ADRA2A Back

adrenergic, alpha-2A-, receptor

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NCBI Description of ADRA2A

Alpha-2-adrenergic receptors are members of the G protein-coupled receptor superfamily. They include 3 highly homologous subtypes: alpha2A, alpha2B, and alpha2C. These receptors have a critical role in regulating neurotransmitter release from sympathetic nerves and from adrenergic neurons in the central nervous system. Studies in mouse revealed that both the alpha2A and alpha2C subtypes were required for normal presynaptic control of transmitter release from sympathetic nerves in the heart and from central noradrenergic neurons; the alpha2A subtype inhibited transmitter release at high stimulation frequencies, whereas the alpha2C subtype modulated neurotransmission at lower levels of nerve activity. This gene encodes alpha2A subtype and it contains no introns in either its coding or untranslated sequences. Sequence Note: The 5'-most in-frame translation initiation codon is selected for this RefSeq based on good conservation across mammalian species. A possible downstream start codon would result in a protein that is 15 aa shorter at the N-terminus. The literature, including PMIDs:2823383, 2568356, 1354394 and 1678390, assumes the use of the downstream start codon based on initial cloning reports, but there is no experimental evidence indicating which start codon is preferentially used in vivo.

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Figure notes


• "Mouse over" a mutation to see details.
• Missense green saturation indicates evolutionary conservation of the mutated positions.
• Red hashes in protein strip are splice sites.
• Blue-white-red bars are log2 copy ratio distributions (–1 to +1) from Zack et al. (2013).


Legend

ADRA2A is highly significantly mutated in
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ADRA2A is significantly mutated in
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ADRA2A is near significance in
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Data details


Mutation list for ADRA2A