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Deficiency in Ikk beta gene enhances arsenic-induced gadd45alpha expression.

Authors
Zhang-Y; Lu-Y; Ding-M; Castranova-V; Shi-X; Chen-F
Source
Mol Cell Biochem 2005 Nov; 279(1-2):163-168
NIOSHTIC No.
20028862
Abstract
Chronic arsenic exposure is implicated in the pathophysiology of various human diseases, including cancer and diabetes. Using Ikkbeta gene knockout mouse embryonic fibroblast cells (Ikkbeta(-/-)), in the present study we demonstrated that NF-kappaB inhibition due to Ikkbeta deficiency up-regulated basal and arsenic-induced expression of gadd45alpha. In addition to gadd45alpha, the basal expression of other gadd family members including gadd45beta, gadd45gamma and gadd153 was substantially increased in Ikkbeta(-/-) cells. Ikkbeta deficiency prevented the induction of gadd45beta and gadd45gamma by arsenic, whereas the induction of gadd45alpha and gadd153 was appreciably enhanced in Ikkbeta(-/-) cells. Furthermore, a substantial decrease in the expression of c-myc, an established endogenous transcriptional repressor of gadd45alpha and gadd153 genes, was noted. Thus, these results uncover the molecular mechanism by which NF-kappaB signalling contributes to the regulation of gadd family gene expression induced by arsenic.
Keywords
Arsenic-compounds; Chronic-exposure; Diseases; Cancer; Laboratory-animals; Animals; Animal-studies
Contact
F. Chen, Pathology and Physiology Research Branch, National Institute for Occupational Safety and Health, 1095 Willowdale Road, Morgantown, WV 26505, USA
CODEN
MCBIB8
CAS No.
7440-38-2
Publication Date
20051101
Document Type
Journal Article
Email Address
lfd3@cdc.gov
Fiscal Year
2006
NTIS Accession No.
NTIS Price
Issue of Publication
1-2
ISSN
0300-8177
NIOSH Division
HELD
Source Name
Molecular and Cellular Biochemistry
State
WV
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