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

  • microtubule assembly by the APC protein is regulated by importin β rangtp
    Journal of Cell Science, 2010
    Co-Authors: Dina Dikovskaya, Ian P. Newton, Iain Davidson, James R. A. Hutchins, Petr Kalab, Paul R. Clarke, Inke S. Näthke

    Abstract:

    Mutations in the tumour suppressor Adenomatous polyposis coli (APC) initiate most sporadic colorectal cancers. APC is implicated in regulating microtubule (MT) dynamics in interphase and mitosis. However, little is known about the underlying mechanism or regulation of this APC function. We identified importin-β as a binding partner of APC that regulates its effect on MTs. APC binds importin-β in vitro and in Xenopus egg extracts, and RanGTP inhibits this interaction. The armadillo-like repeat domain of importin-β binds to the middle of APC, where it can compete with β-catenin. In addition, two independent sites in the C terminus of APC bind the N-terminal region of importin-β. Binding to importin-β reduces the ability of APC to assemble and bundle MTs in vitro and to promote assembly of microtubule asters in Xenopus egg extracts, but does not affect the binding of APC to MTs or to EB1. Depletion of APC decreases the formation of cold-stable spindles in Xenopus egg extracts. Importantly, the ability of purified APC to rescue this phenotype was reduced when it was constitutively bound to importin-β. Thus, importin-β binds to APC and negatively regulates the MT-assembly and spindle-promoting activity of APC in a Ran-regulatable manner.

  • Microtubule assembly by the APC protein is regulated by importin-β—RanGTP
    Journal of Cell Science, 2010
    Co-Authors: Dina Dikovskaya, Ian P. Newton, Iain Davidson, James R. A. Hutchins, Petr Kalab, Paul R. Clarke, Inke S. Näthke

    Abstract:

    Mutations in the tumour suppressor Adenomatous polyposis coli (APC) initiate most sporadic colorectal cancers. APC is implicated in regulating microtubule (MT) dynamics in interphase and mitosis. However, little is known about the underlying mechanism or regulation of this APC function. We identified importin-β as a binding partner of APC that regulates its effect on MTs. APC binds importin-β in vitro and in Xenopus egg extracts, and RanGTP inhibits this interaction. The armadillo-like repeat domain of importin-β binds to the middle of APC, where it can compete with β-catenin. In addition, two independent sites in the C terminus of APC bind the N-terminal region of importin-β. Binding to importin-β reduces the ability of APC to assemble and bundle MTs in vitro and to promote assembly of microtubule asters in Xenopus egg extracts, but does not affect the binding of APC to MTs or to EB1. Depletion of APC decreases the formation of cold-stable spindles in Xenopus egg extracts. Importantly, the ability of purified APC to rescue this phenotype was reduced when it was constitutively bound to importin-β. Thus, importin-β binds to APC and negatively regulates the MT-assembly and spindle-promoting activity of APC in a Ran-regulatable manner.

  • Microtubule assembly by the APC protein is regulated by importin-beta–RanGTP.
    Journal of cell science, 2010
    Co-Authors: Dina Dikovskaya, Ian P. Newton, Iain Davidson, James R. A. Hutchins, Petr Kalab, Paul R. Clarke, Inke S. Näthke

    Abstract:

    Mutations in the tumour suppressor Adenomatous polyposis coli (APC) initiate most sporadic colorectal cancers. APC is implicated in regulating microtubule (MT) dynamics in interphase and mitosis. However, little is known about the underlying mechanism or regulation of this APC function. We identified importin-beta as a binding partner of APC that regulates its effect on MTs. APC binds importin-beta in vitro and in Xenopus egg extracts, and RanGTP inhibits this interaction. The armadillo-like repeat domain of importin-beta binds to the middle of APC, where it can compete with beta-catenin. In addition, two independent sites in the C terminus of APC bind the N-terminal region of importin-beta. Binding to importin-beta reduces the ability of APC to assemble and bundle MTs in vitro and to promote assembly of microtubule asters in Xenopus egg extracts, but does not affect the binding of APC to MTs or to EB1. Depletion of APC decreases the formation of cold-stable spindles in Xenopus egg extracts. Importantly, the ability of purified APC to rescue this phenotype was reduced when it was constitutively bound to importin-beta. Thus, importin-beta binds to APC and negatively regulates the MT-assembly and spindle-promoting activity of APC in a Ran-regulatable manner.

