Smu1 and RED function both as alternative splicing regulators and as general splicing factors and are required predominantly for efficient splicing of short introns.
Investigated and identified antiviral agents targeting the assembly of the human RED-SMU1 splicing complex and results demonstrate possibility of RED-SMU1 destabilizing molecules to be used in antiviral therapy.
Data suggest that two human spliceosomal factors RED and SMU1 are recruited to control expression and alternative splicing of viral exportins via PB2 (polymerase PB2) of influenza A virus (H3N2) and are required for efficient viral multiplication.
At least three genes orthologous to loci in this LD block HBEGF IK and SRA1 result independently in a phenotype of myocardial contractile dysfunction when their expression is reduced with morpholino antisense reagents.
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