Description: Homo sapiens adrenoceptor alpha 1A (ADRA1A), transcript variant 3, mRNA. RefSeq Summary (NM_033302): Alpha-1-adrenergic receptors (alpha-1-ARs) are members of the G protein-coupled receptor superfamily. They activate mitogenic responses and regulate growth and proliferation of many cells. There are 3 alpha-1-AR subtypes: alpha-1A, -1B and -1D, all of which signal through the Gq/11 family of G-proteins and different subtypes show different patterns of activation. This gene encodes alpha-1A-adrenergic receptor. Alternative splicing of this gene generates four transcript variants, which encode four different isoforms with distinct C-termini but having similar ligand binding properties. [provided by RefSeq, Jul 2008]. Transcript (Including UTRs) Position: hg19 chr8:26,613,913-26,722,922 Size: 109,010 Total Exon Count: 2 Strand: - Coding Region Position: hg19 chr8:26,614,061-26,722,486 Size: 108,426 Coding Exon Count: 2
hypertension Gu, D. et al. 2006, Association of alpha1A adrenergic receptor gene variants on chromosome 8p21 with human stage 2 hypertension, J Hypertens 2006 24(6) 1057-1064.
[PubMed 16685204]
Our findings suggest that the genetic variations in the ADRA1A gene are significantly associated with essential hypertension, and may play an important role in the development of essential hypertension in this Chinese population.
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
SCOP Domains: 81321 - Family A G protein-coupled receptor-like
ModBase Predicted Comparative 3D Structure on P35348-9
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.