Fibroblast growth factor receptor influences primary cilium length through an interaction with intestinal cell kinase
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985904%3A_____%2F19%3A00504030" target="_blank" >RIV/67985904:_____/19:00504030 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216224:14110/19:00107404 RIV/00159816:_____/19:00071073 RIV/60076658:12310/19:43899170
Výsledek na webu
<a href="https://www.pnas.org/content/116/10/4316" target="_blank" >https://www.pnas.org/content/116/10/4316</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1073/pnas.1800338116" target="_blank" >10.1073/pnas.1800338116</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Fibroblast growth factor receptor influences primary cilium length through an interaction with intestinal cell kinase
Popis výsledku v původním jazyce
Vertebrate primary cilium is a Hedgehog signaling center but the extent of its involvement in other signaling systems is less well understood. This report delineates a mechanism by which fibroblast growth factor (FGF) controls primary cilia. Employing proteomic approaches to characterize proteins associated with the FGF-receptor, FGFR3, we identified the serine/threonine kinase intestinal cell kinase (ICK) as an FGFR interactor. ICK is involved in ciliogenesis and participates in control of ciliary length. FGF signaling partially abolished ICK's kinase activity, through FGFR-mediated ICK phosphorylation at conserved residue Tyr15, which interfered with optimal ATP binding. Activation of the FGF signaling pathway affected both primary cilia length and function in a manner consistent with cilia effects caused by inhibition of ICK activity. Moreover, knockdown and knockout of ICK rescued the FGF-mediated effect on cilia. We provide conclusive evidence that FGF signaling controls cilia via interaction with ICK.
Název v anglickém jazyce
Fibroblast growth factor receptor influences primary cilium length through an interaction with intestinal cell kinase
Popis výsledku anglicky
Vertebrate primary cilium is a Hedgehog signaling center but the extent of its involvement in other signaling systems is less well understood. This report delineates a mechanism by which fibroblast growth factor (FGF) controls primary cilia. Employing proteomic approaches to characterize proteins associated with the FGF-receptor, FGFR3, we identified the serine/threonine kinase intestinal cell kinase (ICK) as an FGFR interactor. ICK is involved in ciliogenesis and participates in control of ciliary length. FGF signaling partially abolished ICK's kinase activity, through FGFR-mediated ICK phosphorylation at conserved residue Tyr15, which interfered with optimal ATP binding. Activation of the FGF signaling pathway affected both primary cilia length and function in a manner consistent with cilia effects caused by inhibition of ICK activity. Moreover, knockdown and knockout of ICK rescued the FGF-mediated effect on cilia. We provide conclusive evidence that FGF signaling controls cilia via interaction with ICK.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10608 - Biochemistry and molecular biology
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2019
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Proceedings of the National Academy of Sciences of the United States of America
ISSN
0027-8424
e-ISSN
—
Svazek periodika
116
Číslo periodika v rámci svazku
10
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
10
Strana od-do
4316-4325
Kód UT WoS článku
000460242100061
EID výsledku v databázi Scopus
2-s2.0-85062661279