Leo Grady – One of the best experts on this subject based on the ideXlab platform.

  • identification of high risk plaques destined to cause acute coronary syndrome using coronary computed tomographic angiography and computational fluid dynamics
    Jacc-cardiovascular Imaging, 2019
    Co-Authors: Gilwoo Choi, Doyeon Hwang, Jonghanne Park, Jinlong Zhang, Yaliang Tong, Leo Grady, Eunseok Shin, Su Yeon Choi, Eun Ju Chun, Jinho Choi

    Abstract:

    Abstract Objectives The authors investigated the utility of noninvasive hemodynamic assessment in the identification of high-risk plaques that caused subsequent acute coronary syndrome (ACS). Background ACS is a critical event that impacts the prognosis of patients with coronary artery disease. However, the role of hemodynamic factors in the development of ACS is not well-known. Methods Seventy-two patients with clearly documented ACS and available coronary computed tomographic angiography (CTA) acquired between 1 month and 2 years before the development of ACS were included. In 66 culprit and 150 nonculprit lesions as a case-control design, the presence of adverse plaque characteristics (APC) was assessed and hemodynamic parameters (fractional flow reserve derived by coronary computed tomographic angiography [FFRCT], change in FFRCT across the lesion [△FFRCT], wall shear stress [WSS], and axial plaque stress) were analyzed using computational fluid dynamics. The best cut-off values for FFRCT, △FFRCT, WSS, and axial plaque stress were used to define the presence of adverse hemodynamic characteristics (AHC). The incremental discriminant and reclassification abilities for ACS prediction were compared among 3 models (model 1: percent diameter stenosis [%DS] and lesion length, model 2: model 1 + APC, and model 3: model 2 + AHC). Results The culprit lesions showed higher %DS (55.5 ± 15.4% vs. 43.1 ± 15.0%; p  Conclusions Noninvasive hemodynamic assessment enhanced the identification of high-risk plaques that subsequently caused ACS. The integration of noninvasive hemodynamic assessments may improve the identification of culprit lesions for future ACS. (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary CT Angiography and Computational Fluid Dynamic [EMERALD]; NCT02374775)

  • identification of high risk plaques destined to cause acute coronary syndrome using coronary computed tomographic angiography and computational fluid dynamics
    Jacc-cardiovascular Imaging, 2019
    Co-Authors: Joo Myung Lee, Gilwoo Choi, Doyeon Hwang, Jonghanne Park, Jinlong Zhang, Yaliang Tong, Bonkwon Koo, Kyung Jin Kim, Hyunjin Kim, Leo Grady

    Abstract:

    Abstract Objectives The authors investigated the utility of noninvasive hemodynamic assessment in the identification of high-risk plaques that caused subsequent acute coronary syndrome (ACS). Background ACS is a critical event that impacts the prognosis of patients with coronary artery disease. However, the role of hemodynamic factors in the development of ACS is not well-known. Methods Seventy-two patients with clearly documented ACS and available coronary computed tomographic angiography (CTA) acquired between 1 month and 2 years before the development of ACS were included. In 66 culprit and 150 nonculprit lesions as a case-control design, the presence of adverse plaque characteristics (APC) was assessed and hemodynamic parameters (fractional flow reserve derived by coronary computed tomographic angiography [FFR CT ], change in FFR CT across the lesion [△FFR CT ], wall shear stress [WSS], and axial plaque stress) were analyzed using computational fluid dynamics. The best cut-off values for FFR CT , △FFR CT , WSS, and axial plaque stress were used to define the presence of adverse hemodynamic characteristics (AHC). The incremental discriminant and reclassification abilities for ACS prediction were compared among 3 models (model 1: percent diameter stenosis [%DS] and lesion length, model 2: model 1 + APC, and model 3: model 2 + AHC). Results The culprit lesions showed higher %DS (55.5 ± 15.4% vs. 43.1 ± 15.0%; p  CT and higher △FFR CT , WSS, and axial plaque stress than nonculprit lesions (all p values  Conclusions Noninvasive hemodynamic assessment enhanced the identification of high-risk plaques that subsequently caused ACS. The integration of noninvasive hemodynamic assessments may improve the identification of culprit lesions for future ACS. (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary CT Angiography and Computational Fluid Dynamic [EMERALD]; NCT02374775)

Gilwoo Choi – One of the best experts on this subject based on the ideXlab platform.

