Abstract:
:HBV particles with genome derived from spliced mRNAs accumulate in patients with virus-derived severe liver necrosis and fibrosis. We investigated the role of an intronic element (intronic splicing silencer-long, ISS(L)) on splicing of HBV minigene transcripts. Removal of the entire ISS(L) showed two-fold increase in splicing while shorter deletions within ISS(L) indicated isolated clusters of activator and repressor domains. Activator domains stimulated splicing in presence of PRE, a long HBV 3' exon and even when present in a heterologous context. Mutations in the repressor domain unexpectedly augmented repression. The role of this intronic splicing regulatory element could be important for HBV pathogenesis.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Chowdhury JB,Roy D,Ghosh Sdoi
10.1016/j.febslet.2011.09.026subject
Has Abstractpub_date
2011-10-20 00:00:00pages
3348-53issue
20eissn
0014-5793issn
1873-3468pii
S0014-5793(11)00705-8journal_volume
585pub_type
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