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Correction: Corrigendum: Megakaryocyte-specific Profilin1-deficiency alters microtubule stability and causes a Wiskott–Aldrich syndrome-like platelet defect

Markus Bender
Simon Stritt
Bernhard Nieswandt
Amendments and Corrections06 Mar 2015
Nature Communications

Volume: 6, P: 1
Megakaryocyte-specific Profilin1-deficiency alters microtubule stability and causes a Wiskott–Aldrich syndrome-like platelet defect

Patients with mutations in the gene encoding the cytoskeleton regulator WAS have platelet defects. Here the authors show that the WAS-binding protein, Profilin1, is essential for platelet formation in mice, and that its deficiency reproduces the bleeding disorder of patients with WAS mutations.

Markus Bender
Simon Stritt
Bernhard Nieswandt
Research04 Sept 2014
Nature Communications

Volume: 5, P: 1-14
A Cdc42/RhoA regulatory circuit downstream of glycoprotein Ib guides transendothelial platelet biogenesis

Platelets derive from large precursor cells (megakaryocytes) in the bone marrow. Düttinget al. show that megakaryocyte polarization and platelet biogenesis in the bone-marrow sinusoids are directed by adhesion receptor GPIb signalling and resulting balanced antagonism between RhoA (stop-signal) and Cdc42 (go-signal).

Sebastian Dütting
Frederique Gaits-Iacovoni
Bernhard Nieswandt
ResearchOpen Access15 Jun 2017
Nature Communications

Volume: 8, P: 1-13
Defects in TRPM7 channel function deregulate thrombopoiesis through altered cellular Mg²⁺ homeostasis and cytoskeletal architecture

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.

Simon Stritt
Paquita Nurden
Attila Braun
ResearchOpen Access29 Mar 2016
Nature Communications

Volume: 7, P: 1-13
Thrombopoiesis is spatially regulated by the bone marrow vasculature

Megakaryocyte maturation is thought to occur as the cells migrate from a vessel-distant (endosteal) niche to the vessel within the bone. Here, the authors show that megakaryocytes represent largely sessile cells in close contact with the vasculature and homogeneously distributed in the bone marrow.

David Stegner
Judith M. M. vanEeuwijk
Katrin G. Heinze
ResearchOpen Access25 Jul 2017
Nature Communications

Volume: 8, P: 1-11

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Correction: Corrigendum: Megakaryocyte-specific Profilin1-deficiency alters microtubule stability and causes a Wiskott–Aldrich syndrome-like platelet defect

Megakaryocyte-specific Profilin1-deficiency alters microtubule stability and causes a Wiskott–Aldrich syndrome-like platelet defect

A Cdc42/RhoA regulatory circuit downstream of glycoprotein Ib guides transendothelial platelet biogenesis

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

Thrombopoiesis is spatially regulated by the bone marrow vasculature

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