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Role of TAB1 in nit...
Role of TAB1 in nitric oxide-induced p38 activation in insulin-producing cells
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- Makeeva, Natalia (author)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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- Roomans, Godfried M. (author)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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- Welsh, Nils (author)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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(creator_code:org_t)
- 2007
- 2007
- English.
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In: International Journal of Biological Sciences. - 1449-2288. ; 3:2, s. 71-76
- Related links:
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https://urn.kb.se/re...
Abstract
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- The aim of present study was to elucidate the role of TAB1 in nitric oxide-induced activation of p38 MAPK. For this purpose we over-expressed TAB1 in insulin-producing beta-TC6 cells. We observed in cells transiently over-expressing TAB1 that p38 activation was enhanced in response to DETA/NONOate. A lowering of TAB1 levels, using the siRNA technique, resulted in the opposite effect. The DETA/NONOate-induced cell death rate was increased in cells transiently overexpressing TAB1. In stable beta-TC6 cell clones with very high TAB1 levels p38 phosphorylation was enhanced also at basal conditions. DETA/NONOate increased also the phosphorylation of JNK and ERK in beta-TC6 cells, but these events were not affected by TAB1. Interestingly, the inhibitory effect of SB203580 on p38 phosphorylation was paralleled by a stimulatory effect on JNK phosphorylation and an inhibitory effect on ERK phosphorylation. In summary, we propose that TAB1 promotes nitric oxide-induced p38 autophosphorylation. In addition, nitric oxide-induced p38 activation seems to promote JNK inhibition and ERK activation, but this effect appears to not require TAB1. A better understanding of how the TAB1/p38 pathway promotes beta-cell death in response to nitric oxide might help in the development of novel pharmacological approaches in the treatment of diabetes.
Keyword
- apoptosis
- nitric oxide
- insulin producing cell
- TAB1
- p38 MAPK
- MEDICINE
- MEDICIN
Publication and Content Type
- ref (subject category)
- art (subject category)
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