEIN: The Achilles Heel of the Gut Epithelium
Annual review of cell and developmental biology, 2004Co-Authors: Inke S. NäthkeAbstract:The Adenomatous Polyposis Coli (APC) gene is mutated or lost in most colon cancers, and the APC protein has emerged as a multifunctional protein that is not only involved in the Wnt-regulated degradation of -catenin, but also regulates cytoskeletal proteins and thus plays a role in cell migration, cell adhesion, and mitosis. The gut epithelium is uniquely dependent on an intricate balance between a number of fundamental cellular processes including migration, differentiation, adhesion, apoptosis, and mitosis. In this review, I discuss the molecular mechanisms that govern the various functions of APC and their relationship to the role of APC in colon cancer.
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a role for the Adenomatous Polyposis Coli protein in chromosome segregation
Nature Cell Biology, 2001Co-Authors: Kenneth B Kaplan, Aurora A Burds, Jason R Swedlow, Songiil S Bekir, Peter K Sorger, Inke S. NäthkeAbstract:Mutations in the Adenomatous Polyposis Coli (APC) gene are responsible for familial colon cancer and also occur in the early stages of sporadic colon cancer. APC functions in the Wnt signalling pathway to regulate the degradation of beta-catenin (reviewed in refs 1-3). APC also binds to and stabilizes microtubules in vivo and in vitro, localizes to clusters at the ends of microtubules near the plasma membrane of interphase cells, and is an important regulator of cytoskeletal function. Here we show that cells carrying a truncated APC gene (Min) are defective in chromosome segregation. Moreover, during mitosis, APC localizes to the ends of microtubules embedded in kinetochores and forms a complex with the checkpoint proteins Bub1 and Bub3. In vitro, APC is a high-affinity substrate for Bub kinases. Our data are consistent with a role for APC in kinetochore-microtubule attachment and suggest that truncations in APC that eliminate microtubule binding may contribute to chromosomal instability in cancer cells.
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The Adenomatous Polyposis Coli protein: in the limelight out at the edge.
Trends in cell biology, 2001Co-Authors: Dina Dikovskaya, Jürg Zumbrunn, George A. Penman, Inke S. NäthkeAbstract:Truncation mutations in the Adenomatous Polyposis Coli protein (APC) are responsible for familial and sporadic colonic tumours. APC is best known for its role in regulating β-catenin, an important mediator of cell adhesion and a transcriptional activator. However, recent studies indicate that APC has additional roles in cytoskeletal regulation. It binds to microtubules directly and indirectly. Furthermore, indirect connections between APC and the actin cytoskeleton have also been described. Here, we integrate recent information describing the association between APC and the cytoskeleton to illustrate how this multifaceted protein might link different cytoskeletal elements to each other and to cellular signaling pathways.
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The Adenomatous Polyposis Coli protein.
Molecular pathology : MP, 1999Co-Authors: Inke S. NäthkeAbstract:Mutations in the Adenomatous Polyposis Coli (APC) gene are associated with most colorectal cancers. The APC protein has been implicated in many aspects of tumour development. This article will discuss recent data suggesting that APC may have multiple functions in the cell. First, APC is a component of the Wnt signalling pathway; second, APC may have a role in cell migration; finally, APC may regulate proliferation and apoptosis.
Violet Votin - One of the best experts on this subject based on the ideXlab platform.
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neurite outgrowth involves Adenomatous Polyposis Coli protein and β catenin
Journal of Cell Science, 2005Co-Authors: Violet Votin, James W Nelson, Angela I M BarthAbstract: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.
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Neurite outgrowth involves Adenomatous Polyposis Coli protein and beta-catenin.
Journal of cell science, 2005Co-Authors: Violet Votin, W James Nelson, Angela I M BarthAbstract: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.
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A novel function of Adenomatous Polyposis Coli (APC) in regulating DNA repair.
Cancer letters, 2008Co-Authors: Aruna S. Jaiswal, Satya NarayanAbstract:Abstract Prevailing literature suggests diversified cellular functions for the Adenomatous Polyposis Coli (APC) gene. Among them a recently discovered unique role of APC is in DNA repair. The APC gene can modulate the base excision repair (BER) pathway through an interaction with DNA polymerase β (Pol-β) and flap endonuclease 1 (Fen-1). Taken together with the transcriptional activation of APC gene by alkylating agents and modulation of BER activity, APC may play an important role in carcinogenesis and chemotherapy by determining whether cells with DNA damage survive or undergo apoptosis. In this review, we summarize the evidence supporting this novel concept and suggest that these results will have implications for the development of more effective strategies for chemoprevention, prognosis and chemotherapy of certain types of tumors.
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Cigarette smoke condensate-induced level of Adenomatous Polyposis Coli blocks long-patch base excision repair in breast epithelial cells.
Oncogene, 2006Co-Authors: Chanakya Nath Kundu, Ramesh Balusu, Aruna S. Jaiswal, C G Gairola, Satya NarayanAbstract:Cigarette smoke condensate-induced level of Adenomatous Polyposis Coli blocks long-patch base excision repair in breast epithelial cells
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Involvement of Adenomatous Polyposis Coli in colorectal tumorigenesis.
Frontiers in bioscience : a journal and virtual library, 2005Co-Authors: Aruna S. Jaiswal, Ramesh Balusu, Satya NarayanAbstract:Abstract Colorectal cancer arises after a series of mutations in various tumor suppressor and proto-oncogenes, each of which is accompanied by specific alterations and pathological conditions. Recent advances have contributed a great deal of understanding of the molecular basis of events that lead to colorectal tumorigenesis. Mutation in the Adenomatous Polyposis Coli (APC) gene is considered to be one of the earliest events in the colon cancer development. The familial Adenomatous Polyposis (FAP) and hereditary nonPolyposis colorectal cancer (HNPCC) are the most commonly inherited colorectal cancers. FAP and HNPCC develop due to mutations in APC and DNA mismatch repair (MMR) genes, respectively. APC is known to regulate the levels of beta-catenin, an important mediator of cell-cell adhesion and transcriptional regulator. Mutations in APC gene are also linked with chromosomal instability in colon cancer cells. The role of APC is also implicated in cell migration, cell-cell adhesion, cell cycle control, and apoptosis. This article summarizes the structure-function studies and the role of APC mutations in colon cancer development.
W James Nelson - One of the best experts on this subject based on the ideXlab platform.
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Neurite outgrowth involves Adenomatous Polyposis Coli protein and beta-catenin.
Journal of cell science, 2005Co-Authors: Violet Votin, W James Nelson, Angela I M BarthAbstract: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.
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What can humans learn from flies about Adenomatous Polyposis Coli
BioEssays, 2002Co-Authors: Angela I M Barth, W James NelsonAbstract: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.
