Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The fine tuning of Ca(2+) excretion in the kidney takes place in the distal nephron, which consists of the distal convoluted tubule, connecting tubule, and initial portion of the cortical collecting duct. In these segments, Ca(2+) is reabsorbed through an active transcellular pathway. The apical influx of Ca(2+) into the distal renal cell is presumably the rate-limiting step in this process, and its molecular identity has remained obscure so far. The recently discovered epithelial Ca(2+) channel (ECaC) exhibits the expected properties for being the gatekeeper in transcellular Ca(2+) reabsorption. The characteristics and potential physiological role of ECaC will be discussed in this review. Our knowledge of the mechanisms involved in the regulation of transcellular Ca(2+) transport has advanced rapidly since the development of cell models originating from distal tubular cells. Studies using these models indicate that hormones including arginine vasopressin, PGE(2), adenosine, ATP, and atrial natriuretic peptide should be considered as calciotropic hormones controlling renal Ca(2+) handling. Evidence is now beginning to emerge that the stimulating calciotropic hormones utilize new cAMP-independent pathways to stimulate Ca(2+) reabsorption. These new findings allow the development of a comprehensive and detailed model of the process of transcellular calcium transport in the kidney whereby the individual contribution of the participating transporters can now be fully appreciated.
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PMID:Toward a comprehensive molecular model of active calcium reabsorption. 1071 May 38

The organization of Na(+) and Ca(2+) transport pathways along the mouse distal nephron is incompletely known. We revealed by immunohistochemistry a set of Ca(2+) and Na(+) transport proteins along the mouse distal convolution. The thiazide-sensitive Na(+)-Cl(-) cotransporter (NCC) characterized the distal convoluted tubule (DCT). The amiloride-sensitive epithelial Na(+) channel (ENaC) colocalized with NCC in late DCT (DCT2) and extended to the downstream connecting tubule (CNT) and collecting duct (CD). In early DCT (DCT1), the basolateral Ca(2+)-extruding proteins [Na(+)/Ca(2+) exchanger (NCX), plasma membrane Ca(2+)-ATPase (PCMA)] and the cytoplasmic Ca(2+)-binding protein calbindin D(28K) (CB) were found at very low levels, whereas the cytoplasmic Ca(2+)/Mg(2+)-binding protein parvalbumin was highly abundant. NCX, PMCA, and CB prevailed in DCT2 and CNT, where we located the apical epithelial Ca(2+) channel (ECaC1). Its subcellular localization changed from apical in DCT2 to exclusively cytoplasmic at the end of CNT. NCX and PMCA decreased in parallel with the fading of ECaC1 in the apical membrane. All three of them were undetectable in CD. These findings disclose DCT2 and CNT as major sites for transcellular Ca(2+) transport in the mouse distal nephron. Cellular colocalization of Ca(2+) and Na(+) transport pathways suggests their mutual interactions in transport regulation.
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PMID:Distribution of transcellular calcium and sodium transport pathways along mouse distal nephron. 1170 51