CHERP

(redirected from SRA1)

CHERP

A gene on chromosome 19p13.1 that encodes a protein involved in calcium homeostasis, growth and proliferation. CHERP is expressed in the brain, placenta, lungs, liver, kidneys, pancreas, and cardiac and skeletal muscle.
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References in periodicals archive ?
SRA1 was the first gene shown to function through both its protein and noncoding, functional RNA products (62).
Idiopathic Hypogonadotropic Hypogonadism Caused by Inactivating Mutations in SRA1. J Clin Res Pediatr Endocrinol 2016;8:125-134.
Eighty-four Nellore steers (18-mo age, and 350.5 [+ or -] 26.5 kg initial BW, mean [+ or -] SD) were distributed into seven groups according to the initial BW, and groups were randomly assigned to receive one of the experimental diets: control (CON), feed grade urea at 10 or 20 g/kg diet DM (U1 and U2, respectively; Reforce N, Petrobras, Rio de Janeiro, Brazil), coated SRA2 at 10 or 20 g/kg diet DM (SRA1 and SRA2, respectively; Polymer-coated slow-release urea without sulphur in composition Petrobras), and coated slow-release urea B at 10 or 20 g/kg diet DM (SRB1 and SRB2, respectively; Polymer coated slow-release urea with 29.5 g/kg DM of sulphur content, Petrobras).
Animals fed urea at 20 g/kg DM (U2, SRA2 and SRB2) had lower (p<0.01) final BW and ADG compared to those fed urea at 10 g/kg DM (U1, SRA1 and SRB1).
Safety inspection and culture (SRA1) and audit (SIA) SC10.
Founded in 1976, the hall has 14 historic aircraft, including the only SRA1 jet flying boat in the world, as well as an M24 Spitfire and S6B Schneider.
SRA1 (Steroid receptor RNA activator 1) encodes for a nuclear hormone receptor coregulator.
SRA1 was originally described as a functional ncRNA involved in the regulation of gene expression by steroid receptors.
It is evident from the eloquent studies reported here that inactivating mutations of the SRA1 gene cause complete normosmic IHH, hence pubertal failure in humans.
In consideration of the known roles of the SRA1 with other nuclear receptors, any disorders associated with a potential dysfunction of these receptors were actively ruled out.
Analysis of targeted exome sequencing data for the autozygous regions revealed that the only plausible candidate variant to account for the phenotype is in the SRA1 gene.
Family 3: A Sanger screening for SRA1 showed that the proband and his affected brother had a heterozygous mutations (a C-to-T change at cDNA 59 predicting substitution of proline at residue 20 for leucine, p.P20L) (Figure 2).