  • identification of high risk plaques destined to cause acute coronary syndrome using coronary computed tomographic angiography and computational fluid dynamics
    Jacc-cardiovascular Imaging, 2019
    Co-Authors: Gilwoo Choi, Doyeon Hwang, Jonghanne Park, Jinlong Zhang, Yaliang Tong, Leo Grady, Eunseok Shin, Su Yeon Choi, Eun Ju Chun, Jinho Choi

    Abstract:

    Abstract Objectives The authors investigated the utility of noninvasive hemodynamic assessment in the identification of high-risk plaques that caused subsequent acute coronary syndrome (ACS). Background ACS is a critical event that impacts the prognosis of patients with coronary artery disease. However, the role of hemodynamic factors in the development of ACS is not well-known. Methods Seventy-two patients with clearly documented ACS and available coronary computed tomographic angiography (CTA) acquired between 1 month and 2 years before the development of ACS were included. In 66 culprit and 150 nonculprit lesions as a case-control design, the presence of adverse plaque characteristics (APC) was assessed and hemodynamic parameters (fractional flow reserve derived by coronary computed tomographic angiography [FFRCT], change in FFRCT across the lesion [△FFRCT], wall shear stress [WSS], and axial plaque stress) were analyzed using computational fluid dynamics. The best cut-off values for FFRCT, △FFRCT, WSS, and axial plaque stress were used to define the presence of adverse hemodynamic characteristics (AHC). The incremental discriminant and reclassification abilities for ACS prediction were compared among 3 models (model 1: percent diameter stenosis [%DS] and lesion length, model 2: model 1 + APC, and model 3: model 2 + AHC). Results The culprit lesions showed higher %DS (55.5 ± 15.4% vs. 43.1 ± 15.0%; p  Conclusions Noninvasive hemodynamic assessment enhanced the identification of high-risk plaques that subsequently caused ACS. The integration of noninvasive hemodynamic assessments may improve the identification of culprit lesions for future ACS. (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary CT Angiography and Computational Fluid Dynamic [EMERALD]; NCT02374775)

  • identification of high risk plaques destined to cause acute coronary syndrome using coronary computed tomographic angiography and computational fluid dynamics
    Jacc-cardiovascular Imaging, 2019
    Co-Authors: Joo Myung Lee, Gilwoo Choi, Doyeon Hwang, Jonghanne Park, Jinlong Zhang, Yaliang Tong, Bonkwon Koo, Kyung Jin Kim, Hyunjin Kim, Leo Grady

    Abstract:

    Abstract Objectives The authors investigated the utility of noninvasive hemodynamic assessment in the identification of high-risk plaques that caused subsequent acute coronary syndrome (ACS). Background ACS is a critical event that impacts the prognosis of patients with coronary artery disease. However, the role of hemodynamic factors in the development of ACS is not well-known. Methods Seventy-two patients with clearly documented ACS and available coronary computed tomographic angiography (CTA) acquired between 1 month and 2 years before the development of ACS were included. In 66 culprit and 150 nonculprit lesions as a case-control design, the presence of adverse plaque characteristics (APC) was assessed and hemodynamic parameters (fractional flow reserve derived by coronary computed tomographic angiography [FFR CT ], change in FFR CT across the lesion [△FFR CT ], wall shear stress [WSS], and axial plaque stress) were analyzed using computational fluid dynamics. The best cut-off values for FFR CT , △FFR CT , WSS, and axial plaque stress were used to define the presence of adverse hemodynamic characteristics (AHC). The incremental discriminant and reclassification abilities for ACS prediction were compared among 3 models (model 1: percent diameter stenosis [%DS] and lesion length, model 2: model 1 + APC, and model 3: model 2 + AHC). Results The culprit lesions showed higher %DS (55.5 ± 15.4% vs. 43.1 ± 15.0%; p  CT and higher △FFR CT , WSS, and axial plaque stress than nonculprit lesions (all p values  Conclusions Noninvasive hemodynamic assessment enhanced the identification of high-risk plaques that subsequently caused ACS. The integration of noninvasive hemodynamic assessments may improve the identification of culprit lesions for future ACS. (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary CT Angiography and Computational Fluid Dynamic [EMERALD]; NCT02374775)