Btk is a positive regulator in the TREM-1/DAP12 signaling pathway
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F11%3A00370093" target="_blank" >RIV/68378050:_____/11:00370093 - isvavai.cz</a>
Výsledek na webu
<a href="http://dx.doi.org/10.1182/blood-2010-11-317016" target="_blank" >http://dx.doi.org/10.1182/blood-2010-11-317016</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1182/blood-2010-11-317016" target="_blank" >10.1182/blood-2010-11-317016</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Btk is a positive regulator in the TREM-1/DAP12 signaling pathway
Popis výsledku v původním jazyce
TREM-1 receptor has been implicated in the production of proinflammatory cytokines and chemokines during bacterial infection and sepsis. For downstream signal transduction, TREM-1 is coupled to the ITAM-containing adaptor DAP12. We demonstrate that Bruton tyrosine kinase (Btk), becomes phosphorylated upon TREM-1 triggering. In cell lines, in which expression of Btk was diminished by shRNA-mediated knockdown, phosphorylation of Erk1/2 and PLC?1 and Ca+ mobilization were reduced after TREM-1 stimulation.TREM-1-induced production of the pro-inflammatory cytokines, TNF-? and IL-8, and up-regulation of activation/differentiation cell surface markers were impaired in Btk knockdown cells.Intact membrane localization and a functional kinase domain were required for TREM-1-mediated signaling. After TREM-1 engagement, TNF-? production by PBMCs was reduced in the patients suffering from XLA, a disease caused by mutations in the BTK gene.
Název v anglickém jazyce
Btk is a positive regulator in the TREM-1/DAP12 signaling pathway
Popis výsledku anglicky
TREM-1 receptor has been implicated in the production of proinflammatory cytokines and chemokines during bacterial infection and sepsis. For downstream signal transduction, TREM-1 is coupled to the ITAM-containing adaptor DAP12. We demonstrate that Bruton tyrosine kinase (Btk), becomes phosphorylated upon TREM-1 triggering. In cell lines, in which expression of Btk was diminished by shRNA-mediated knockdown, phosphorylation of Erk1/2 and PLC?1 and Ca+ mobilization were reduced after TREM-1 stimulation.TREM-1-induced production of the pro-inflammatory cytokines, TNF-? and IL-8, and up-regulation of activation/differentiation cell surface markers were impaired in Btk knockdown cells.Intact membrane localization and a functional kinase domain were required for TREM-1-mediated signaling. After TREM-1 engagement, TNF-? production by PBMCs was reduced in the patients suffering from XLA, a disease caused by mutations in the BTK gene.
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
EB - Genetika a molekulární biologie
OECD FORD obor
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Návaznosti výsledku
Projekt
<a href="/cs/project/1M0506" target="_blank" >1M0506: Centrum molekulární a buněčné imunologie</a><br>
Návaznosti
Z - Vyzkumny zamer (s odkazem do CEZ)
Ostatní
Rok uplatnění
2011
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Blood
ISSN
0006-4971
e-ISSN
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Svazek periodika
118
Číslo periodika v rámci svazku
4
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
10
Strana od-do
936-945
Kód UT WoS článku
000293221700020
EID výsledku v databázi Scopus
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