The B1 H + -ATPase (Atp6v1b1) Subunit in Non-Type A Intercalated Cells is Required for Driving Pendrin Activity and the Renal Defense Against Alkalosis.
1) Atp6v1b1+/- mice developed a mild incomplete dRTA. dRTA is partly compensated by respiration. 2) Compensatory mechanisms for the absence of B1 take place only in the collecting duct of Atp6v1b1-/- kidneys.
RhCG and H+ATPases are located within the same cellular protein complex in the kidney and this interaction is required for maximal urinary acidification by H+-ATPases a prerequisite for efficient NH3 secretion and urine excretion of NH4+.
Gene ablation abolished the enhanced urinary acidification stimulated by exposure of dissected outer medullary collecting ducts to high (5.0 mM) extracellular Ca(2+).
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