adenyl

PKC: protein kinase C: MEK-ERK activator kinase; ERK: extracellular signal-regulated kinase; JNK: c-Jun N-terminal kinases; SP-1: specificity protein 1; PI3K: phosphoinositide 3-kinase; Akt: protein kinase B; mTOR: mammalian target of rapamycin kinase; p70S6K: ribosomal S6 kinase; eNOS: endothelial NOS; AMPK: 5'-AMP-activated kinase: AC: adenyl cyclase; PKA: protein kinase A; ATP: adenosine triphosphate; cAMP: cyclic adenosine monophosphate; c-JUN: transcription factor c-JUN; c-FOS: transcription factor c-FOS.

IKK: inhibitor of kappa B kinase; P: phosphate group; M: methyl group; A: adenyl group; JARID1B: lysine-specific demethylase 5B; HDAC1: histone deacetylase 1; Site B: 9-10 base pair DNA sites where p50 and p65 subunits bind.

McCune-Albright Syndrome (MAS, MIM 174800) is caused by post-zygotic activating mutations in the Gs[alpha] subunit of G proteins (encoded by GNAS, MIM 139320), leading to a mosaic distribution of cells bearing constitutively active adenyl cyclase activity.

Cellular levels of cAMP responded to increasing or decreasing concentrations of TSH concluding that TSH in thyroid cells activates adenyl cyclase so that cAMP production is augmented.

Therefore, forskolin treatment results in a reduced amount of AH accumulation in the anterior chamber (decreased secretion and increased outflow) in response to adenyl cyclase activation [27, 37].

Stimulation of these receptors on central nervous system neurons causes an intracellular inhibition of adenyl cyclase, closing of influx membrane calcium channels and opening of membrane potassium channels.

Surface binding and sensing by germ tube is an important step for activation of membrane bound adenyl cyclase to form cAMP as external application of cAMP could nullify surface influence as well as temperature influence.

This will lead to the production of prostaglandin which couple with Gi protein and inhibits adenyl cyclase and thus decrease HCl production.18

We conclude that decreased vagal modulation of heart rate may occur in hyperthyroidism, which may be restored following adequate treatment by blocking [beta]-receptors and thereby inhibiting the adenyl cyclase-cyclic AMP pathway.

This would then inhibit cAMP generation by adenyl cyclase and block the triggered release of calcium from the sarcoplasmic reticulum even in the presence of normal calcium storage.

Stimulation of intestinal adenyl cyclase by cholera toxin.