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  PAR1 Scaffolds TGF beta RII to Downregulate TGF-beta Signaling and Activate ESC Differentiation to Endothelial Cells

Gong, H., An, S., Sassmann, A., Liu, M., Mastej, V., Mittal, M., et al. (2016). PAR1 Scaffolds TGF beta RII to Downregulate TGF-beta Signaling and Activate ESC Differentiation to Endothelial Cells. STEM CELL REPORTS, 7(6), 1050-1058. doi:10.1016/j.stemcr.2016.10.006.

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 Urheber:
Gong, Haixia, Autor
An, Shejuan, Autor
Sassmann, Antonia1, Autor           
Liu, Menglin, Autor
Mastej, Victoria, Autor
Mittal, Manish, Autor
Zhang, Wei, Autor
Hong, Zhigang, Autor
Offermanns, Stefan1, Autor           
Rehman, Jalees, Autor
Malik, Asrar B., Autor
Affiliations:
1Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591696              

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Schlagwörter: PROTEIN-COUPLED RECEPTORS; HUMAN EMBRYONIC STEM; THROMBIN; PLURIPOTENCY; G-ALPHA(13); MAINTENANCE; MECHANISMS; DISEASES; GPR56Cell Biology;
 Zusammenfassung: We studied the function of the G-protein-coupled receptor PAR1 in mediating the differentiation of mouse embryonic stem cells (mESCs) to endothelial cells (ECs) that are capable of inducing neovascularization. We observed that either deletion or activation of PAR1 suppressed mouse embryonic stem cell (mESC) differentiation to ECs and neovascularization in mice. This was mediated by induction of TGF beta RII/TGF beta RI interaction, forming an active complex, which in turn induced SMAD2 phosphorylation. Inhibition of TGF-beta signaling in PAR1-deficient mESCs restored the EC differentiation potential of mESCs. Thus, PAR1 in its inactive unligated state functions as a scaffold for TGF beta RII to downregulate TGF-beta signaling, and thereby promote ESC transition to functional ECs. The PAR1 scaffold function in ESCs is an essential mechanism for dampening TGF-beta signaling and regulating ESC differentiation.

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Sprache(n): eng - English
 Datum: 2016
 Publikationsstatus: Erschienen
 Seiten: 9
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: -
 Identifikatoren: ISI: 000393188500004
DOI: 10.1016/j.stemcr.2016.10.006
 Art des Abschluß: -

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Titel: STEM CELL REPORTS
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA : CELL PRESS
Seiten: - Band / Heft: 7 (6) Artikelnummer: - Start- / Endseite: 1050 - 1058 Identifikator: ISSN: 2213-6711