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ADRB2 — TNF

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: TNF → ADRB2 (increases, TNF Activity)
  Evidence: Thus, insulin resistance in rats caused by chronic growth-hormone treatment is accompanied by a decrease in insulin-stimulated insulin receptor activity and IRS protein phosphorylation in vivo

Text-mined interactions from Literome

Nakamura et al., Cytokine 2000 : These findings indicate that beta2-adrenoceptor stimulation during an LPS challenge prevented TNF-alpha production as a consequence of MAPK inhibition and enhanced cAMP generation, which at a later stage was associated with an anti-inflammatory effect of IL-6
Nakamura et al., Nephrol Dial Transplant 2000 (Endotoxemia) : beta(2)-Adrenoceptor activation regulates tumour necrosis factor (TNF)-alpha and interleukin-6 (IL-6) production in cultured renal cells
Nakamura et al., J Am Soc Nephrol 2001 : In summary, the downregulation of TNF-alpha transcription by terbutaline was mediated by an inhibitory effect of beta(2)-adrenoceptor activation on MAPK ( p42/p44, p38 ) and NF-kappa B ( p50/p65 ), which were exerted through a cAMP-PKA pathway and a cAMP independent mechanism ... It is likely that cAMP-PKA and MAPK ( p42/p44, p38 ) may play a critical role in the regulation of the Stx-2 induced TNF-alpha transcription via beta(2)-adrenoceptor activation
Nakamura et al., Inflamm Res 2003 : The present study examined the inhibitory effect of beta2-adrenoceptor activation on the mitogen activated protein kinase ( MAPK ) cascades and the contribution of these pathways to the suppression of tumor necrosis factor (TNF)-alpha in lipopolysaccharide (LPS) stimulated rat renal mesangial cells
Asehnoune et al., Cytokine 2006 (Shock, Hemorrhagic) : beta2-Adrenoceptor blockade partially restores ex vivo TNF production following hemorrhagic shock
Hadri et al., J Biol Chem 1997 : Nuclear run-on assays on isolated nuclei and mRNA stability measurements showed that TNF-alpha increased both beta2-adrenoreceptor gene transcription and beta2-adrenoreceptor mRNA half-life, while beta1- and beta3-adrenoreceptor gene expression was modulated only at the transcriptional level by the cytokine