MHC-I-induced apoptosis in human B-lymphoma cells is dependent on protein tyrosine and serine/threonine kinases.

Anders Elm Pedersen; S Bregenholt; B Johansen; S Skov; M H Claesson

doi:10.1006/excr.1999.4571

MHC-I-induced apoptosis in human B-lymphoma cells is dependent on protein tyrosine and serine/threonine kinases.

Anders Elm Pedersen, S Bregenholt, B Johansen, S Skov, M H Claesson

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

13 Citationer (Scopus)

Abstract

Udgivelsesdato: 1999-Aug-25

Originalsprog	Engelsk
Tidsskrift	Experimental Cell Research
Vol/bind	251
Udgave nummer	1
Sider (fra-til)	128-34
Antal sider	6
ISSN	0014-4827
DOI	https://doi.org/10.1006/excr.1999.4571
Status	Udgivet - 1999

Bibliografisk note

Adgang til dokumentet

10.1006/excr.1999.4571

Citationsformater

@article{17336b90ac0611ddb5e9000ea68e967b,

title = "MHC-I-induced apoptosis in human B-lymphoma cells is dependent on protein tyrosine and serine/threonine kinases.",

abstract = "In addition to providing the framework for peptide presentation, major histocompatibility complex class I (MHC-I) molecules can act as signal transducing molecules in lymphoid cells. Here we show that the mobilization of intracellular calcium, which follows crosslinking of MHC-I molecules on human B lymphoma cells, is dependent on protein tyrosine kinases and the phosphatidylinositol 3 (PI-3) kinase. Functional studies showed that MHC-I crosslinking induced almost complete inhibition of the spontaneous proliferation of the B lymphoma cells as early as 6 h post-crosslinking and apoptosis 24 h post-crosslinking. Preincubation with either protein tyrosine kinase or protein serine/threonine kinase inhibitors reduced the MHC-I-induced apoptosis to background levels, whereas inhibition of PI-3 kinase had no effect. These data demonstrate a pivotal role for protein tyrosine and serine/threonine kinases in MHC-I-mediated apoptosis in human B-cells and suggest the presence of several MHC-I signaling pathways leading to diverse effects in these cells.",

author = "Pedersen, {Anders Elm} and S Bregenholt and B Johansen and S Skov and Claesson, {M H}",

note = "Keywords: 1-Phosphatidylinositol 3-Kinase; Androstadienes; Apoptosis; Benzoquinones; Calcium; Cell Division; Chromones; Enzyme Activation; Histocompatibility Antigens Class I; Humans; Lactams, Macrocyclic; Lymphoma, B-Cell; Morpholines; Protein-Serine-Threonine Kinases; Protein-Tyrosine Kinases; Proto-Oncogene Proteins c-bcl-2; Quinones; Receptor Aggregation; Signal Transduction; Time Factors; Tumor Cells, Cultured; beta 2-Microglobulin",

year = "1999",

doi = "10.1006/excr.1999.4571",

language = "English",

volume = "251",

pages = "128--34",

journal = "Experimental Cell Research",

issn = "0014-4827",

publisher = "Academic Press",

number = "1",

}

TY - JOUR

T1 - MHC-I-induced apoptosis in human B-lymphoma cells is dependent on protein tyrosine and serine/threonine kinases.

AU - Pedersen, Anders Elm

AU - Bregenholt, S

AU - Johansen, B

AU - Skov, S

AU - Claesson, M H

N1 - Keywords: 1-Phosphatidylinositol 3-Kinase; Androstadienes; Apoptosis; Benzoquinones; Calcium; Cell Division; Chromones; Enzyme Activation; Histocompatibility Antigens Class I; Humans; Lactams, Macrocyclic; Lymphoma, B-Cell; Morpholines; Protein-Serine-Threonine Kinases; Protein-Tyrosine Kinases; Proto-Oncogene Proteins c-bcl-2; Quinones; Receptor Aggregation; Signal Transduction; Time Factors; Tumor Cells, Cultured; beta 2-Microglobulin

PY - 1999

Y1 - 1999

N2 - In addition to providing the framework for peptide presentation, major histocompatibility complex class I (MHC-I) molecules can act as signal transducing molecules in lymphoid cells. Here we show that the mobilization of intracellular calcium, which follows crosslinking of MHC-I molecules on human B lymphoma cells, is dependent on protein tyrosine kinases and the phosphatidylinositol 3 (PI-3) kinase. Functional studies showed that MHC-I crosslinking induced almost complete inhibition of the spontaneous proliferation of the B lymphoma cells as early as 6 h post-crosslinking and apoptosis 24 h post-crosslinking. Preincubation with either protein tyrosine kinase or protein serine/threonine kinase inhibitors reduced the MHC-I-induced apoptosis to background levels, whereas inhibition of PI-3 kinase had no effect. These data demonstrate a pivotal role for protein tyrosine and serine/threonine kinases in MHC-I-mediated apoptosis in human B-cells and suggest the presence of several MHC-I signaling pathways leading to diverse effects in these cells.

AB - In addition to providing the framework for peptide presentation, major histocompatibility complex class I (MHC-I) molecules can act as signal transducing molecules in lymphoid cells. Here we show that the mobilization of intracellular calcium, which follows crosslinking of MHC-I molecules on human B lymphoma cells, is dependent on protein tyrosine kinases and the phosphatidylinositol 3 (PI-3) kinase. Functional studies showed that MHC-I crosslinking induced almost complete inhibition of the spontaneous proliferation of the B lymphoma cells as early as 6 h post-crosslinking and apoptosis 24 h post-crosslinking. Preincubation with either protein tyrosine kinase or protein serine/threonine kinase inhibitors reduced the MHC-I-induced apoptosis to background levels, whereas inhibition of PI-3 kinase had no effect. These data demonstrate a pivotal role for protein tyrosine and serine/threonine kinases in MHC-I-mediated apoptosis in human B-cells and suggest the presence of several MHC-I signaling pathways leading to diverse effects in these cells.

U2 - 10.1006/excr.1999.4571

DO - 10.1006/excr.1999.4571

M3 - Journal article

C2 - 10438578

VL - 251

SP - 128

EP - 134

JO - Experimental Cell Research

JF - Experimental Cell Research

SN - 0014-4827

IS - 1

ER -