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Gene Symbol |
NPR3 |
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Aliases |
ANP-C, ANPR-C, ANPRC, C5orf23, GUCY2B, NPR-C, NPRC |
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Entrez Gene ID |
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Gene Name |
Natriuretic peptide receptor 3 |
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Chromosomal Location |
5p13.3 |
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HGNC ID |
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Summary |
This gene encodes one of three natriuretic peptide receptors. Natriutetic peptides are small peptides which regulate blood volume and pressure, pulmonary hypertension, and cardiac function as well as some metabolic and growth processes. The product of this gene encodes a natriuretic peptide receptor responsible for clearing circulating and extracellular natriuretic peptides through endocytosis of the receptor. Multiple transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Feb 2011]
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RefSeq DNA |
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RefSeq mRNA |
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e!Ensembl
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| Protein Information |
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Protein Name |
Atrial natriuretic peptide receptor 3, atrial natriuretic peptide clearance receptor, atrial natriuretic peptide receptor type C, atrionatriuretic peptide receptor C, guanylate cyclase C, natriuretic peptide receptor C/guanylate cyclase C (atrionatriuretic peptide receptor C) |
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Function |
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Receptor for the natriuretic peptide hormones, binding with similar affinities atrial natriuretic peptide NPPA/ANP, brain natriuretic peptide NPPB/BNP, and C-type natriuretic peptide NPPC/CNP. May function as a clearance receptor for NPPA, NPPB and NPPC, regulating their local concentrations and effects. May regulate diuresis, blood pressure and skeletal development. Does not have guanylate cyclase activity. |
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UniProt |
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PDB |
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Pfam |
| Pfam Accession |
Pfam ID |
| PF01094 |
ANF_receptor |
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Interactions |
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| STRING |
MINT |
IntAct |
| ENSP00000339467 |
P84095 |
P84095 |
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View interactions
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Associated Diseases
| Disease group | Disease Name | References |
| Ear Or Mastoid Diseases |
| Meniere Disease |
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| Endocrine System Diseases |
| PCOS |
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| Neoplasms |
| Prostate cancer |
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| Psychiatric/Brain disorders |
| Obstructive Sleep Apnea |
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References |
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| Corton Marta, Botella-Carretero Jose I, Benguria Alberto, Villuendas Gemma, Zaballos Angel, San Millan Jose L, Escobar-Morreale Hector F, Peral Belen |
| Instituto de Investigaciones Biomedicas, Consejo Superior de Investigaciones Cientificas and Universidad Autonoma de Madrid, E-28029 Madrid, Spain. |
| J Clin Endocrinol Metab. 2007 Jan;92(1):328-37. doi: 10.1210/jc.2006-1665. Epub |
Abstract
CONTEXT: The polycystic ovary syndrome (PCOS) is frequently associated with visceral obesity, suggesting that omental adipose tissue might play an important role in the pathogenesis of the syndrome. OBJECTIVE: The objective was to study the expression profiles of omental fat biopsy samples obtained from morbidly obese women with or without PCOS at the time of bariatric surgery. DESIGN: This was a case-control study. SETTINGS: We conducted the study in an academic hospital. PATIENTS: Eight PCOS patients and seven nonhyperandrogenic women submitted to bariatric surgery because of morbid obesity. INTERVENTIONS: Biopsy samples of omental fat were obtained during bariatric surgery. MAIN OUTCOME MEASURE: The main outcome measure was high-density oligonucleotide arrays. RESULTS: After statistical analysis, we identified changes in the expression patterns of 63 genes between PCOS and control samples. Gene classification was assessed through data mining of Gene Ontology annotations and cluster analysis of dysregulated genes between both groups. These methods highlighted abnormal expression of genes encoding certain components of several biological pathways related to insulin signaling and Wnt signaling, oxidative stress, inflammation, immune function, and lipid metabolism, as well as other genes previously related to PCOS or to the metabolic syndrome. CONCLUSION: The differences in the gene expression profiles in visceral adipose tissue of PCOS patients compared with nonhyperandrogenic women involve multiple genes related to several biological pathways, suggesting that the involvement of abdominal obesity in the pathogenesis of PCOS is more ample than previously thought and is not restricted to the induction of insulin resistance. |
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