Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
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Gene/Protein
Disease
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Target Concepts:
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Query: UMLS:C0020438 (
hypercalciuria
)
2,502
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The combination of hyperoxaluria and hypocitraturia can trigger Ca(2+)-oxalate stone formation, even in the absence of
hypercalciuria
, but the molecular mechanisms that control urinary oxalate and citrate levels are not understood completely. Here, we examined the relationship between the oxalate transporter SLC26A6 and the citrate transporter
NaDC-1
in citrate and oxalate homeostasis. Compared with wild-type mice, Slc26a6-null mice exhibited increased renal and intestinal sodium-dependent succinate uptake, as well as urinary hyperoxaluria and hypocitraturia, but no change in urinary pH, indicating enhanced transport activity of
NaDC-1
. When co-expressed in Xenopus oocytes,
NaDC-1
enhanced Slc26a6 transport activity. In contrast, Slc26a6 inhibited
NaDC-1
transport activity in an activity dependent manner to restricted tubular citrate absorption. Biochemical and physiologic analysis revealed that the STAS domain of Slc26a6 and the first intracellular loop of
NaDC-1
mediated both the physical and functional interactions of these transporters. These findings reveal a molecular pathway that senses and tightly regulates oxalate and citrate levels and may control Ca(2+)-oxalate stone formation.
...
PMID:SLC26A6 and NaDC-1 transporters interact to regulate oxalate and citrate homeostasis. 2383 57
