Background
RBM4 functions as an RNA-binding protein and precursor mRNA splicing factor that antagonizes activity of PTBP1-mediated splicing. Upon phosphorylation at Ser309, RBM4 accumulates in stress granules and suppresses cap-dependent translation through eIF4A. Exon skipping of MEF2C by RBM4 has been shown to play a key role in the differentiation of brown adipocytes. The splicing activities of RBM4 seem to suppress tumorigenesis in the context of multiple cancer types.
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