Ribotoxic stress activates p38 and JNK kinases and modulates the antigen-presenting activity of dendritic cells. (Q44345790)

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1 November 2019

title

Ribotoxic stress activates p38 and JNK kinases and modulates the antigen-presenting activity of dendritic cells (English)

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1 November 2019

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10

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1 November 2019

author name string

Peter Bunyard

1

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1 November 2019

Matthew Handley

2

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1 November 2019

Gabriel Pollara

3

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1 November 2019

Karine Rutault

4

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1 November 2019

Isabelle Wood

5

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1 November 2019

Manika Chaudry

6

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1 November 2019

Charles Alderman

7

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1 November 2019

John Foreman

8

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1 November 2019

David R Katz

9

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1 November 2019

publication date

1 March 2003

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1 November 2019

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1 November 2019

volume

39

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1 November 2019

page(s)

815-827

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1 November 2019

issue

13

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The PI3 kinase, p38 SAP kinase, and NF-kappaB signal transduction pathways are involved in the survival and maturation of lipopolysaccharide-stimulated human monocyte-derived dendritic cells

1 November 2019

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The protein kinase PKR is required for p38 MAPK activation and the innate immune response to bacterial endotoxin

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Cell type-specific activation of mitogen-activated protein kinases by CpG-DNA controls interleukin-12 release from antigen-presenting cells

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The injured cell: the role of the dendritic cell system as a sentinel receptor pathway

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Ribotoxic stress response: activation of the stress-activated protein kinase JNK1 by inhibitors of the peptidyl transferase reaction and by sequence-specific RNA damage to the alpha-sarcin/ricin loop in the 28S rRNA.

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Activation of p38 mitogen-activated protein kinase and c-Jun NH(2)-terminal kinase by double-stranded RNA and encephalomyocarditis virus: involvement of RNase L, protein kinase R, and alternative pathways.

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Human tonsillar dendritic cell-induced T cell responses: analysis of molecular mechanisms using monoclonal antibodies

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Stress-activated protein kinase/Jun N-terminal kinase is required for interleukin (IL)-1-induced IL-6 and IL-8 gene expression in the human epidermal carcinoma cell line KB.

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Defective IL-12 production in mitogen-activated protein (MAP) kinase kinase 3 (Mkk3)-deficient mice

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Tolerance, danger, and the extended family

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Protein-damaging stresses activate c-Jun N-terminal kinase via inhibition of its dephosphorylation: a novel pathway controlled by HSP72.

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Dendritic cell survival and maturation are regulated by different signaling pathways.

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Trichothecene mycotoxins trigger a ribotoxic stress response that activates c-Jun N-terminal kinase and p38 mitogen-activated protein kinase and induces apoptosis

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Identifiers

DOI

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1 November 2019

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