Atp6v0a4 knockout mouse is a model of distal renal tubular acidosis with hearing loss, with additional extrarenal phenotype
Author:
Publisher
Proceedings of the National Academy of Sciences
Subject
Multidisciplinary
Reference28 articles.
1. Impaired glycosylation and cutis laxa caused by mutations in the vesicular H+-ATPase subunit ATP6V0A2
2. Defects in TCIRG1 subunit of the vacuolar proton pump are responsible for a subset of human autosomal recessive osteopetrosis
3. Mutations in the a3 subunit of the vacuolar H+-ATPase cause infantile malignant osteopetrosis
4. Mutations in the chloride-bicarbonate exchanger gene AE1 cause autosomal dominant but not autosomal recessive distal renal tubular acidosis
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3. Neonatal Onset Distal Renal Tubular Acidosis: Description of Two Novel Variants on the ATP6V0A4 Gene and Review of the Literature on Associated Extrarenal Manifestations;Journal of Pediatric Genetics;2023-08-08
4. The pathophysiology of distal renal tubular acidosis;Nature Reviews Nephrology;2023-04-04
5. Hearing Loss Related to Gene Mutations in Distal Renal Tubular Acidosis;Audiology and Neurotology;2023
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