High impact information on Slc14a1

• The facilitated urea transporter (UT-B) in erythrocytes permits these cells to lose urea rapidly as they traverse the ascending vasa recta, thereby preventing loss of urea from the medulla and decreasing urine-concentrating ability by decreasing the efficiency of countercurrent exchange, as occurs in Jk null individuals (who lack Kidd antigen) [1].
• Additionally, both UT-A2 and UT-B protein abundances in the outer medulla increased during urea-induced osmotic diuresis but not in NaCl or glucose diuresis [2].
• Regulated expression of renal and intestinal UT-B urea transporter in response to varying urea load [3].
• We identified expression of UT-B in the rat colon, as a 2-kb mRNA transcript and as an approximately 45-kDa protein, with apical localization in superficial colon epithelial cells [3].
• UT-B also is expressed in rat small intestine [3].

Biological context of Slc14a1

• We conclude that during osmotic diuresis, UT-A1 abundance increases when the percentage of urea in total urinary solute is low and UT-A2 and UT-B abundances increase when the urea concentration in the medullary interstitium is high [2].
• Immunocytochemistry confirmed downregulation of UT-A1 and UT-A3 in IM collecting duct and UT-B in the descending vasa recta [4].
• METHODS: To test whether lithium alters UT-A1 or UT-B urea transporter protein abundance or UT-A1 phosphorylation, rats were fed a standard diet supplemented with LiCl for 10 or 25 days, and then compared to pair-fed control rats [5].
• The distribution of UT-A and UT-B in the inner ear suggests that the cells that surround the inner ear fluids may be involved in urea transport and thus play an important role in fluid homeostasis in the inner ear [6].

Anatomical context of Slc14a1

• Urea transport in the kidney is mediated by a family of transporter proteins that includes renal urea transporters (UT-A) and erythrocyte urea transporters (UT-B) [7].
• UT-B protein and mRNA are detected in rat brain, colon, heart, liver, lung, and testis [8].
• UT-B protein is detected in cultured bovine endothelial cells [8].
• In conclusion, reduced expression of UT-A1, UT-A3, and UT-B levels in both BUO and UUO rats suggests that urea transporters play important roles in the impaired urinary concentrating capacity in response to urinary tract obstruction [4].
• UT-B was expressed in the plasma membrane of the descending vasa recta of both control and experimental animals [9].

Associations of Slc14a1 with chemical compounds

• RESULTS: In lithium-fed rats (25 days), UT-A1 abundance was reduced to 50% of control rats in IM tip and to 25% in IM base, and UT-B abundance was reduced to 40% in IM base [5].

Regulatory relationships of Slc14a1

• UT-B protein was expressed on Sertoli cell membranes of stage II-III tubules [10].

Other interactions of Slc14a1

• UrT1-C has 70 and 62% amino acid identity to rat UrT1-B and UrT2 (UT3), respectively, and 99% identity to a recently reported rat isoform (UT-A3; Karakashian A, Timmer RT, Klein JD, Gunn RB, Sands JM, and Bagnasco SM. J Am Soc Nephrol 10: 230-237, 1999) [11].

Analytical, diagnostic and therapeutic context of Slc14a1

• Because newborn rats are not capable of producing concentrated urine, we examined the time of expression and the distribution of UT-A and UT-B in the developing rat kidney by light and electron microscopic immunocytochemistry [7].
• Using in vitro perfusion, we determined that a phloretin-inhibitable urea pathway exists across the SMTs of rat testis and conclude that UT-B is likely to participate in this pathway [10].
• There was no difference in immunoblot expression of UT-B in the bladder or ureteral homogenates between groups of rats fed high- or low-protein or high- or low-sodium diets [12].
• In view of the wide distribution of UT-B in rat vasculature, elevated blood urea nitrogen may lead to endothelial L-Arg deficiency in vivo [13].
• In this study, we examined the expression of the UT-B urea transporter in rats fed a low-protein diet (LPD), a high-protein diet (HPD), and a 20% urea-supplemented diet [3].

References