In:
American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 283, No. 2 ( 2002-08-01), p. G270-G281
Abstract:
The eukaryotic transcription factor nuclear factor-κB (NF-κB)/Rel is activated by a large variety of stimuli. It has been demonstrated that NF-κB/Rel is induced during the course of cerulein pancreatitis. Here, we show that NF-κB/Rel is differentially activated in pancreatic lobules. Cerulein induces NF-κB/Rel via activation of IκB kinase (IKK), which causes degradation of IκBα but not IκBβ. Tumor necrosis factor-α-mediated IKK activation leads to IκBα and IκBβ degradation. In contrast, oxidative stress induced by H 2 O 2 activates NF-κB/Rel independent of IKK activation and IκBα degradation; instead IκBα is phosphorylated on tyrosine. H 2 O 2 but not cerulein-mediated NF-κB/Rel activation can be blocked by stabilizing microtubules with Taxol. Inhibition of tubulin polymerization with nocodazole causes NF-κB/Rel activation in pancreatic lobules. These results propose three different pathways of NF-κB/Rel activation in pancreatic acinar cells. Furthermore, these data demonstrate that microtubules play a key role in IKK-independent NF-κB/Rel activation following oxidative stress.
Type of Medium:
Online Resource
ISSN:
0193-1857
,
1522-1547
DOI:
10.1152/ajpgi.00407.2001
Language:
English
Publisher:
American Physiological Society
Publication Date:
2002
detail.hit.zdb_id:
1477329-6
SSG:
12
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