Inhibition of p38 mitogen-activated protein kinase reduces TNF-induced activation of NF-kappaB, elicits caspase activity, and enhances cytotoxicity (Q42832279)

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scientific article published on February 2004

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English	Inhibition of p38 mitogen-activated protein kinase reduces TNF-induced activation of NF-kappaB, elicits caspase activity, and enhances cytotoxicity	scientific article published on February 2004

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scholarly article

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Europe PubMed Central

PubMed publication ID

8 November 2017

Inhibition of p38 mitogen-activated protein kinase reduces TNF-induced activation of NF-kappaB, elicits caspase activity, and enhances cytotoxicity (English)

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Europe PubMed Central

PubMed publication ID

8 November 2017

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Silke Lüschen

1

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Europe PubMed Central

PubMed publication ID

8 November 2017

Gudrun Scherer

2

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Europe PubMed Central

PubMed publication ID

8 November 2017

Sandra Ussat

3

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Europe PubMed Central

PubMed publication ID

8 November 2017

Hendrik Ungefroren

4

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8 November 2017

Sabine Adam-Klages

5

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8 November 2017

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publication date

1 February 2004

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Europe PubMed Central

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8 November 2017

Experimental Cell Research

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Europe PubMed Central

PubMed publication ID

8 November 2017

293

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Europe PubMed Central

PubMed publication ID

8 November 2017

2

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Europe PubMed Central

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8 November 2017

196-206

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Europe PubMed Central

PubMed publication ID

8 November 2017

Tumor necrosis factor receptor and Fas signaling mechanisms.

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Apoptosis signaling in lymphocytes.

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The death domain kinase RIP mediates the TNF-induced NF-kappaB signal

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NF-kappaB antiapoptosis: induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to suppress caspase-8 activation

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Inhibition of TNF-induced apoptosis by NF-kappa B.

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NF-kappaB signals induce the expression of c-FLIP.

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Apoptotic and necrotic cell death induced by death domain receptors.

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Tumor necrosis factor (TNF)-mediated kinase cascades: bifurcation of nuclear factor-kappaB and c-jun N-terminal kinase (JNK/SAPK) pathways at TNF receptor-associated factor 2

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NF-kappaB activation by tumour necrosis factor requires the Akt serine-threonine kinase

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Pro-inflammatory cytokines and environmental stress cause p38 mitogen-activated protein kinase activation by dual phosphorylation on tyrosine and threonine

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AP-1 as a regulator of cell life and death

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The p38 MAP kinase pathway signals for cytokine-induced mRNA stabilization via MAP kinase-activated protein kinase 2 and an AU-rich region-targeted mechanism.

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The p38 signal transduction pathway: activation and function

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Osmotic shock induces G1 arrest through p53 phosphorylation at Ser33 by activated p38MAPK without phosphorylation at Ser15 and Ser20.

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Phosphorylation of human p53 by p38 kinase coordinates N-terminal phosphorylation and apoptosis in response to UV radiation

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Activation of the p38 mitogen-activated protein kinase pathway arrests cell cycle progression and differentiation of immature thymocytes in vivo

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Regulation of biglycan gene expression by transforming growth factor-beta requires MKK6-p38 mitogen-activated protein Kinase signaling downstream of Smad signaling

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Transfecting mammalian cells: optimization of critical parameters affecting calcium-phosphate precipitate formation

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Overexpression of acid ceramidase protects from tumor necrosis factor-induced cell death

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Activation of ERK1/2 and cPLA(2) by the p55 TNF receptor occurs independently of FAN

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Inhibition of caspases increases the sensitivity of L929 cells to necrosis mediated by tumor necrosis factor.

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Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade

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Mammalian caspases: structure, activation, substrates, and functions during apoptosis

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Importance of poly(ADP-ribose) polymerase and its cleavage in apoptosis. Lesson from an uncleavable mutant

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Acquisition of sensitivity of stress-activated protein kinases to the p38 inhibitor, SB 203580, by alteration of one or more amino acids within the ATP binding pocket

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Activation of stress-activated protein kinase-3 (SAPK3) by cytokines and cellular stresses is mediated via SAPKK3 (MKK6); comparison of the specificities of SAPK3 and SAPK2 (RK/p38)

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Characterization of the structure and function of the fourth member of p38 group mitogen-activated protein kinases, p38delta

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The phosphoinositide 3-kinase pathway

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Four deaths and a funeral: from caspases to alternative mechanisms.

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Sodium salicylate induces apoptosis via p38 mitogen-activated protein kinase but inhibits tumor necrosis factor-induced c-Jun N-terminal kinase/stress-activated protein kinase activation.

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Activation of p38 mitogen-activated protein kinase by sodium salicylate leads to inhibition of tumor necrosis factor-induced IkappaB alpha phosphorylation and degradation

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Cell stress and MKK6b-mediated p38 MAP kinase activation inhibit tumor necrosis factor-induced IkappaB phosphorylation and NF-kappaB activation

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Apoptosis induced by withdrawal of trophic factors is mediated by p38 mitogen-activated protein kinase

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The p38-MAPK inhibitor, SB203580, inhibits cardiac stress-activated protein kinases/c-Jun N-terminal kinases (SAPKs/JNKs)

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p38 and extracellular signal-regulated kinase mitogen-activated protein kinase pathways are required for nuclear factor-kappaB p65 transactivation mediated by tumor necrosis factor.

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Identifiers

10.1016/J.YEXCR.2003.10.009

1 reference

Europe PubMed Central

PubMed publication ID

8 November 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

8 November 2017

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