Zoltan Nagy (0000-0001-6517-2071)

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Dr. Zoltan Nagy leads an independent laboratory, dedicated to uncovering phosphorylation-dependent signal transduction pathways crucial for regulating megakaryocyte development and platelet biogenesis, supported by the DFG Emmy Noether Program. Dr. Nagy completed his PhD under the supervision of Dr. Albert Smolenski in Dublin, Ireland, and his postdoctoral training with Prof. Yotis Senis in Birmingham, UK, focusing on the role of kinases and phosphatases in platelet signaling. Subsequently, he joined the institute of Prof. Bernhard Nieswandt in Würzburg, Germany, where he developed biochemical analytical methods and applied single-cell RNA sequencing to study megakaryocyte biology.

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Universitätsklinikum Würzburg: Würzburg, DE

2023-07-01 to present | Emmy Noether Group Leader – Experimental Hematology (Institute of Experimental Biomedicine)

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Zoltan Nagy

https://orcid.org/0000-0001-6517-2071

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Employment (4)

Universitätsklinikum Würzburg: Würzburg, DE

University of Würzburg: Würzburg, DE

University of Birmingham: Birmingham, GB

University College Dublin: Dublin, IE

Professional activities (1)

Faculty Opinions: London, GB

Funding (2)

Single-cell roadmap of megakaryocyte development

Mechanisms of megakaryocyte polarisation and platelet biogenesis (A01)

Works (28)

LAIR-1 and PECAM-1 function via the same signaling pathway to inhibit GPVI-mediated platelet activation

Signaling network analysis reveals fostamatinib as a potential drug to control platelet hyperactivation during SARS-CoV-2 infection.

PDE5A: Key Enzyme to Overcome Platelet Inhibition.

Impaired microtubule dynamics contribute to microthrombocytopenia in RhoB-deficient mice

G6b-B regulates an essential step in megakaryocyte maturation

Reduced platelet forces underlie impaired hemostasis in mouse models of <i>MYH9</i> -related disease

G6b-B regulates an essential step in megakaryocyte maturation

Reduced platelet forces underlie impaired hemostasis in mouse models of <i>MYH9</i>-related disease

Microthrombocytopenia caused by impaired microtubule stability in RhoB-deficient mice

Thymosin β4 is essential for thrombus formation by controlling the G-actin/F-actin equilibrium in platelets.

RhoA/Cdc42 signaling drives cytoplasmic maturation but not endomitosis in megakaryocytes.

Lymphatic blood filling in CLEC-2-deficient mouse models

Platelet Src family kinases: A tale of reversible phosphorylation

Severity of megakaryocyte-driven osteosclerosis in Mpig6b-deficient mice is sex-linked.

The RhoA regulators Myo9b and GEF‐H1 are targets of cyclic nucleotide‐dependent kinases in platelets

Actin/microtubule crosstalk during platelet biogenesis in mice is critically regulated by Twinfilin1 and Cofilin1

Interplay between the tyrosine kinases Chk and Csk and phosphatase PTPRJ is critical for regulating platelets in mice

Heparan sulfates are critical regulators of the inhibitory megakaryocyte-platelet receptor G6b-B

Heparan sulfates are critical regulators of the inhibitory megakaryocyte-platelet receptor G6b-B

The Gp1ba-Cre transgenic mouse: a new model to delineate platelet and leukocyte functions

Evaluation of the Total Thrombus-Formation System (T-TAS): application to human and mouse blood analysis.

Analysis of Protein Phosphorylation Using Phos‐Tag Gels

Cyclic nucleotide‐dependent inhibitory signaling interweaves with activating pathways to determine platelet responses

Maintenance of murine platelet homeostasis by the kinase Csk and phosphatase CD148

Ups and downs of the ADP phosphoproteome.

Cyclic Nucleotide-dependent Protein Kinases Target ARHGAP17 and ARHGEF6 Complexes in Platelets

Cyclic Nucleotide Dependent Dephosphorylation of Regulator of G-Protein Signaling 18 in Human Platelets

CLP36 Is a Negative Regulator of Glycoprotein VI Signaling in Platelets

Peer review (7 reviews for 3 publications/grants)