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巨核细胞和血小板中的formin 蛋白:肌动蛋白和微管动力学的调节。

Formin proteins in megakaryocytes and platelets: regulation of actin and microtubule dynamics.

机构信息

a Institute of Cardiovascular Sciences , University of Birmingham , Birmingham , UK.

b Centre of Membrane Proteins and Receptors (COMPARE) , University of Birmingham and University of Nottingham , Midlands , UK.

出版信息

Platelets. 2019;30(1):23-30. doi: 10.1080/09537104.2018.1481937. Epub 2018 Jun 18.

DOI:10.1080/09537104.2018.1481937
PMID:29913076
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6406210/
Abstract

The platelet and megakaryocyte cytoskeletons are essential for formation and function of these cells. A dynamic, properly organised tubulin and actin cytoskeleton is critical for the development of the megakaryocyte and the extension of proplatelets. Tubulin in particular plays a pivotal role in the extension of these proplatelets and the release of platelets from them. Tubulin is further required for the maintenance of platelet size, and actin is the driving force for shape change, spreading and platelet contraction during platelet activation. Whilst several key proteins which regulate these cytoskeletons have been described in detail, the formin family of proteins has received less attention. Formins are intriguing as, although they were initially believed to simply be a nucleator of actin polymerisation, increasing evidence shows they are important regulators of the crosstalk between the actin and microtubule cytoskeletons. In this review, we will introduce the formin proteins and consider the recent evidence that they play an important role in platelets and megakaryocytes in mediating both the actin and tubulin cytoskeletons.

摘要

血小板和巨核细胞的细胞骨架对于这些细胞的形成和功能至关重要。一个动态的、组织良好的微管和肌动蛋白细胞骨架对于巨核细胞的发育和伪足的延伸至关重要。微管蛋白在这些伪足的延伸和血小板从伪足中释放中起着关键作用。微管蛋白进一步需要维持血小板的大小,肌动蛋白是血小板激活过程中形状变化、扩散和血小板收缩的驱动力。虽然已经详细描述了几种调节这些细胞骨架的关键蛋白,但形成蛋白家族受到的关注较少。形成蛋白很有趣,因为尽管最初它们被认为只是肌动蛋白聚合的起始因子,但越来越多的证据表明,它们是调节肌动蛋白和微管细胞骨架之间串扰的重要调节剂。在这篇综述中,我们将介绍形成蛋白,并考虑最近的证据,表明它们在调节血小板和巨核细胞中的肌动蛋白和微管细胞骨架方面发挥着重要作用。

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Neural Regen Res. 2017 Dec;12(12):1971-1973. doi: 10.4103/1673-5374.221148.
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Loss of mDia1 causes neutropenia via attenuated CD11b endocytosis and increased neutrophil adhesion to the endothelium.mDia1的缺失通过减弱CD11b内吞作用和增加中性粒细胞与内皮细胞的黏附导致中性粒细胞减少。
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The actin-organizing formin protein Fhod3 is required for postnatal development and functional maintenance of the adult heart in mice.
巨噬细胞中SHP2的特异性敲除促进巨噬细胞M2极化并减轻肾脏缺血再灌注损伤。
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4
mDia formins form hetero-oligomers and cooperatively maintain murine hematopoiesis.mDia 形成蛋白形成异型寡聚体,并协同维持小鼠造血。
PLoS Genet. 2023 Dec 29;19(12):e1011084. doi: 10.1371/journal.pgen.1011084. eCollection 2023 Dec.
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Dynamic actin/septin network in megakaryocytes coordinates proplatelet elaboration.巨核细胞中动态肌动蛋白/栓系蛋白网络协调血小板前体细胞的延伸。
Haematologica. 2024 Mar 1;109(3):915-928. doi: 10.3324/haematol.2023.283369.
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Impaired microtubule dynamics contribute to microthrombocytopenia in RhoB-deficient mice.RhoB 缺陷型小鼠的微管动力学障碍导致微小血小板减少症。
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Cells. 2021 Sep 27;10(10):2554. doi: 10.3390/cells10102554.
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