Double-stranded RNA (dsRNA) endoribonuclease playing a central role in short dsRNA-mediated post-transcriptional gene silencing. Cleaves naturally occurring long dsRNAs and short hairpin pre-microRNAs (miRNA) into fragments of twenty-one to twenty-three nucleotides with 3' overhang of two nucleotides, producing respectively short interfering RNAs (siRNA) and mature microRNAs. SiRNAs and miRNAs serve as guide to direct the RNA-induced silencing complex (RISC) to complementary RNAs to degrade them or prevent their translation. Gene silencing mediated by siRNAs, also called RNA interference, controls the elimination of transcripts from mobile and repetitive DNA elements of the genome but also the degradation of exogenous RNA of viral origin for instance. The miRNA pathway on the other side is a mean to specifically regulate the expression of target genes (By similarity). More active than isoform 1 to process long double-stranded RNA into siRNAs. Responsible for the accumulation of endogenous siRNAs observed in mouse oocytes compared to somatic cells and it regulates meiotic spindle organization in female germline. Endonucleolytic cleavage to 5'-phosphomonoester. Binds 2 magnesium or manganese ions per subunit. Component of the RISC loading complex (RLC), or micro-RNA (miRNA) loading complex (miRLC), which is composed of DICER1, AGO2 and TARBP2; DICER1 and TARBP2 are required to process precursor miRNAs (pre-miRNAs) to mature miRNAs and then load them onto AGO2. Note that the trimeric RLC/miRLC is also referred to as RISC. Interacts with DHX9, AGO1, PIWIL1 and PRKRA. Interacts with AGO2, TARBP2, EIF6, MOV10 and RPL7A (60S ribosome subunit); they form a large RNA-induced silencing complex (RISC). Interacts with BCDIN3D (By similarity). Interacts (via Dicer dsRNA-binding fold domain) with ALOX5 (via PLAT domain); this interaction enhances arachidonate 5-lipoxygenase activity and modifies the miRNA precursor processing activity of DICER1 (By similarity). Isoform 1 is expressed in a wide variety of tissues. Isoform 2 is specifically expressed in oocytes during their growth (at protein level). Mice lacking isoform 2 are viable and males are fertile. However, females are sterile, their oocytes displaying meiotic spindle defects. An MT-C retrotransposon in intron 6 of the mouse DICER gene functions as a promoter producing a transcript lacking exons 1 to 6. A new alternative first exon is directly derived from the retrotransposon. Belongs to the helicase family. Dicer subfamily. It is uncertain whether Met-1 or Met-11 is the initiator. Truncated N-terminus.