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

• Main Authors: Natapol Duangtum, Mutita Junking, Suratchanee Phadngam, Nunghathai Sawasdee, Andrea Castiglioni, Komgrid Charngkaew, Thawornchai Limjindaporn, Ciro Isidoro, Pa Thai Yenchitsomanus
• Other Authors: Mahidol University
• Format: Article
• Published: 2018
• Subjects: Biochemistry, Genetics and Molecular Biology
• Online Access: https://repository.li.mahidol.ac.th/handle/123456789/41833

© 2017 The Author(s); published by Portland Press Limited on behalf of the Biochemical Society. 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...