Gene interactions and pathways from curated databases and text-mining

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ADCY10 — PRKACB

Text-mined interactions from Literome

Kageyama et al., J Cardiovasc Pharmacol 2003 : Both SQ22536, an adenylate cyclase inhibitor, and Rp-8-Br-cAMPS, a protein kinase A (PKA) inhibitor , were found to attenuate the urocortin II-induced vasodilation
Chen et al., Neuroscience 2003 : A cAMP dependent protein kinase (PKA) selective inhibitor and an adenylate cyclase inhibitor blocked both PKA activation and the subsequent filopodia formation
Li et al., American journal of physiology. Renal physiology 2004 : The stimulatory effect of CHA and CGS-21680 was completely blocked by H89, an inhibitor of protein kinase A (PKA) , or by inhibition of adenylate cyclase with SQ-22536
van der Heyden et al., Cardiovasc Res 2005 (Ion Channel Gating) : Stimulation of beta-adrenergic receptors ( ARs ) results in an increased cyclic adenosine monophosphate ( cAMP ) production by adenylate cyclase ( AC ) and consequently activation of protein kinase (PK) A and phosphorylation of L-type Ca ( 2+ ) channels by this enzyme
Gu et al., J Appl Physiol 2007 : Furthermore, pretreatment with SQ 22536 ( 100-300 microM, 15 min ), an adenylate cyclase inhibitor, and H89 ( 3 microM, 15 min ), a PKA inhibitor , completely abolished the potentiating effect of epinephrine
Wales et al., J Neurochem 2007 : In one clone ( PC47 ), ICP10PK inhibited caspase-3 activation through up-regulation/stabilization of adenylate cyclase ( AC ) , activation of PKA and MEK, and the convergence of the two pathways on extracellular signal regulated kinase activation
Manna et al., Mol Immunol 2009 (Neoplasms) : The PKA inhibition was independent of adenylate cyclase activity or cAMP level
Pernalete et al., Endocrinology 1990 : Recent studies indicate that PTH binding promotes not only stimulation of adenylate cyclase and activation of protein kinase-A (PK-A) , but also, stimulation of phospholipase-C, leading to activation of PK-C
Deyts et al., J Neurosci 2012 : We found that accumulation of APP C-terminal fragments or expression of membrane tethered APP intracellular domain results in adenylate cyclase dependent activation of PKA ( protein kinase A ) and inhibition of GSK3ß signaling cascades, and enhancement of axodendritic arborization in rat immortalized hippocampal neurons, mouse primary cortical neurons, and mouse neuroblastoma
Murai et al., J Neurophysiol 2012 : The Ca ( 2+ ) /calmodulin stimulated adenylate cyclase may contribute to the activation of PKA
Gwosdow et al., Am J Physiol 1994 : Inhibition of adenylate cyclase with 2'5'-dideoxyadenosine ( 2'5'-DDA ) did not affect IL-1 alpha induced increases in PKA activity and ACTH secretion
Wong et al., Neuroendocrinology 1995 : Stimulation of cytosolic PKA activity in rat somatotrophs by the adenylate cyclase activator forskolin ( 10 nM-1 microM ) and membrane permeant cAMP analog db.cAMP ( 5 microM-0.5 mM ) mimicked the GH-releasing effect of GRF
Janulis et al., Endocrinology 1993 : The adenylate cyclase inhibitor 2',5'-dideoxyadenosine ( 10 ( -4 ) M ) reduced PTH- ( 1-34 ) -stimulated PKA activity by 60 %, but failed to block the rise in 1,25- ( OH ) 2D3 secretion
Li et al., Exp Eye Res 1999 (Second Messenger Systems) : SQ22536 ( 100 microM ), an adenylate cyclase inhibitor, and H-89, a PKA inhibitor , had no inhibitory effect on bFGF induced down-regulation of IGF-I expression