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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Congenital jaundice in rats with a mutation in a multidrug resistance-associated protein gene.

The human Dubin-Johnson syndrome and its animal model, the TR(-) rat, are characterized by a chronic conjugated hyperbilirubinemia. TR(-) rats are defective in the canalicular multispecific organic anion transporter ( cMOAT), which mediates hepatobiliary excretion of numerous organic anions. The complementary DNA for rat cmoat, a homolog of the human multidrug resistance gene (hMRP1), was isolated and shown to be expressed in the canalicular membrane of hepatocytes. In the TR(-) rat, a single-nucleotide deletion in this gene resulted in a reduced messenger RNA level and absence of the protein. It is likely that this mutation accounts for the TR(-) phenotype.[1]

References

  1. Congenital jaundice in rats with a mutation in a multidrug resistance-associated protein gene. Paulusma, C.C., Bosma, P.J., Zaman, G.J., Bakker, C.T., Otter, M., Scheffer, G.L., Scheper, R.J., Borst, P., Oude Elferink, R.P. Science (1996) [Pubmed]
 
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