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Gene Review

Atp6v1b1  -  ATPase, H+ transporting, lysosomal V1...

Mus musculus

Synonyms: AW208839, Atp6b1, D630003L15, D630030L16Rik, D630039P21Rik, ...
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Disease relevance of Atp6v1b1

  • Urine pH is more alkaline and metabolic acidosis is more severe in Atp6v1b1(-/-) mice after oral acid challenge, demonstrating a failure of normal urinary acidification [1].

High impact information on Atp6v1b1

  • Apical expression of the alternative B-subunit isoform, B2, is increased in Atp6v1b1(-/-) medulla and colocalizes with the H(+)ATPase E-subunit; however, the greater severity of metabolic acidosis in Atp6v1b1(-/-) mice after oral acid challenge indicates that the B2-subunit cannot fully functionally compensate for the loss of B1 [1].
  • In Atp6v1b1(-/-) mice, the normal urinary acidification induced by a lumen-negative potential in response to furosemide infusion is abolished [1].
  • Northern blotting detects a 2.2-kb Atp6v1b1 transcript in the kidney and testis, but not other major organs [2].
  • Auditory brainstem response tests revealed normal hearing in mice lacking Atp6b1 [3].
  • Our data demonstrate that Atp6b1 is not critical for normal inner ear development or normal inner ear function in mice and suggest that other proton-transporting mechanisms or pH buffering systems must allow the mouse inner ear to compensate for lack of normal Atp6b1 activity [3].

Anatomical context of Atp6v1b1

  • Atp6b1 mRNA was first detected at embryonic day 11.5 (E11.5) in the endolymphatic duct epithelia [3].
  • From E16.5 onward, Atp6b1 was also observed in the presumptive interdental cell layer of the spiral limbus in the cochlea [3].

Analytical, diagnostic and therapeutic context of Atp6v1b1

  • After an acute intracellular acidification, Na(+)-independent pH recovery rates of individual Atp6v1b1(-/-) intercalated cells of the cortical collecting duct are markedly reduced and show no further decrease after treatment with the selective H(+)ATPase inhibitor concanamycin [1].
  • Standard in situ hybridization was used for the expression study with routine morphologic and physiologic assessments of hearing and balance in H(+)-ATPase B1 subunit (Atp6b1) null mutant mice [3].


  1. The B1-subunit of the H(+) ATPase is required for maximal urinary acidification. Finberg, K.E., Wagner, C.A., Bailey, M.A., Paunescu, T.G., Breton, S., Brown, D., Giebisch, G., Geibel, J.P., Lifton, R.P. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  2. Molecular cloning and characterization of Atp6v1b1, the murine vacuolar H+ -ATPase B1-subunit. Finberg, K.E., Wagner, C.A., Stehberger, P.A., Geibel, J.P., Lifton, R.P. Gene (2003) [Pubmed]
  3. Mice lacking the B1 subunit of H+ -ATPase have normal hearing. Dou, H., Finberg, K., Cardell, E.L., Lifton, R., Choo, D. Hear. Res. (2003) [Pubmed]
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