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Btk is a positive regulator in the TREM-1/DAP12 signaling pathway
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SYSNO ASEP 0370093 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Btk is a positive regulator in the TREM-1/DAP12 signaling pathway Tvůrce(i) Ormsby, Tereza (UMG-J)
Schlecker, E. (DE)
Ferdin, J. (DE)
Tessarz, A.S. (DE)
Angelisová, Pavla (UMG-J) RID
Koprulu, A.D. (AT)
Borte, M. (DE)
Warnatz, K. (DE)
Schulze, I. (DE)
Ellmeier, W. (DE)
Hořejší, Václav (UMG-J) RID
Cerwenka, A. (DE)Zdroj.dok. Blood. - : American Society of Hematology - ISSN 0006-4971
Roč. 118, č. 4 (2011), s. 936-945Poč.str. 10 s. Jazyk dok. eng - angličtina Země vyd. US - Spojené státy americké Klíč. slova TREM-1 ; DAP-12 ; Btk Vědní obor RIV EB - Genetika a molekulární biologie CEP 1M0506 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy CEZ AV0Z50520514 - UMG-J (2005-2011) UT WOS 000293221700020 DOI 10.1182/blood-2010-11-317016 Anotace 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 PLCγ1 and Ca²+ mobilization were reduced after TREM-1 stimulation. TREM-1-induced production of the pro-inflammatory cytokines, TNF-α 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-α production by PBMCs was reduced in the patients suffering from XLA, a disease caused by mutations in the BTK gene. Pracoviště Ústav molekulární genetiky Kontakt Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Rok sběru 2012
Počet záznamů: 1