Disease relevance of ADCY6

• Capacitative Ca2+ entry exclusively inhibits cAMP synthesis in C6-2B glioma cells. Evidence that physiologically evoked Ca2+ entry regulates Ca(2+)-inhibitable adenylyl cyclase in non-excitable cells [1].

High impact information on ADCY6

• Ca(2+)-inhibitable adenylyl cyclase modulates pulmonary artery endothelial cell cAMP content and barrier function [2].
• Residence of the endogenous Ca(2+)-inhibitable adenylyl cyclase of C6-2B glioma cells in cholesterol-enriched caveolae is essential for its regulation by CCE (Fagan, K. A., Smith, K. E., and Cooper, D. M. F. (2000) J. Biol. Chem. 275, 26530-26537) [3].
• Paralleling this phenotype, expression of the variant was associated with attenuation of the forskolin-mediated reduction in cell growth rate to 64% +/- 5% of the effect seen with expression of the wild-type ADCY6 (n = 4; P = .001) [4].
• Activation of a novel PKC isoform synergistically enhances D2L dopamine receptor-mediated sensitization of adenylate cyclase type 6 [5].
• Recently, protein kinase signaling and phosphorylation have been implicated in the sensitization of adenylate cyclase type 6 (AC6) [5].

Biological context of ADCY6

• We have successfully cloned a 5200-nucleotide cDNA from VNO of garter snakes containing an open reading frame++ encoding 1150 amino acids of AC-VI protein [6].

Analytical, diagnostic and therapeutic context of ADCY6

• A 250-bp fragment of adenylate cyclase type VI (AC-VI) was obtained from brain cDNA of garter snake by RT-PCR with degenerate primers [6].

References