RHCG Antibody, FITC conjugated

1. RhCG and H+ATPases are located within the same cellular protein complex in the kidney and this interaction is required for maximal urinary acidification by H+-ATPases, a prerequisite for efficient NH3 secretion and urine excretion of NH4+. PMID: 29054531
2. RHCG was down-regulated in cervical cancers compared to that in normal cervical tissues, and further decreased in cervical cancer cell lines. Functionally, RHCG overexpression reduced cervical cancer cell proliferation and migration, as evidenced by the decreased transforming growth factor (TGF)-beta1, matrix metalloproteinase (MMP)-2 and MMP-9 expressions in cancer cells. PMID: 29852177
3. The results support the notion that RHCG is a novel tumor suppressor gene that plays an important role in the development and progression of ESCC. PMID: 29290801
4. The molecular mechanism of NH4(+) recruitment and NH3 transport by RHCG is described. PMID: 26190573
5. Rh B Glycoprotein (Rhbg) and Rh C Glycoprotein (Rhcg) are identified as ammonia transporters. They are expressed in specific cell populations and membrane domains in distal renal epithelial cells, where they facilitate ammonia secretion. PMID: 24647713
6. RhAG, RhBG and RhCG-exhibit significant permeability to NH3 and show for the first time that RhBG and RhCG can conduct CO2. PMID: 24077989
7. Amt and Rh proteins are not functionally equivalent and that permeation takes place according to two distinct mechanisms. PMID: 24021113
8. X-ray crystallographic structure of human RhCG, determined at 2.1 A resolution, reveals the mechanism of ammonia transport. PMID: 20457942
9. major finding of this study is that RhCG protein is active as an NH(3) channel and that this function does not require any protein partner PMID: 20126667
10. RhBG and RhCG facilitate ammonium movement across the plasma membrane; these results favor the hypothesis that these Rh glycoproteins, together with their homolog RhAG, constitute a family of NH3 channels in mammalian cells. PMID: 15929723
11. RhCG expression enhanced the ammonium-induced initial alkalinization (related to NH3 influx)& secondary acidification (related to NH4+ influx). Sub-millimolar NH4+ concentrations induced inward currents in voltage-clamped RhCG-expressing cells. PMID: 16564724
12. Review. Mutations at positions F74, V137 and F235 resulted in a severe reduction of NH3 transport. PMID: 16580862
13. This study concludes that under normal conditions, RhCG is the major putative ammonia transporter expressed in the human kidney and RhBG is not expressed at detectable levels. PMID: 19357182
14. Rhbg and Rhcg may contribute to bronchial epithelial cell ammonia metabolism and suggest that they do not contribute to pulmonary carbon dioxide transport. PMID: 19429772

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HGNC: 18140

OMIM: 605381

KEGG: hsa:51458

STRING: 9606.ENSP00000268122

UniGene: Hs.459284