Vaughan et al. (1995) described a rat cDNA for a member of the corticotropin-releasing hormone
(CRH) family that is expressed in a region of the rat midbrain. The deduced peptide is 63%
identical to fish urotensin and 45% identical to CRH. Synthetic urocortin was shown to cause
secretion of ACTH and to bind to CRH receptor-1 . The authors showed that
the peptide also bound CRH receptor-2 better than CRH itself.
NCBI Summary:
This gene encodes a member of the sauvagine/corticotropin-releasing factor/urotensin I family. The encoded preproprotein is proteolytically processed to generate the mature peptide, an endogenous ligand for both corticotropin-releasing factor receptor 1 and corticotropin-releasing factor receptor 2. In the brain this peptide may be responsible for the effects of stress on appetite. This peptide may also play a role in mood disorders, neurodegeneration, and skeletal system disorders. In spite of the gene family name similarity, the product of this gene has no sequence similarity to urotensin-2. [provided by RefSeq, Feb 2016]
General function
Ligand, Hormone
Comment
Cellular localization
Secreted
Comment
Ovarian function
Luteolysis
Comment
Expression regulated by
Comment
Ovarian localization
Luteal cells, Small luteal cells
Comment
Muramatsu Y, et al reported Urocortin and Corticotropin-Releasing Factor Receptor Expression in Normal
Cycling Human Ovaries.
CRF has been detected in the
human ovary and has been demonstrated to suppress ovarian
steroidogenesis in vitro. The authoors examined urocortin and CRF
receptor expression in normal cycling human ovaries, using
immunohistochemistry and RT-PCR. Normal cycling human ovaries were
obtained at oophorectomy and hysterectomy from patients who
underwent surgery for cervical cancer or myoma uteri. Intense urocortin
immunoreactivity was detected in luteinized thecal cells of regressing
corpora lutea, in which only luteinized thecal cells have the capacity for
steroidogenesis. Immunoreactive urocortin was also detected in luteinized
granulosa and thecal cells of functioning corpora lutea, in which both cell
components are capable of producing steroids. RT-PCR analyses
revealed that messenger ribonucleic acid levels for urocortin, CRF, and
CRF receptor type 1 and type 2alpha were significantly higher in the
regressing corpus luteum than in the functioning corpus luteum. The
spatial and temporal immunolocalization patterns of CRF receptor were
similar to those of urocortin. These results suggest that urocortin is locally
synthesized in steroidogenic luteal cells and acts on them as an autocrine
and/or paracrine regulator of ovarian steroidogenesis, especially during
luteal regression.
Follicle stages
Corpus luteum
Comment
Effect of ovarian stimulation with recombinant follicle-stimulating hormone, gonadotropin-releasing hormone agonist and antagonists, on follicular fluid stem cell factor and serum urocortin 1 levels on the day of oocyte retrieval. Celik O et al. To compare the serum and follicular fluid (FF) concentrations of stem cell factor (SCF) as well as the serum urocortin 1 (UCN1) concentration in gonadotropin-releasing hormone antagonist (GnRH-ant) and gonadotropin-releasing hormone agonist (GnRH-a) protocols for controlled ovarian hyperstimulation (COH) in IVF patients.
Phenotypes
Mutations
1 mutations
Species: human
Mutation name: type: naturally occurring fertility: fertile Comment: A genome-wide association study of early menopause and the combined impact of identified variants. Perry JR et al. (2013) Early menopause (EM) affects up to 10% of the female population, reducing reproductive lifespan considerably. Currently, it constitutes the leading cause of infertility in the western world, affecting mainly those women who postpone their first pregnancy beyond the age of 30 years. The genetic aetiology of EM is largely unknown in the majority of cases. We have undertaken a meta-analysis of genome-wide association studies (GWASs) in 3493 EM cases and 13 598 controls from 10 independent studies. No novel genetic variants were discovered, but the 17 variants previously associated with normal age at natural menopause as a quantitative trait (QT) were also associated with EM and primary ovarian insufficiency (POI). Thus, EM has a genetic aetiology which overlaps variation in normal age at menopause and is at least partly explained by the additive effects of the same polygenic variants. The combined effect of the common variants captured by the single nucleotide polymorphism arrays was estimated to account for ∼30% of the variance in EM. The association between the combined 17 variants and the risk of EM was greater than the best validated non-genetic risk factor, smoking.//////////////////