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Article

γ-COPI mediates the retention of kAE1 G701D protein in Golgi apparatus - a mechanistic explanation of distal renal tubular acidosis associated with the G701D mutation.

The Biochemical journal - 17 Jul 2017

Duangtum Natapol, Junking Mutita, Phadngam Suratchanee, Sawasdee Nunghathai, Castiglioni Andrea, Charngkaew Komgrid, Limjindaporn Thawornchai, Isidoro Ciro, Yenchitsomanus Pa-Thai

Abstract excerpt

Mutations of the solute carrier family 4 member 1 (SLC4A1) gene encoding kidney anion (chloride/bicarbonate ion) exchanger 1 (kAE1) can cause genetic distal renal tubular acidosis (dRTA). Different SLC4A1 mutations give rise to mutant kAE1 proteins with distinct defects in protein trafficking. The mutant kAE1 protein may be retained in endoplasmic reticulum (ER) or Golgi apparatus, or mis-targeted to the apical...

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Share to Acidosis, Renal Tubular
Share to Anion Exchange Protein 1, Erythrocyte

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Gene Knockdown Techniques

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Identifiers

PMID: 28646128
DOI: 10.1042/BCJ20170088

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