Human Molecular Genetics, Vol 7, 203-207, Copyright © 1998 by Oxford University Press
M Wada, S Toh, K Taniguchi, T Nakamura, T Uchiumi, K Kohno, I Yoshida, A Kimura, S Sakisaka, Y Adachi and M Kuwano
Members of the ATP-binding cassette (ABC) transporter superfamily are
mutated to cause diseases that include cystic fibrosis, hyperinsulinemia,
adrenoleukodystrophy, Stargardt disease and multidrug resistance. We
recently isolated a novel human member of ABC transporter superfamily as
the candidate transporter for the glucuronide and glutathione-conjugated
antitumor agents, and found it highly homologous to the rat cmoat gene.
consistent with recent findings of defects in the homologous cmoat gene in
two rat models of hyperbilirubinemia (TR- and Eisai), we report two
deletions and a missense mutation in the active transport family signature
region in the gene in patients with hyperbilirubinemia II/Dubin-Johnson
syndrome (DJS; MIM 237500), respectively. These results strongly implicate
the cMOAT gene as responsible for the defects in DJS patients.
ARTICLES
Mutations in the canilicular multispecific organic anion transporter (cMOAT) gene, a novel ABC transporter, in patients with hyperbilirubinemia II/Dubin-Johnson syndrome
Department of Biochemistry, Kyushu University School of Medicine, Fukuoka 812-82, Japan. wada@biochem1.med.kyushu-u.ac.jp
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