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Induction of β-Transducin Repeat-containing Protein by JNK Signaling and Its Role in the Activation of NF-κB

Spiegelman, Vladimir S. ; Stavropoulos, Pete ; Latres, Esther ; Pagano, Michele ; Ronai, Ze'ev ; Slaga, Tomas J. ; Fuchs, Serge Y.

The Journal of biological chemistry, 2001-07, Vol.276 (29), p.27152-27158 [Periódico revisado por pares]

Elsevier Inc

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  • Título:
    Induction of β-Transducin Repeat-containing Protein by JNK Signaling and Its Role in the Activation of NF-κB
  • Autor: Spiegelman, Vladimir S. ; Stavropoulos, Pete ; Latres, Esther ; Pagano, Michele ; Ronai, Ze'ev ; Slaga, Tomas J. ; Fuchs, Serge Y.
  • Assuntos: b-transducin repeat-containing protein ; b-TrCP protein ; IKK protein ; JNK protein
  • É parte de: The Journal of biological chemistry, 2001-07, Vol.276 (29), p.27152-27158
  • Notas: ObjectType-Article-2
    SourceType-Scholarly Journals-1
    ObjectType-Feature-1
    content type line 23
  • Descrição: Activation of Jun N-kinase (JNK) and NF-κB transcription factor are the hallmarks of cellular response to stress. Phosphorylation of NF-κB inhibitor (IκB) by respective stress-inducible kinases (IKK) is a key event in NF-κB activation. β-TrCP F-box protein mediates ubiquitination of phosphorylated IκB via recruitment of SCFβ-TrCP-Roc1 E3 ubiquitin ligase complex. Subsequent proteasome-dependent degradation of IκB results in activation of the NF-κB pathway. We found that a variety of cellular stress stimuli induce an increase in the steady state levels of β-TrCP mRNA and protein levels in human cells. Activation of stress-activated protein kinases JNK (and, to a lesser extent, p38) by forced expression of constitutively active mutants of JNKK2 and MKK6 (but not MEK1 or IKKβ) also leads to accumulation of β-TrCP. Transcription of the β-TrCP gene is not required for JNK-mediated induction of β-TrCP. A synergistic effect of stimulation of IKK and JNK on the transcriptional activity of NF-κB was observed. The mechanisms of β-TrCP induction via stress and its role in NF-κB activation are discussed.
  • Editor: Elsevier Inc
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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