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Nina Wettschureck

Researcher at Max Planck Society

Publications -  83
Citations -  7293

Nina Wettschureck is an academic researcher from Max Planck Society. The author has contributed to research in topics: Heterotrimeric G protein & Receptor. The author has an hindex of 36, co-authored 79 publications receiving 6044 citations. Previous affiliations of Nina Wettschureck include Heidelberg University & Goethe University Frankfurt.

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Mammalian G proteins and their cell type specific functions

TL;DR: In this review, some of the functions of heterotrimeric G proteins in defined cells and tissues are described.
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G12-G13-LARG-mediated signaling in vascular smooth muscle is required for salt-induced hypertension.

TL;DR: It is shown that Gq-G11-mediated signaling in smooth muscle cells is required for maintenance of basal blood pressure and for the development of salt-induced hypertension, which identifies the G12-G13–LARG–mediated signaling pathway as a new target for antihypertensive therapies that would be expected to leave normal blood pressure regulation unaffected.
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Conditional mutation of the ErbB2(HER2) receptor in cardiomyocytes leads to dilated cardiomyopathy.

TL;DR: It is inferred that signaling from the ErbB2 receptor, which is enriched in T-tubules in cardiomyocytes, is crucial for adult heart function.
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Platelet-Derived Nucleotides Promote Tumor-Cell Transendothelial Migration and Metastasis via P2Y2 Receptor

TL;DR: It is shown that adenine nucleotides released from tumor cell-activated platelets induce opening of the endothelial barrier to allow transendothelial migration of tumor cells and thereby promote cancer cell extravasation.
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Endothelial cation channel PIEZO1 controls blood pressure by mediating flow-induced ATP release

TL;DR: It is shown that the endothelial mechanosensitive cation channel PIEZO1 is required for flow-induced ATP release and subsequent P2Y2/Gq/G11-mediated activation of downstream signaling that results in phosphorylation and activation of AKT and endothelial NOS and that PIEzO1-dependent ATP release is mediated in part by pannexin channels.