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c-Jun NH2-terminal kinase (JNK)1 and JNK2 have similar and stage-dependent roles in regulating T cell apoptosis and proliferation

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c-Jun NH2-terminal kinase (JNK)1 and JNK2 have similar and stage-dependent roles in regulating T cell apoptosis and proliferation. / Sabapathy, K; Kallunki, T; David, J P; Graef, I; Karin, M; Wagner, E F.

In: J EXP MED, Vol. 193, No. 3, 05.02.2001, p. 317-28.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Sabapathy, K, Kallunki, T, David, JP, Graef, I, Karin, M & Wagner, EF 2001, 'c-Jun NH2-terminal kinase (JNK)1 and JNK2 have similar and stage-dependent roles in regulating T cell apoptosis and proliferation', J EXP MED, vol. 193, no. 3, pp. 317-28.

APA

Sabapathy, K., Kallunki, T., David, J. P., Graef, I., Karin, M., & Wagner, E. F. (2001). c-Jun NH2-terminal kinase (JNK)1 and JNK2 have similar and stage-dependent roles in regulating T cell apoptosis and proliferation. J EXP MED, 193(3), 317-28.

Vancouver

Sabapathy K, Kallunki T, David JP, Graef I, Karin M, Wagner EF. c-Jun NH2-terminal kinase (JNK)1 and JNK2 have similar and stage-dependent roles in regulating T cell apoptosis and proliferation. J EXP MED. 2001 Feb 5;193(3):317-28.

Bibtex

@article{a1ad57dd55384dcda7e5261d1b1e5384,
title = "c-Jun NH2-terminal kinase (JNK)1 and JNK2 have similar and stage-dependent roles in regulating T cell apoptosis and proliferation",
abstract = "Apoptotic and mitogenic stimuli activate c-Jun NH2-terminal kinases (JNKs) in T cells. Although T cells express both JNK1 and JNK2 isozymes, the absence of JNK2 alone can result in resistance to anti-CD3-induced thymocyte apoptosis and defective mature T cell proliferation. Similar defects in thymocyte apoptosis and mature T cell proliferation, the latter due to reduced interleukin 2 production, are also caused by JNK1 deficiency. Importantly, T cell function was compromised in Jnk1(+/-)Jnk2(+/-) double heterozygous mice, indicating that JNK1 and JNK2 play similar roles in regulating T cell function. The reduced JNK dose results in defective c-Jun NH2-terminal phosphorylation in thymocytes but not in peripheral T cells, in which nuclear factors of activated T cells (NK-ATs)-DNA binding activity is affected. Thus, JNK1 and JNK2 control similar functions during T cell maturation through differential targeting of distinct substrates.",
keywords = "Animals, Antigens, CD3, Apoptosis, B-Lymphocytes, Cell Differentiation, Cell Division, Cell Survival, DNA-Binding Proteins, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitogen-Activated Protein Kinase 8, Mitogen-Activated Protein Kinase 9, Mitogen-Activated Protein Kinases, NFATC Transcription Factors, Nuclear Proteins, Phosphorylation, T-Lymphocytes, Transcription Factors",
author = "K Sabapathy and T Kallunki and David, {J P} and I Graef and M Karin and Wagner, {E F}",
year = "2001",
month = feb,
day = "5",
language = "English",
volume = "193",
pages = "317--28",
journal = "J EXP MED",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "3",

}

RIS

TY - JOUR

T1 - c-Jun NH2-terminal kinase (JNK)1 and JNK2 have similar and stage-dependent roles in regulating T cell apoptosis and proliferation

AU - Sabapathy, K

AU - Kallunki, T

AU - David, J P

AU - Graef, I

AU - Karin, M

AU - Wagner, E F

PY - 2001/2/5

Y1 - 2001/2/5

N2 - Apoptotic and mitogenic stimuli activate c-Jun NH2-terminal kinases (JNKs) in T cells. Although T cells express both JNK1 and JNK2 isozymes, the absence of JNK2 alone can result in resistance to anti-CD3-induced thymocyte apoptosis and defective mature T cell proliferation. Similar defects in thymocyte apoptosis and mature T cell proliferation, the latter due to reduced interleukin 2 production, are also caused by JNK1 deficiency. Importantly, T cell function was compromised in Jnk1(+/-)Jnk2(+/-) double heterozygous mice, indicating that JNK1 and JNK2 play similar roles in regulating T cell function. The reduced JNK dose results in defective c-Jun NH2-terminal phosphorylation in thymocytes but not in peripheral T cells, in which nuclear factors of activated T cells (NK-ATs)-DNA binding activity is affected. Thus, JNK1 and JNK2 control similar functions during T cell maturation through differential targeting of distinct substrates.

AB - Apoptotic and mitogenic stimuli activate c-Jun NH2-terminal kinases (JNKs) in T cells. Although T cells express both JNK1 and JNK2 isozymes, the absence of JNK2 alone can result in resistance to anti-CD3-induced thymocyte apoptosis and defective mature T cell proliferation. Similar defects in thymocyte apoptosis and mature T cell proliferation, the latter due to reduced interleukin 2 production, are also caused by JNK1 deficiency. Importantly, T cell function was compromised in Jnk1(+/-)Jnk2(+/-) double heterozygous mice, indicating that JNK1 and JNK2 play similar roles in regulating T cell function. The reduced JNK dose results in defective c-Jun NH2-terminal phosphorylation in thymocytes but not in peripheral T cells, in which nuclear factors of activated T cells (NK-ATs)-DNA binding activity is affected. Thus, JNK1 and JNK2 control similar functions during T cell maturation through differential targeting of distinct substrates.

KW - Animals

KW - Antigens, CD3

KW - Apoptosis

KW - B-Lymphocytes

KW - Cell Differentiation

KW - Cell Division

KW - Cell Survival

KW - DNA-Binding Proteins

KW - Lymphocyte Activation

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Mitogen-Activated Protein Kinase 8

KW - Mitogen-Activated Protein Kinase 9

KW - Mitogen-Activated Protein Kinases

KW - NFATC Transcription Factors

KW - Nuclear Proteins

KW - Phosphorylation

KW - T-Lymphocytes

KW - Transcription Factors

M3 - SCORING: Journal article

C2 - 11157052

VL - 193

SP - 317

EP - 328

JO - J EXP MED

JF - J EXP MED

SN - 0022-1007

IS - 3

ER -