Adenylate cyclase 1

T

he membrane-bound adenylyl cyclases (ACs) represent one of the major families of effector enzymes for G protein-coupled receptors.  Nine human AC isoforms (AC-1 through AC-9), encoded by separate genes, have been identified up to now (1).  Most of the adenylate cyclase genes are comprise of 11-26 exons and distributed over a q6-430 kb.  Majority of the adenylate cyclases previously described are expressed discretely in defined peripheral tissues, the type 1 adenylate cyclase (AC-1) is localized on chromosome 11, expressed predominantly in brain and is sensitive to Ca/Calmodulin stimulation.  Genes for at least nine adenylate cyclase (AC-1-AC-9) have been cloned characterized and sequenced.  All, but AC-9, are activated by Forskolin and GTP bound Gs reported.  The type I Ca(2+)-sensitive adenylyl cyclase has been implicated in several forms of synaptic plasticity in vertebrates, mutations in the AC-1 gene led to deficits in learning and memory (2).  Mutant mice in which this enzyme was inactivated by targeted mutagenesis show deficient spatial memory and altered long-term potentiation (3).  During first two weeks of postnatal development, there is significant increase in AC-1 mRNA and enzymatic activity in hippocampus, cerebellum and cortex that corresponds to appearance of long-term potentiation which supports the notion that AC-1 activity is important for neuronal plasticity and spatial memory (4).

For research use only, not for diagnostic or therapeutic use.