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Risk alleles for 6 loci increased glucose levels from birth to 5 years of age (ADCY5, ADRA2A (show ADRA2A Proteins), CDKAL1 (show CDKAL1 Proteins), CDKN2A/B, GRB10 (show GRB10 Proteins), and TCF7L2 (show TCF7L2 Proteins)
changes in adipose tissue ADCY5 expression are related to obesity and fat distribution.
This study identification of ADCY5 mutations in one family with dyskinesia-facial myokymia and in two unrelated sporadic cases of paxoysmal choreic/dystonia-facial myokymia.
these results suggest that AnxA4 (show ANXA4 Proteins) is a novel direct negative regulator of AC5, adding a new facet to the functions of annexins.
Mutations in ADCY5 were linked to benign hereditary chorea.
LRs are essential not only for the proper membrane distribution and maintenance of AC5/6 activity but also for the regulation of D1R- and D5R-mediated AC signaling.
Alterations in beta-cell ADCY5 expression and impaired glucose signaling thus provide a likely route through which ADCY5 gene polymorphisms influence fasting glucose levels and T2D risk, while exerting more minor effects on incretin action
the functional effect of missense mutations in adenylyl cyclase 5 (ADCY5) in sporadic and inherited cases of autosomal dominant familial dyskinesia with facial myokymia
AC5, by binding active Galphai1, interferes with G-protein deactivation and reassembly and thereby might sensitize its own regulation.
Polymorphisms ADCY5 are associated with an alcohol-dependent phenotype in females, which is distinguished by comorbid signs of depression.
These results identify the AC5 and mGluR system in the dorsal striatum as molecular on/off switches to direct decisions on behavioral preferences for cue-oriented options
deficiency of AC5 protects against obesity, glucose intolerance, and insulin (show INS Proteins) resistance.
Myocardial adrenergic receptor beta 1 (show ADRB1 Proteins) preferentially associates with AC5.
Disruption of AC5 prevents cardiomyopathy induced by chronically enhanced beta-AR signaling in mice with overexpressed beta-AR, potentially by enhancing resistance to oxidative stress and apoptosis, suggesting a novel, alternative approach to beta-AR blockade.
AC5 knockout mice delayed age-related tumor incidence significantly.
These results identify the AC5/cAMP system in the dorsal striatum as a therapeutic target for the treatment of L-DOPA-induced dyskinesia in patients with Parkinson's disease.
Cytokine-induced iNOS and ERK1/2 inhibit adenylyl cyclase type 5/6 activity and stimulate phosphodiesterase 4D5 activity in intestinal longitudinal smooth muscle, contributing to colonic dysmotility during inflammation.
Overexpression of AC5 exacerbates the cardiomyopathy induced by chronic catecholamine stress by altering regulation of SIRT1 (show SIRT1 Proteins)/FoxO3a (show FOXO3 Proteins), MEK (show MDK Proteins)/ERK (show EPHB2 Proteins), and MnSOD (show SOD2 Proteins).
Describe developmental expression of adenylyl cyclase 5.
our data suggest that AC5 is the prevalent adenylyl cyclase isoform in rabbit renal cortex
This gene encodes a member of the membrane-bound adenylyl cyclase enzymes. Adenylyl cyclases mediate G protein-coupled receptor signaling through the synthesis of the second messenger cAMP. Activity of the encoded protein is stimulated by the Gs alpha subunit of G protein-coupled receptors and is inhibited by protein kinase A, calcium and Gi alpha subunits. Single nucleotide polymorphisms in this gene may be associated with low birth weight and type 2 diabetes. Alternatively spliced transcript variants that encode different isoforms have been observed for this gene.
adenylate cyclase type 5
, adenylyl cyclase type V
, adenylate cyclase 5
, ATP pyrophosphate-lyase 5
, adenylate cyclase type V
, adenylyl cyclase 5
, ca(2+)-inhibitable adenylyl cyclase