FZD(10)-G alpha(13) signalling axis points to a role of FZD(10) in CNS angiogenesis

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F17%3A00100422" target="_blank" >RIV/00216224:14310/17:00100422 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.cellsig.2017.01.023" target="_blank" >http://dx.doi.org/10.1016/j.cellsig.2017.01.023</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.cellsig.2017.01.023" target="_blank" >10.1016/j.cellsig.2017.01.023</a>

Jazyk výsledku

angličtina

Název v původním jazyce

FZD(10)-G alpha(13) signalling axis points to a role of FZD(10) in CNS angiogenesis

Popis výsledku v původním jazyce

Among the 10 Frizzled (FZD) isoforms belonging to the Class F of G protein-coupled receptors (GPCRs), FZD(10) remains the most enigmatic. FZD10 shows homology to FZD(4) and FZD(9) and was previously implicated in both beta-catenin-dependent and-independent signalling. In normal tissue, FZD(10) levels are generally very low; however, its upregulation in synovial carcinoma has attracted some attention for therapy. Our findings identify FZD(10), as a receptor interacting with and signalling through the heterotrimeric G protein G alpha(13) but not G alpha(12), G alpha(i1,) G alpha(oA), G alpha(s), or G alpha(q). Stimulation with the FZD agonist WNT induced the dissociation of the G alpha(13) protein from FZD(10), and led to global G alpha(12/13)-dependent cell changes assessed by dynamic mass redistribution measurements. Furthermore, we show that FZD(10) mediates G alpha(12/13) activation-dependent induction of YAP/TAZ transcriptional activity. In addition, we show a distinct expression of FZD(10) in embryonic CNS endothelial cells at E11.5-E14.5. Given the well-known importance of G alpha(13) signalling for the development of the vascular system, the selective expression of FZD(10) in brain vascular endothelial cells points at a potential role of FZD(10)-G alpha(13) signalling in CNS angiogenesis. (C) 2017 Elsevier Inc. All rights reserved.

Název v anglickém jazyce

FZD(10)-G alpha(13) signalling axis points to a role of FZD(10) in CNS angiogenesis

Popis výsledku anglicky

Among the 10 Frizzled (FZD) isoforms belonging to the Class F of G protein-coupled receptors (GPCRs), FZD(10) remains the most enigmatic. FZD10 shows homology to FZD(4) and FZD(9) and was previously implicated in both beta-catenin-dependent and-independent signalling. In normal tissue, FZD(10) levels are generally very low; however, its upregulation in synovial carcinoma has attracted some attention for therapy. Our findings identify FZD(10), as a receptor interacting with and signalling through the heterotrimeric G protein G alpha(13) but not G alpha(12), G alpha(i1,) G alpha(oA), G alpha(s), or G alpha(q). Stimulation with the FZD agonist WNT induced the dissociation of the G alpha(13) protein from FZD(10), and led to global G alpha(12/13)-dependent cell changes assessed by dynamic mass redistribution measurements. Furthermore, we show that FZD(10) mediates G alpha(12/13) activation-dependent induction of YAP/TAZ transcriptional activity. In addition, we show a distinct expression of FZD(10) in embryonic CNS endothelial cells at E11.5-E14.5. Given the well-known importance of G alpha(13) signalling for the development of the vascular system, the selective expression of FZD(10) in brain vascular endothelial cells points at a potential role of FZD(10)-G alpha(13) signalling in CNS angiogenesis. (C) 2017 Elsevier Inc. All rights reserved.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10608 - Biochemistry and molecular biology

Projekt

<a href="/cs/project/EE2.3.20.0180" target="_blank" >EE2.3.20.0180: Spolupráce mezi Masarykovou univerzitou a Karolinska Institutet, Stockholm na poli biomedicíny</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2017

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Cellular Signalling

ISSN

0898-6568

e-ISSN

—

Svazek periodika

32

Číslo periodika v rámci svazku

April

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

93-103

Kód UT WoS článku

000395953400010

EID výsledku v databázi Scopus

—