Description: Homo sapiens relaxin 3 (RLN3), mRNA. RefSeq Summary (NM_080864): This gene encodes a member of the relaxin family of insulin-like hormones that is expressed predominantly in the brain and plays a role in physiological processes such as stress, memory and appetite regulation. The encoded protein is a precursor that is proteolytically processed to generate a heterodimeric mature form consisting A and B chains interlinked by disulfide bonds. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Jul 2015]. Transcript (Including UTRs) Position: hg19 chr19:14,139,017-14,141,783 Size: 2,767 Total Exon Count: 2 Strand: + Coding Region Position: hg19 chr19:14,139,017-14,141,760 Size: 2,744 Coding Exon Count: 2
ID:REL3_HUMAN DESCRIPTION: RecName: Full=Relaxin-3; AltName: Full=Insulin-like peptide INSL7; Short=Insulin-like peptide 7; AltName: Full=Prorelaxin H3; Contains: RecName: Full=Relaxin-3 B chain; Contains: RecName: Full=Relaxin-3 A chain; Flags: Precursor; FUNCTION: May play a role in neuropeptide signaling processes. Ligand for LGR7, relaxin-3 receptor-1 (GPCR135) and relaxin-3 receptor-2 (GPCR142). SUBUNIT: Heterodimer of a B chain and an A chain linked by two disulfide bonds. SUBCELLULAR LOCATION: Secreted. SIMILARITY: Belongs to the insulin family. SEQUENCE CAUTION: Sequence=AAQ88548.1; Type=Erroneous initiation;
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 Q8WXF3
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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.