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Intermediate-sized non-coding RNA 761 could interact with DEAD-box helicase 6 (DDX6) to induce NTERA-2 (NT2 (testicular embryonal carcinoma cell)) cell apoptosis and proliferation inhibition via the p53 pathway.
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The abrogation of DDX6 expression inhibited iPSC generation, which was mediated by RNA decay targeting parental mRNAs supporting mesenchymal phenotypes, along with microRNAs, such as miR-302b-3p
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Results showed that DDX6 was overexpressed in gastric cancer (GC) and acted as an oncogene through the regulation of c-Myc mRNA in GC cells.
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Results provide evidence for a dual mechanisms regulating the nucleocytoplasmic localization of DDX6. First, data show that DDX6 can be transported by 4E-T in a piggyback manner. Furthermore, a novel nuclear targeting mechanism was detected in which DDX6 enters the newly formed nuclei by "hitch-hiking" on mitotic chromosomes with its C-terminal domain during M phase progression.
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Results showed that DDX6 protein was overexpressed in gastric cancer (GC) and provided evidence that DDX6 acted as an upstream molecule that positively regulated the expression of HER2 and FGFR2 at the post-transcriptional step in GC cells.
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These findings imply a novel function for DDX6 as an RNA co-sensor and signaling enhancer for RIG-I.
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Identification of the DEAD box RNA helicase DDX6 as a new partner that acts in cooperation with Tau to increase miRNA activity.
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DDX6 modulates interaction of miR-122 with the 5' untranslated region of hepatitis C virus RNA.
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we demonstrate that joint deletion of two short conserved motifs that bind UNR and DDX6 relieves repression of 4E-T-bound mRNA, in part reliant on the 4E-T-DDX6-CNOT1 axis.
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miRNAs, AGOs, GW182, the CCR4-NOT complex, and DDX6/Me31B repress and degrade polyadenylated mRNA targets that are translated via scanning-independent mechanisms in both human and Drosophila melanogaster cells
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DDX6 may have a role in radio- and chemoresistance in glioblastoma
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Functional analysis of the 11q23.3 glioma susceptibility locus implicates PHLDB1 and DDX6 in glioma susceptibility.
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DDX6 repression complexes are required for P-body assembly.
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Protein Interactome Analysis of DDX6
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Results indicate that progenitor function is maintained by DDX6 complexes through two distinct pathways that include the degradation of differentiation-inducing transcripts and by promoting the translation of self-renewal and proliferation mRNAs.
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CNOT1 facilitates recruitment of DDX6 to miRNA-targeted mRNAs, placing DDX6 as a downstream effector in the miRNA silencing pathway.
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study discovered multiple susceptibility variants for systemic lupus erythematosus in the 11q23.3 region, including variants in/near PHLDB1 (rs11603023), DDX6 (rs638893) and CXCR5 (rs10892301)
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Crystal structures of the DDX6, CNOT1 and CNOT9 complexes.
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Crystal structure of the DDX6, CNOT9 and CNOT1 complex.
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DDX6 and miR-122 modulate HCV through distinct pathways.
