Abstract:
:The NFkappaB family of transcription factors is regulated by inhibitory IkappaB proteins. A diversity of stimuli leads to the phosphorylation and subsequent degradation of IkappaB, releasing NFkappaB to act on its target genes. Calmodulin (CaM) is a key regulator of numerous cellular processes and is the predominant intracellular receptor for Ca2+ signals. Here we report that several CaM antagonists inhibit the activation of NFkappaB, and that this is due to the prevention of inducible IkappaB phosphorylation. Our results suggest that CaM is involved in the phosphorylation of IkappaB, a finding that may help in elucidating the mechanism of this critical step of NFkappaB activation.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Hughes K,Antonsson A,Grundstrøm Tdoi
10.1016/s0014-5793(98)01537-3subject
Has Abstractpub_date
1998-12-11 00:00:00pages
132-6issue
1eissn
0014-5793issn
1873-3468pii
S0014-5793(98)01537-3journal_volume
441pub_type
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