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Functional deficiency of all UTs caused a urea-selective urine-concentrating defect with little physiological abnormality in extrarenal organs.
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results suggest that GSK3 may in part modulate the hypertonic-induced intracellular UT-A1 redistribution and its accumulation on the plasma membrane, which may constitute another mechanism by which GSK3 modulates urine concentration
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UT2 is a negative regulator shared across STAT3 and mTORC2 signaling cascades, functioning as a tumor suppressor in hematologic malignancies driven by those pathways.
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Studies indicate that urea transporter Slc14a2 (UT-A1/3) knockout mouse models showed the essential role of urea for producing maximally concentrated urine.
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It is concluded that NaCl and urea synergistically induce the expression of UTA2 rather than AQP2 in mIMCD3 cells, and hyperosmolality probably mediates the expression of AQP2 and UTA2 through different mechanisms.
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These results suggest that in wild-type mice UT-A2 facilitates urea absorption by urea efflux from the thin descending limb of short loops of Henle.
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Levels of UTA mRNA were increased in thirsted mice compared with control animals
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potassium depletion is associated with reduced expression of UT-A1, UT-A3, and UT-B but increased expression of UT-A2.
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mUT-A3 is a basolateral membrane transporter expressed in inner medullary collecting duct cells.
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lack of UT-B does not result in a change in expression of urea transporters involved in urea reabsorption from the inner medullary collecting duct (UT-A1 and UT-A3).
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UT-A2 is important for maintaining a high concentration of urea in the inner medulla when urea supply to the kidney is limited
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These results demonstrate that 4.2 kb of the UT-Aalpha promoter is sufficient to drive expression of a heterologous reporter gene in a tissue-specific and cell-specific fashion in transgenic mice.
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Urea transporter UT-A2 is acutely sensitive to AVP, cAMP, or increased intracellular calcium.
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data suggest that the Gamble phenomenon is largely a manifestation of facilitated urea transport in the inner medulla collecting dut by UT-A1 and UT-A3
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UT-A1 is a target gene of KLF12.
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results indicate that UT-A3 is acutely regulated by arginine vasopressin, via a protein kinase A-dependent pathway in MDCK type I cells
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Biophysical characterization of mouse UT-A2 and UT-A3 undertaken by expression in Xenopus laevis oocytes and preparation of plasma membrane vesicles for use in stopped-flow fluorometry.
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ubiquitination regulates the plasma membrane expression of all three major UT-A urea transporters, but that this is not the mechanism primarily used by vasopressin to produce its physiological effects.
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Three distinct variations in the appearance of the renal pelvis were found in UT-A1/3(-/-) mice
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study investigated the vasopressin regulation of the basolateral urea transporter UT-A3 using an MDCK-mUT-A3 cell line; vasopressin significantly increases UT-A3 localization at the basolateral membrane
