(Q40010639)

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Ectodomain shedding of TNF receptor 1 induced by protein synthesis inhibitors regulates TNF-alpha-mediated activation of NF-kappaB and caspase-8.

scientific article published on 6 February 2008

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Europe PubMed Central

PubMed publication ID

16 September 2017

Ectodomain shedding of TNF receptor 1 induced by protein synthesis inhibitors regulates TNF-alpha-mediated activation of NF-kappaB and caspase-8. (English)

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Europe PubMed Central

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16 September 2017

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Hirotsugu Ogura

1

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Europe PubMed Central

PubMed publication ID

16 September 2017

Yoshinori Tsukumo

2

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16 September 2017

Hikaru Sugimoto

3

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Europe PubMed Central

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16 September 2017

Masayuki Igarashi

4

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16 September 2017

Kazuo Nagai

5

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16 September 2017

Takao Kataoka

6

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16 September 2017

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6 February 2008

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16 September 2017

Experimental Cell Research

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16 September 2017

314

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16 September 2017

6

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16 September 2017

1406-1414

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16 September 2017

The TNF and TNF receptor superfamilies: integrating mammalian biology

1 reference

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Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes

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The caspase-8 modulator c-FLIP.

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cFLIP regulation of lymphocyte activation and development

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Rapid turnover of c-FLIPshort is determined by its unique C-terminal tail

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The E3 ubiquitin ligase itch couples JNK activation to TNFalpha-induced cell death by inducing c-FLIP(L) turnover

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A metalloproteinase disintegrin that releases tumour-necrosis factor-alpha from cells

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NF-kappaB inducers upregulate cFLIP, a cycloheximide-sensitive inhibitor of death receptor signaling

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

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GLUTARIMIDE ANTIBIOTICS. VII. THE SYNTHESIS OF DL-NEOCYCLOHEXIMIDE AND THE DETERMINATION OF THE CYCLOHEXANONE RING STEREOCHEMISTRY OF CYCLOHEXIMIDE, ITS ISOMERS, AND INACTONE

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Glutarimide antibiotics. XIII. Stereochemistry of streptovitacin A and E-73

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E-73, an acetoxyl analogue of cycloheximide, blocks the tumor necrosis factor-induced NF-kappaB signaling pathway

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Expression of TNF receptors and related signaling molecules in the bone marrow from patients with myelodysplastic syndromes

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The tumor necrosis factor-alpha converting enzyme (TACE): a unique metalloproteinase with highly defined substrate selectivity

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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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Protein synthesis inhibitors exhibit a nonspecific effect on phenobarbital-inducible cytochome P450 gene expression in primary rat hepatocytes

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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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Shiga toxin 1 triggers a ribotoxic stress response leading to p38 and JNK activation and induction of apoptosis in intestinal epithelial cells

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Acetoxycycloheximide (E-73) rapidly induces apoptosis mediated by the release of cytochrome c via activation of c-Jun N-terminal kinase

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Ribotoxic stress response to the trichothecene deoxynivalenol in the macrophage involves the SRC family kinase Hck.

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Inhibition of protein synthesis and activation of stress-activated protein kinases by onnamide A and theopederin B, antitumor marine natural products

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Shiga toxin 1-induced cytokine production is mediated by MAP kinase pathways and translation initiation factor eIF4E in the macrophage-like THP-1 cell line

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Extracellular signal-regulated kinase phosphorylates tumor necrosis factor alpha-converting enzyme at threonine 735: a potential role in regulated shedding.

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Evidence for a critical role of the tumor necrosis factor alpha convertase (TACE) in ectodomain shedding of the p75 neurotrophin receptor (p75NTR).

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ERK-mediated phosphorylation of Thr735 in TNFalpha-converting enzyme and its potential role in TACE protein trafficking

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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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Relationship of structure to fungitoxicity of cycloheximide and related glutarimide derivatives

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10.1016/J.YEXCR.2008.01.019

1 reference

Europe PubMed Central

PubMed publication ID

16 September 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

16 September 2017

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