Human Gene MC3R (ENST00000243911.2) from GENCODE V44
Description: Homo sapiens melanocortin 3 receptor (MC3R), mRNA. (from RefSeq NM_019888) RefSeq Summary (NM_019888): This gene encodes a G-protein-coupled receptor for melanocyte-stimulating hormone and adrenocorticotropic hormone that is expressed in tissues other than the adrenal cortex and melanocytes. This gene maps to the same region as the locus for benign neonatal epilepsy. Mice deficient for this gene have increased fat mass despite decreased food intake, suggesting a role for this gene product in the regulation of energy homeostasis. Mutations in this gene are associated with a susceptibility to obesity in humans. [provided by RefSeq, Jul 2008]. Sequence Note: A downstream start codon is selected for this RefSeq based on conservation with homologs and for consistency with other family members, including the human melanocortin 4 and melanocortin 5 receptors. The use of an alternative upstream start codon, which is specific to primate species, would increase the protein length from 323 aa to 360 aa. This longer protein is referred to in the literature, including PMIDs 15292330 and 8463333. Gencode Transcript: ENST00000243911.2 Gencode Gene: ENSG00000124089.4 Transcript (Including UTRs) Position: hg38 chr20:56,248,732-56,249,815 Size: 1,084 Total Exon Count: 1 Strand: + Coding Region Position: hg38 chr20:56,248,844-56,249,815 Size: 972 Coding Exon Count: 1
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.
ModBase Predicted Comparative 3D Structure on P41968
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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.