You are viewing an incomplete version of our website. Please click to reload the website as full version.

Adenylate Cyclase 8 (Brain) (ADCY8) Peptide

Details for Product No. ABIN493202, Supplier: Login to see New
Request Want additional data for this product?

The Independent Validation Initiative strives to provide you with high quality data. Find out more

Protein Name
(2), (1), (1), (1)
Control Peptide (CP)
Pubmed 4 references available
Supplier Login to see New
Catalog number from supplier Login to see New
Quantity 0.25 mg
Shipping to United States ( )
Background The membrane-bound adenylyl cyclases (ACs) represent one of the major families of effector enzymes for G protein-coupled receptors (GPCRs). Using the high inter-species homology of mammalian AC isoforms, nine Adenylyl cyclase (AC) isoforms, encoded by separate genes, have been identified until today. Human adenylate cyclase genes comprise of 11 to 26 exons, which are distributed over 16 to 430kb. The expression profile of these 9 AC isoforms in a panel of 16 human tissues and in human embryonic kidney (HEK) cells have been demonstrated earlier (1). The cAMP synthesizing enzymes are found in two forms: cytosolic (soluble) and membrane-bound (particulate). Stimulation of adenylate cyclases produce cAMP form ATP in response to the activation of GPCRs by various hormones, neurotransmitters and other regulatory molecules. cAMP, in subsequent steps down the signal transduction pathway, can stimulate cAMP-dependent protein kinase A (cPKA), and several other target molecules. Activation of cPKA can phosphorylate a broad range of substrates that regulate various metabolic pathways, gene expression, and affect memory functions etc., (3, 4). The stimulation of adenylate cyclases starts with interactions with GPCRs mediated signals initiated by Gs and Gi heterotrimeric G-proteins. The interaction of GPCR agonist (eg. Interaction of isopreternol to beta2 receptors) catalyses the exchange of GDP to GTP that is bound to G proteins. The GTP binding reduces the affinity of Gs to other GTP binding proteins and Gs-GTP complex stimulate the adenylate cyclase (5). In last several years, new members of particulate and soluble adenylate cyclase family have been identified and significant progress is made in understanding of the molecular mechanisms that underlie the regulation of these families of enzymes. The Ca2+/calmodulin-stimulated adenylyl cyclase (AC) isoforms AC1 and AC8, couple NMDA receptor activation to cAMP signaling pathways in neurons and are important for development, learning and memory, drug addiction and persistent pain. PAC8 has been linked to interleukin induced cell differentiation of vascular smooth muscle in to secretory cells (6).Synonyms: ADCY8, ATP pyrophosphate-lyase 8, Adenylate cyclase type VIII, Adenylyl cyclase 8
Gene ID 114
NCBI Accession NP_001106
UniProt P40145
Research Area Cancer, Neurotransmitters
Application Notes Optimal working dilution should be determined by the investigator.

Antigenic blocking peptide for ABIN493203

Restrictions For Research Use only
Handling Advice Avoid repeated freezing and thawing.
Storage -20 °C
Storage Comment Store (in aliquots) at -20 °C.
Background publications Clément, Glorian, Raymondjean et al.: "PGE2 amplifies the effects of IL-1beta on vascular smooth muscle cell de-differentiation: a consequence of the versatility of PGE2 receptors 3 due to the emerging expression of adenylyl cyclase 8." in: Journal of cellular physiology, Vol. 208, Issue 3, pp. 495-505, 2006 (PubMed).

Taussig, Tang, Hepler et al.: "Distinct patterns of bidirectional regulation of mammalian adenylyl cyclases." in: The Journal of biological chemistry, Vol. 269, Issue 8, pp. 6093-100, 1994 (PubMed).

Gilman: "G proteins: transducers of receptor-generated signals." in: Annual review of biochemistry, Vol. 56, pp. 615-49, 1987 (PubMed).

Bourne, Sanders, McCormick: "The GTPase superfamily: a conserved switch for diverse cell functions." in: Nature, Vol. 348, Issue 6297, pp. 125-32, 1990 (PubMed).

Catalog No. ABIN493202

Order hotline:

  • +1 877 302 8632
  • +1 888 205 9894 (TF)