The pool of preactivated Lck in the initiation of T-cell signaling: a critical re-evaluation of the Lck standby model

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F15%3A10314282" target="_blank" >RIV/00216208:11310/15:10314282 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68378050:_____/15:00455198

Výsledek na webu

<a href="http://dx.doi.org/10.1038/icb.2014.100" target="_blank" >http://dx.doi.org/10.1038/icb.2014.100</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/icb.2014.100" target="_blank" >10.1038/icb.2014.100</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The pool of preactivated Lck in the initiation of T-cell signaling: a critical re-evaluation of the Lck standby model

Popis výsledku v původním jazyce

The initiation of T-cell receptor (TCR) signaling, based on the cobinding of TCR and CD4-Lck heterodimer to a peptide-major histocompatibility complex II on antigen presenting cells, represents a classical model of T-cell signaling. What is less clear however, is the mechanism which translates TCR engagement to the phosphorylation of immunoreceptor tyrosine-based activation motifs on CD3 chains and how this event is coupled to the delivery of Lck function. Recently proposed ' standby model of Lck' posits that resting T-cells contain an abundant pool of constitutively active Lck (pY394(Lck)) required for TCR triggering, and this amount, upon TCR engagement, remains constant. Here, we show that although maintenance of the limited pool of pY394(Lck) is necessary for the generation of TCR proximal signals in a time-restricted fashion, the total amount of this pool, similar to 2%, is much smaller than previously reported (similar to 40%). We provide evidence that this dramatic discrepancy i

Název v anglickém jazyce

The pool of preactivated Lck in the initiation of T-cell signaling: a critical re-evaluation of the Lck standby model

Popis výsledku anglicky

The initiation of T-cell receptor (TCR) signaling, based on the cobinding of TCR and CD4-Lck heterodimer to a peptide-major histocompatibility complex II on antigen presenting cells, represents a classical model of T-cell signaling. What is less clear however, is the mechanism which translates TCR engagement to the phosphorylation of immunoreceptor tyrosine-based activation motifs on CD3 chains and how this event is coupled to the delivery of Lck function. Recently proposed ' standby model of Lck' posits that resting T-cells contain an abundant pool of constitutively active Lck (pY394(Lck)) required for TCR triggering, and this amount, upon TCR engagement, remains constant. Here, we show that although maintenance of the limited pool of pY394(Lck) is necessary for the generation of TCR proximal signals in a time-restricted fashion, the total amount of this pool, similar to 2%, is much smaller than previously reported (similar to 40%). We provide evidence that this dramatic discrepancy i

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EC - Imunologie

OECD FORD obor

—

Projekt

<a href="/cs/project/GA310%2F09%2F2084" target="_blank" >GA310/09/2084: Charakterizace molekulárního mechanismu regulujícího kompartmentalizaci signálních molekul do lipidových raftů</a><br>

Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2015

Kód důvěrnosti údajů

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

Název periodika

Immunology and Cell Biology

ISSN

0818-9641

e-ISSN

—

Svazek periodika

93

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

AU - Austrálie

Počet stran výsledku

12

Strana od-do

384-395

Kód UT WoS článku

000353302900011

EID výsledku v databázi Scopus

2-s2.0-84928209119