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  1. Article ; Online: Defects in TRPM7 channel function deregulate thrombopoiesis through altered cellular Mg2+ homeostasis and cytoskeletal architecture

    Simon Stritt / Paquita Nurden / Remi Favier / Marie Favier / Silvia Ferioli / Sanjeev K. Gotru / Judith M M. van Eeuwijk / Harald Schulze / Alan T. Nurden / Michele P. Lambert / Ernest Turro / Stephanie Burger-Stritt / Masayuki Matsushita / Lorenz Mittermeier / Paola Ballerini / Susanna Zierler / Michael A. Laffan / Vladimir Chubanov / Thomas Gudermann /
    Bernhard Nieswandt / Attila Braun

    Nature Communications, Vol 7, Iss 1, Pp 1-

    2016  Volume 13

    Abstract: ... still largely unknown. Here, the authors show that TRPM7, a cation channel and a protein kinase ... regulates thrombopoiesis and platelet size by affecting the cytoskeleton of these cells in mice and humans. ... Although Mg2+is vital for platelet activation and aggregation, its regulation in these cells is ...

    Abstract Although Mg2+is vital for platelet activation and aggregation, its regulation in these cells is still largely unknown. Here, the authors show that TRPM7, a cation channel and a protein kinase, regulates thrombopoiesis and platelet size by affecting the cytoskeleton of these cells in mice and humans.
    Keywords Science ; Q
    Language English
    Publishing date 2016-03-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article: Defects in TRPM7 channel function deregulate thrombopoiesis through altered cellular Mg2+ homeostasis and cytoskeletal architecture

    Stritt, Simon / Nurden, Paquita / Favier, Remi / Favier, Marie / Ferioli, Silvia / Gotru, Sanjeev K. / van Eeuwijk, Judith M. M. / Schulze, Harald / Nurden, Alan T. / Lambert, Michele P. / Turro, Ernest / Burger-Stritt, Stephanie / Matsushita, Masayuki / Mittermeier, Lorenz / Ballerini, Paola / Zierler, Susanna / Laffan, Michael A. / Chubanov, Vladimir / Gudermann, Thomas /
    Nieswandt, Bernhard / Braun, Attila

    Nature Communications (7), . (2016)

    Abstract: ... MKs) and platelets are largely unknown. Transient receptor potential melastatin-like 7 channel (TRPM7 ... critical for embryonic development and cell survival. Here we report that impaired channel function ... mainly caused by cytoskeletal alterations resulting in impaired proplatelet formation by Trpm7(fl/fl ...

    Abstract Mg2+ plays a vital role in platelet function, but despite implications for life-threatening conditions such as stroke or myocardial infarction, the mechanisms controlling [Mg2+](i) in megakaryocytes (MKs) and platelets are largely unknown. Transient receptor potential melastatin-like 7 channel (TRPM7) is a ubiquitous, constitutively active cation channel with a cytosolic alpha-kinase domain that is critical for embryonic development and cell survival. Here we report that impaired channel function of TRPM7 in MKs causes macrothrombocytopenia in mice (Trpm7(fl/fl-Pf4Cre)) and likely in several members of a human pedigree that, in addition, suffer from atrial fibrillation. The defect in platelet biogenesis is mainly caused by cytoskeletal alterations resulting in impaired proplatelet formation by Trpm7(fl/fl-Pf4Cre) MKs, which is rescued by Mg2+ supplementation or chemical inhibition of non-muscle myosin IIA heavy chain activity. Collectively, our findings reveal that TRPM7 dysfunction may cause macrothrombocytopenia in humans and mice.
    Language English
    Document type Article
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  3. Article: Defects in TRPM7 channel function deregulate thrombopoiesis through altered cellular Mg2+ homeostasis and cytoskeletal architecture

    Stritt, Simon / Nurden, Paquita / Favier, Remi / Favier, Marie / Ferioli, Silvia / Gotru, Sanjeev K. / van Eeuwijk, Judith M. M. / Schulze, Harald / Nurden, Alan T. / Lambert, Michele P. / Turro, Ernest / Burger-Stritt, Stephanie / Matsushita, Masayuki / Mittermeier, Lorenz / Ballerini, Paola / Zierler, Susanna / Laffan, Michael A. / Chubanov, Vladimir / Gudermann, Thomas /
    Nieswandt, Bernhard / Braun, Attila

    Nature Communications (7), . (2016)

    Abstract: ... MKs) and platelets are largely unknown. Transient receptor potential melastatin-like 7 channel (TRPM7 ... critical for embryonic development and cell survival. Here we report that impaired channel function ... mainly caused by cytoskeletal alterations resulting in impaired proplatelet formation by Trpm7(fl/fl ...

    Abstract Mg2+ plays a vital role in platelet function, but despite implications for life-threatening conditions such as stroke or myocardial infarction, the mechanisms controlling [Mg2+](i) in megakaryocytes (MKs) and platelets are largely unknown. Transient receptor potential melastatin-like 7 channel (TRPM7) is a ubiquitous, constitutively active cation channel with a cytosolic alpha-kinase domain that is critical for embryonic development and cell survival. Here we report that impaired channel function of TRPM7 in MKs causes macrothrombocytopenia in mice (Trpm7(fl/fl-Pf4Cre)) and likely in several members of a human pedigree that, in addition, suffer from atrial fibrillation. The defect in platelet biogenesis is mainly caused by cytoskeletal alterations resulting in impaired proplatelet formation by Trpm7(fl/fl-Pf4Cre) MKs, which is rescued by Mg2+ supplementation or chemical inhibition of non-muscle myosin IIA heavy chain activity. Collectively, our findings reveal that TRPM7 dysfunction may cause macrothrombocytopenia in humans and mice.
    Language English
    Document type Article
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

    More links

    Kategorien

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

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