Anti-AGO2 (full length) polyclonal antibody

Erasure of DNA methylation and repressive chromatin marks in the mammalian germline leads to risk of transcriptional activation of transposable elements (TEs). Here, we used mouse embryonic stem cells (ESCs) to identify an endosiRNA-based mechanism involved in suppression of TE transcription. In ESCs with DNA demethylation induced by acute deletion of Dnmt1, we saw an increase in sense transcription at TEs, resulting in an abundance of sense/antisense transcripts leading to high levels of ARGONAUTE2 (AGO2)-bound small RNAs. Inhibition of Dicer or Ago2 expression revealed that small RNAs are involved in an immediate response to demethylation-induced transposon activation, while the deposition of repressive histone marks follows as a chronic response. In vivo, we also found TE-specific endo-siRNAs present during primordial germ cell development. Our results suggest that antisense TE transcription is a "trap'' that elicits an endosiRNA response to restrain acute transposon activity during epigenetic reprogramming in the mammalian germline.

AGO2 (Argonaute RISC Catalytic Component 2) plays an important role in small RNA-guided gene silencing processes. It has been implied in tumorigenesis of different types of tumors. In this study, we found that AGO2 expression was remarkably increased in human hepatocellular carcinoma (HCC) tissues when compared with adjacent noncancerous tissues. High expression of AGO2 was associated with poor prognosis in HCC patients. The CRISPR/Cas9-mediated knockout of AGO2 in SMMC-7721 cells inhibited cell proliferation and induced significant G1 phase arrest of cell cycle. Inhibition of cell migration was also observed in SMMC-7721 AGO2(-/-) cells. In vivo experiments showed that tumors grew slower in nude mice transplanted with AGO2(-/-) cells than in SMMC-7721 cell-derived xenograft mice. Microarray analysis and western blot analysis revealed that AGO2 depletion decreased expression of Survivin, Vimentin, and Snail. Overexpression of AGO2 in SMMC-7721 and Huh-7 cells could reverse the knockout-induced inhibition effects on either cell behaviors or expression of Survivin, Vimentin, and Snail Therefore, our data demonstrated that AGO2 might facilitate HCC tumorigenesis and metastasis through modulating expression of Survivin, Vimentin, and Snail.