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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

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8 November 2017

Sandra Ussat

3

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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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1 February 2004

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8 November 2017

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Experimental Cell Research

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8 November 2017

293

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Europe PubMed Central

PubMed publication ID

8 November 2017

2

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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-κB Signal

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Inhibition of TNF-induced apoptosis by NF-κB

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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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Establishment of mouse cell lines which constitutively secrete large quantities of interleukin 2, 3, 4 or 5, using modified cDNA expression vectors

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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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7 January 2021

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, p38δ

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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 IκBα 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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Inhibition of p38 kinase reveals a TNF-alpha-mediated, caspase-dependent, apoptotic death pathway in a human myelomonocyte cell line

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Early Activation of c-Jun N-terminal Kinase and p38 Kinase Regulate Cell Survival in Response to Tumor Necrosis Factor α

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Effect of SB 203580 on the activity of c-Raf in vitro and in vivo

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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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The c-IAP-1 and c-IAP-2 proteins are direct inhibitors of specific caspases

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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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CREB-binding protein/p300 are transcriptional coactivators of p65

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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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