![]() Desir J, Moya G, Reish O, Van Regemorter N, Deconinck H, David KL, Meire FM, Abramowicz M. Electrogenic sodium-dependent bicarbonate secretion by glial cells of the leech central nervous system. Am J Physiol Regul Integr Comp Physiol 293: R2136–R2146, 2007. Molecular expression of SLC4 derived Na + dependent anion transporters in selected human tissues. The relationship of blood- and urine-boron to boron exposure in borax-workers and usefulness of urine-boron as an exposure marker. Culver BD, Shen PT, Taylor TH, Lee-Feldstein A, Anton-Culver H, Strong PL. Cellular and molecular biology of the aquaporin water channels. Molecular mechanisms underlying the corneal endothelial pump. Carbonic anhydrase II increases the activity of the human electrogenic Na +/HCO 3 − cotransporter. Facilitated lactate transport by MCT1 when coexpressed with the sodium bicarbonate cotransporter (NBC) in Xenopus oocytes. Bicarbonate transport in health and disease. Autosomal recessive CHED associated with novel compound heterozygous mutations in SLC4A11. Aldave AJ, Yellore VS, Bourla N, Momi RS, Khan MA, Salem AK, Rayner SA, Glasgow BJ, Kurtz I. Genetics of the corneal endothelial dystrophies: an evidence-based review. Mutational spectrum of SLC4A11 in autosomal recessive CHED in Saudi Arabia. Aldahmesh MA, Khan AO, Meyer BF, Alkuraya FS. When expressed in oocytes, SLC4A11 transported NH 3, not NH 3/H +. This work provides additional support for water and ammonia transport by SLC4A11. These data argue against a role of human SLC4A11 in bicarbonate or borate transport. In mammalian cells, but not oocytes, OH −/H + conductance may arise when SLC4A11 activates another protein or itself is activated by another protein. Voltage-dependent OH − or H + movement was not measurable in SLC4A11-expressing oocytes, but SLC4A11-expressing HEK293 cells manifested low-level cytosolic acidification at baseline. SLC4A11 mediated electroneutral NH 3 transport in oocytes. Studies in oocytes and HEK293 cells could not detect Na +-coupled HCO 3 − transport or Cl −/HCO 3 − exchange by SLC4A11. SLC4A11 supported osmotically driven water accumulation that was electroneutral and Na + independent. The plant water/borate transporter NIP5 1 manifested borate transport, whereas human SLC4A11 did not. Since plant and fungal SLC4A11 orthologs transport borate, we measured cell swelling associated with accumulation of solute borate. To clarify the normal function(s) of SLC4A11, we characterized the protein following expression in the simple, low-background expression system Xenopus laevis oocytes. The role of SLC4A11 in these corneal dystrophies is not firmly established, as SLC4A11 function remains unclear. These diseases are marked by fluid accumulation in the corneal stroma, secondary to defective fluid reabsorption by the corneal endothelium. Mutations of SLC4A11 cause some cases of the blinding corneal dystrophies, congenital hereditary endothelial dystrophy, and Fuchs endothelial corneal dystrophy. SLC4A11, a member of the SLC4 family of bicarbonate transporters, is a widely expressed integral membrane protein, abundant in kidney and cornea. ![]()
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