Human Gene PTGER3 (uc001dfn.3) Description and Page Index
Description: Homo sapiens prostaglandin E receptor 3 (subtype EP3) (PTGER3), transcript variant 6, mRNA. RefSeq Summary (NM_198716): The protein encoded by this gene is a member of the G-protein coupled receptor family. This protein is one of four receptors identified for prostaglandin E2 (PGE2). This receptor may have many biological functions, which involve digestion, nervous system, kidney reabsorption, and uterine contraction activities. Studies of the mouse counterpart suggest that this receptor may also mediate adrenocorticotropic hormone response as well as fever generation in response to exogenous and endogenous stimuli. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Aug 2009]. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Gene record to access additional publications. ##Evidence-Data-START## Transcript exon combination :: X83861.1, BC024229.1 [ECO:0000332] RNAseq introns :: single sample supports all introns SAMEA1966682, SAMEA1968189 [ECO:0000348] ##Evidence-Data-END## Transcript (Including UTRs) Position: hg19 chr1:71,349,439-71,513,491 Size: 164,053 Total Exon Count: 5 Strand: - Coding Region Position: hg19 chr1:71,349,632-71,513,260 Size: 163,629 Coding Exon Count: 5
asthma asthma, aspirin-intolerant Kim, S. H. et al. 2007, Association between polymorphisms in prostanoid receptor genes and aspirin-intolerant asthma, Pharmacogenet Genomics 2007 17(4) 295-304.
These findings suggest that genetic polymorphisms in PTGER2, PTGER3, PTGER4, PTGIR, and TBXA2R play important roles in the pathogenesis of aspirin-intolerant asthma.
Cholesterol Sekar Kathiresan et al. BMC medical genetics 2007, A genome-wide association study for blood lipid phenotypes in the Framingham Heart Study., BMC medical genetics.
Using a 100K genome-wide scan, we have generated a set of putative associations for common sequence variants and lipid phenotypes. Validation of selected hypotheses in additional samples did not identify any new loci underlying variability in blood lipids. Lack of replication may be due to inadequate statistical power to detect modest quantitative trait locus effects (i.e., <1% of trait variance explained) or reduced genomic coverage of the 100K array. GWAS in FHS using a denser genome-wide genotyping platform and a better-powered replication strategy may identify novel loci underlying blood lipids.
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 Q147X8
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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.