Abstract:
:Crigler-Najjar (CN) disease is caused by a deficiency of the hepatic enzyme, bilirubin UDP-glucuronosyltransferase (B-UGT). We have found two CN type II patients, who were homozygous for a leucine to arginine transition at position 15 of B-UGT1. This mutation is expected to disrupt the hydrophobic core of the signal peptide of B-UGT1. Wild type and mutant B-UGT cDNAs were transfected in COS cells. Mutant and wild type mRNA were formed in equal amounts. The mutant protein was expressed with 0.5% efficiency, as compared to wild type. Mutant and wild type mRNAs were translated in vitro. Wild type transferase is processed by microsomes, no processing of the mutant protein was observed.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Seppen J,Steenken E,Lindhout D,Bosma PJ,Elferink RPdoi
10.1016/0014-5793(96)00677-1subject
Has Abstractpub_date
1996-07-29 00:00:00pages
294-8issue
3eissn
0014-5793issn
1873-3468pii
0014579396006771journal_volume
390pub_type
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