Where it comes from
- Made in
- Decidua, trophoblast and prostate, at low levels
- Sent out by
- Unknown
- Acts on
- Uterus and cervix, presumably
What it does
- Arose when the ancestral relaxin gene duplicated in the catarrhine primates, about 44 to 30 million years ago, and the pair survives only in the apes 1
- Acts like relaxin-2 at the receptor; relaxin-2 does the circulating work 2
- Its transcripts turn up in decidua, trophoblast and prostate, the same places as relaxin-2, and no separate function has been shown 3
In medicine
- Nothing is measured or treated with it: no assay used in care separates H1 from H2 relaxin
- A fusion transcript joining RLN1 to RLN2 has been reported in prostate cancer, which is the only clinical thread so far 4
Beyond the body’s own use
- It is studied as a question in evolution rather than as a hormone: why a duplicate kept for 30 million years has no job of its own
- All the human work on relaxin, from pregnancy physiology to the heart failure trials, has used relaxin-2 or its synthetic form, so this gene is read from sequence and tissue expression rather than from experiments 2
Sources
- Arroyo et al., Evolution of the relaxin/insulin-like gene family in anthropoid primates, Genome Biology and Evolution 2014
- Bathgate et al., Relaxin family peptides and their receptors, Physiological Reviews 2013
- Hansell et al., Expression of the human relaxin H1 gene in the decidua, trophoblast and prostate, Journal of Clinical Endocrinology and Metabolism 1991
- Tevz et al., A fusion transcript between human relaxin-1 and relaxin-2 in prostate cancer, Molecular and Cellular Endocrinology 2016
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.