dc.creator | Molinero, Luciana Lorena | |
dc.creator | Fuertes, Mercedes Beatriz | |
dc.creator | Fainboim, Leonardo | |
dc.creator | Rabinovich, Gabriel Adrián | |
dc.creator | Zwirner, Norberto Walter | |
dc.date.accessioned | 2018-02-11T23:48:14Z | |
dc.date.accessioned | 2018-11-06T14:42:41Z | |
dc.date.available | 2018-02-11T23:48:14Z | |
dc.date.available | 2018-11-06T14:42:41Z | |
dc.date.created | 2018-02-11T23:48:14Z | |
dc.date.issued | 2003-06-01 | |
dc.identifier | Molinero, Luciana Lorena; Fuertes, Mercedes Beatriz; Fainboim, Leonardo; Rabinovich, Gabriel Adrián; Zwirner, Norberto Walter; Up-regulated expression of MICA on activated T lymphocytes involves Lck and Fyn kinases, and signaling through MEK1/ERK, p38 MAP kinase and calcineurin; Federation of American Societies for Experimental Biology; Journal of Leukocyte Biology; 73; 6; 1-6-2003; 815-822 | |
dc.identifier | 0741-5400 | |
dc.identifier | http://hdl.handle.net/11336/36414 | |
dc.identifier | CONICET Digital | |
dc.identifier | CONICET | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/1889310 | |
dc.description.abstract | Major histocompatibility complex class I-related chain (MICA) is a cell stress-regulated molecule recognized by cytotoxic cells expressing the NKG2D molecule. MICA can be induced on T cells after CD3 or CD28 engagement. Here, we investigated the intracellular pathways leading to activation-induced expression of MICA. The Src kinase inhibitor PP1 inhibited up-regulated expression of MICA on anti-CD3-stimulated T cells. Downstream signaling routes involved mitogen-activated protein kinase (MAPK) kinase (MEK)1/extracellular signal-regulated kinase (ERK), p38 MAPK, and calcineurin, as MICA expression was prevented by U0126, SB202190, cyclosporin A, and FK506. Also, Lck and Fyn as well as MEK1/ERK and p38 MAPK were found to regulate MICA expression in anti-CD28/phorbol 12-myristate 13-acetate-stimulated T cells. Expression of MICA on activated T cells involved interleukin-2-dependent signaling routes triggered by Janus tyrosine kinases/signal transducer and activators of transcription and p70S6 kinase, as it could be inhibited by AG490 and rapamycin. This is the first demonstration of the intracellular pathways involved in activation-induced expression of MICA, which may reveal potential targets for immune intervention to modulate MICA expression in pathological disorders. | |
dc.language | eng | |
dc.publisher | Federation of American Societies for Experimental Biology | |
dc.relation | info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1189/jlb.0602329/full | |
dc.relation | info:eu-repo/semantics/altIdentifier/url/10.1189/jlb.0602329 | |
dc.relation | info:eu-repo/semantics/altIdentifier/pmid/12773514 | |
dc.rights | https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ | |
dc.rights | info:eu-repo/semantics/restrictedAccess | |
dc.subject | MAJOR HISTOCOMPATIBIBLITY COMPLEX | |
dc.subject | SIGNALING PATHWAYS | |
dc.subject | NKG2D | |
dc.subject | MICA | |
dc.title | Up-regulated expression of MICA on activated T lymphocytes involves Lck and Fyn kinases, and signaling through MEK1/ERK, p38 MAP kinase and calcineurin | |
dc.type | Artículos de revistas | |
dc.type | Artículos de revistas | |
dc.type | Artículos de revistas | |