Expression of a Ca2+/calmodulin-dependent protein kinase, CaM kinase-Gr, in human T lymphocytes. Regulation of kinase activity by T cell receptor signaling.
J Biol Chem
; 268(27): 20055-63, 1993 Sep 25.
Article
em En
| MEDLINE
| ID: mdl-8397199
ABSTRACT
Ca2+/calmodulin-dependent protein kinase type Gr (CaM kinase-Gr) is a Ca2+/calmodulin-dependent protein kinase which is enriched in the brain and thymus. In this study, we examined the expression of CaM kinase-Gr in human lymphocytes and the regulation of its catalytic activity by antigen receptor signaling. CaM kinase-Gr was found selectively expressed in T lymphocytes in a developmentally regulated manner. It was present at severalfold higher levels in immature thymocytes (CD3low, CD4+CD8+) relative to mature thymocytes (CD3high, CD4+CD8-/CD8+CD4-) or to circulating T lymphocytes. The kinase was preferentially expressed in CD4+ T lymphocytes, but was not detected in B lymphocytes or in monocytes. The impact of T cell antigen receptor-CD3 complex (TCR.CD3) signaling on kinase activity was examined using Jurkat human leukemic T lymphocytes as a model. Treatment of Jurkat cells with anti TCR.CD3 monoclonal antibody induced rapid autophosphorylation of the kinase on serine residues and a dramatic, autophosphorylation-dependent enhancement of both Ca2+/calmodulin-dependent and autonomous kinase activity. Enzyme autophosphorylation and activation were dependent on the influx of extracellular Ca2+ following receptor signaling but could not be induced by an influx of extra-cellular Ca2+ triggered by ionophores, indicating that additional signals delivered via TCR.CD3 contribute to the activation of CaM kinase-Gr. These findings suggest a role for CaM kinase-Gr in T lymphocyte development and activation and indicate the presence of stringent regulatory mechanisms governing the activity of this kinase in situ.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas Quinases
/
Receptores de Antígenos de Linfócitos T
/
Linfócitos T
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Transdução de Sinais
/
Isoenzimas
Tipo de estudo:
Prognostic_studies
Limite:
Adult
/
Child
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Humans
Idioma:
En
Revista:
J Biol Chem
Ano de publicação:
1993
Tipo de documento:
Article