Deletion of human tarbp2 reveals cellular microRNA targets and cell cycle function of TRBP

ABSTRACT: TRBP has two known functions as Dicer co-factor and PKR inhibitor. However, the role of TRBP in miRNA biogenesis is controversial and its regulation of PKR in mitosis remains unexplored. Here, we generate TRBP KO HeLa cells and find that TRBP depletion alters Dicer processing sites of a subset of miRNAs, but does not affect Dicer stability, miRNA abundance, or Argonaute loading. By generating PACT, another Dicer interactor, and TRBP/PACT double-KO cells, we further show that TRBP and PACT do not functionally compensate each other and that only TRBP contributes to Dicer processing. We also report that TRBP is hyperphosphorylated by JNK in M phase when PKR is activated by cellular dsRNAs. Hyperphosphorylation potentiates the inhibitory activity of TRBP on PKR, suppressing PKR in M-G1 transit

ORGANISM(S): Homo sapiens

SUBMITTER: Daekwan Seo 

PROVIDER: E-GEOD-61458 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress