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MHC class I signaling in T cells leads to tyrosine kinase activity and PLC-gamma 1 phosphorylation

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Standard

MHC class I signaling in T cells leads to tyrosine kinase activity and PLC-gamma 1 phosphorylation. / Skov, S; Odum, Niels; Claesson, M H.

I: Journal of Immunology, Bind 154, Nr. 3, 1995, s. 1167-76.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Skov, S, Odum, N & Claesson, MH 1995, 'MHC class I signaling in T cells leads to tyrosine kinase activity and PLC-gamma 1 phosphorylation', Journal of Immunology, bind 154, nr. 3, s. 1167-76.

APA

Skov, S., Odum, N., & Claesson, M. H. (1995). MHC class I signaling in T cells leads to tyrosine kinase activity and PLC-gamma 1 phosphorylation. Journal of Immunology, 154(3), 1167-76.

Vancouver

Skov S, Odum N, Claesson MH. MHC class I signaling in T cells leads to tyrosine kinase activity and PLC-gamma 1 phosphorylation. Journal of Immunology. 1995;154(3):1167-76.

Author

Skov, S ; Odum, Niels ; Claesson, M H. / MHC class I signaling in T cells leads to tyrosine kinase activity and PLC-gamma 1 phosphorylation. I: Journal of Immunology. 1995 ; Bind 154, Nr. 3. s. 1167-76.

Bibtex

@article{11432370fd9511ddb219000ea68e967b,
title = "MHC class I signaling in T cells leads to tyrosine kinase activity and PLC-gamma 1 phosphorylation",
abstract = "We have studied the biochemical signal pathway leading to a rise in intracellular free calcium concentration ([Ca2+]i) following cross-linking of MHC class I (MHC-I) molecules on human T leukemic Jurkat cells. Evidence is presented that MHC-I signaling is dependent on tyrosine kinase activity before the observed increase in [Ca2+]i. Thus, tyrosine phosphorylation was detected within 5 s after MHC-I cross-linking, whereas an increase in [Ca2+]i was observed after a lag period of 30 s. Moreover, an inhibitor of tyrosine kinases, herbimycin A, almost completely blocked MHC-I-induced tyrosine phosphorylation and the subsequent calcium response. The early tyrosine kinase activity was found to be dependent on expression of the TCR/CD3 complex and the CD45 molecule on the surface of the T cells. Furthermore, MHC-I cross-linking was shown to tyrosine phosphorylate PLC-gamma 1 (phospholipase C-gamma 1). Collectively, these results indicate that the MHC-I signaling pathway is linked to activation of tyrosine kinase(s) in Jurkat cells.",
author = "S Skov and Niels Odum and Claesson, {M H}",
note = "Keywords: Antigens, CD45; Benzoquinones; Calcium; Histocompatibility Antigens Class I; Humans; Isoenzymes; Lactams, Macrocyclic; Phospholipase C gamma; Phosphotyrosine; Precipitin Tests; Protein-Tyrosine Kinases; Quinones; Receptor-CD3 Complex, Antigen, T-Cell; Signal Transduction; T-Lymphocytes; Tumor Cells, Cultured; Type C Phospholipases; Tyrosine",
year = "1995",
language = "English",
volume = "154",
pages = "1167--76",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "3",

}

RIS

TY - JOUR

T1 - MHC class I signaling in T cells leads to tyrosine kinase activity and PLC-gamma 1 phosphorylation

AU - Skov, S

AU - Odum, Niels

AU - Claesson, M H

N1 - Keywords: Antigens, CD45; Benzoquinones; Calcium; Histocompatibility Antigens Class I; Humans; Isoenzymes; Lactams, Macrocyclic; Phospholipase C gamma; Phosphotyrosine; Precipitin Tests; Protein-Tyrosine Kinases; Quinones; Receptor-CD3 Complex, Antigen, T-Cell; Signal Transduction; T-Lymphocytes; Tumor Cells, Cultured; Type C Phospholipases; Tyrosine

PY - 1995

Y1 - 1995

N2 - We have studied the biochemical signal pathway leading to a rise in intracellular free calcium concentration ([Ca2+]i) following cross-linking of MHC class I (MHC-I) molecules on human T leukemic Jurkat cells. Evidence is presented that MHC-I signaling is dependent on tyrosine kinase activity before the observed increase in [Ca2+]i. Thus, tyrosine phosphorylation was detected within 5 s after MHC-I cross-linking, whereas an increase in [Ca2+]i was observed after a lag period of 30 s. Moreover, an inhibitor of tyrosine kinases, herbimycin A, almost completely blocked MHC-I-induced tyrosine phosphorylation and the subsequent calcium response. The early tyrosine kinase activity was found to be dependent on expression of the TCR/CD3 complex and the CD45 molecule on the surface of the T cells. Furthermore, MHC-I cross-linking was shown to tyrosine phosphorylate PLC-gamma 1 (phospholipase C-gamma 1). Collectively, these results indicate that the MHC-I signaling pathway is linked to activation of tyrosine kinase(s) in Jurkat cells.

AB - We have studied the biochemical signal pathway leading to a rise in intracellular free calcium concentration ([Ca2+]i) following cross-linking of MHC class I (MHC-I) molecules on human T leukemic Jurkat cells. Evidence is presented that MHC-I signaling is dependent on tyrosine kinase activity before the observed increase in [Ca2+]i. Thus, tyrosine phosphorylation was detected within 5 s after MHC-I cross-linking, whereas an increase in [Ca2+]i was observed after a lag period of 30 s. Moreover, an inhibitor of tyrosine kinases, herbimycin A, almost completely blocked MHC-I-induced tyrosine phosphorylation and the subsequent calcium response. The early tyrosine kinase activity was found to be dependent on expression of the TCR/CD3 complex and the CD45 molecule on the surface of the T cells. Furthermore, MHC-I cross-linking was shown to tyrosine phosphorylate PLC-gamma 1 (phospholipase C-gamma 1). Collectively, these results indicate that the MHC-I signaling pathway is linked to activation of tyrosine kinase(s) in Jurkat cells.

M3 - Journal article

C2 - 7529791

VL - 154

SP - 1167

EP - 1176

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 3

ER -

ID: 10635993