Title : Interleukin-1 beta and tumor necrosis factor-alpha suppress dexamethasone induction of glutamine synthetase in primary mouse astrocytes.

Pub. Date : 1998 Oct

PMID : 9751175






5 Functional Relationships(s)
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1 Interleukin-1 beta and tumor necrosis factor-alpha suppress dexamethasone induction of glutamine synthetase in primary mouse astrocytes. Dexamethasone interleukin 1 beta Mus musculus
2 As the glucocorticoid receptor has been shown to interact with transcription factors that may also be activated by the proinflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), we hypothesized that IL-1beta or TNF-alpha might oppose the induction of glutamine synthetase by dexamethasone. Dexamethasone interleukin 1 beta Mus musculus
3 As the glucocorticoid receptor has been shown to interact with transcription factors that may also be activated by the proinflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), we hypothesized that IL-1beta or TNF-alpha might oppose the induction of glutamine synthetase by dexamethasone. Dexamethasone interleukin 1 beta Mus musculus
4 As the glucocorticoid receptor has been shown to interact with transcription factors that may also be activated by the proinflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), we hypothesized that IL-1beta or TNF-alpha might oppose the induction of glutamine synthetase by dexamethasone. Dexamethasone interleukin 1 beta Mus musculus
5 We also found that IL-1beta and TNF-alpha inhibited the induction of glutamine synthetase mRNA by dexamethasone, and that the induction of enzymatic activity was similarly prevented by IL-1beta. Dexamethasone interleukin 1 beta Mus musculus