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Results 1 - 5 of 5
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GlcAT-I promoter activity is suppressed by co-expression of calcineurin and nuclear factors of activated T cells 2, 3, and 4, treatment with WP631 at 50-100 nM completely abolishes ionomycin-mediated induction in GlcAT-I-D reporter activity as well as suppressing basal promoter activity
the enzyme is upregulated 3fold by 5 ng/ml transforming growth factor-beta1. Enzyme expression is increased in idiopathic pulmonary fibrosis, fibrotic rat lungs, and fibrotic lung fibroblasts
treatment with 0.001 mM ionomycin for 24 h results in increased GlcAT-I expression, ionomycin mediated induction of GlcAT-I promoter activity requires TonEBP binding to TonE, calcium regulates GlcAT-I expression in cells of the nucleus pulposus
treatment with both BMP-2 (200 ng/ml) and TGFbeta (10 ng/ml) for 24 h results in increased GlcAT-I mRNA levels in nucleus pulposus cells, however, simultaneous treatment of nucleus pulposus cells with TGFbeta and BMP-2 does not synergize GlcAT-I mRNA expression. GlcAT-I regulation is mediated through transcription factors AP1, Sp1, and TonEBP (NFAT5). Treatment with MAPK inhibitors blocks BMP-2 and TGFbeta induced GlcAT-I expression. p38delta is important in GlcAT-I activation
under hypoxic conditions (1% O2) there is an increase in enzyme expression both in nucleus pulposus cells and in N1511 chondrocytes. Suppression of hypoxia-inducible factor-1alpha and hypoxia-inducible factor-2alpha induces enzyme promoter activity and expression only in nucleus pulposus cells
Results 1 - 5 of 5