Post-transcriptional repressor of mRNAs containing a conserved stem loop motif, called constitutive decay element (CDE), which is often located in the 3'-UTR, as in HMGXB3, ICOS, IER3, NFKBID, NFKBIZ, PPP1R10, TNF and in many more mRNAs. Binds to CDE and promotes mRNA deadenylation and degradation. This process does not involve miRNAs (PubMed:23663784). In follicular helper T (Tfh) cells, represses of ICOS and TNFRSF4 expression, thus preventing spontaneous Tfh cell differentiation, germinal center B-cell differentiation in the absence of immunization and autoimmunity. In resting or LPS-stimulated macrophages, controls inflammation by suppressing TNF expression. Also recognizes CDE in its own mRNA and in that of paralogous RC3H1, possibly leading to feedback loop regulation (PubMed:23583643, PubMed:23583642). Inhibits cooperatively with ZC3H12A the differentiation of helper T cells Th17 in lungs. They repress target mRNA encoding the Th17 cell-promoting factors IL6, ICOS, REL, IRF4, NFKBID and NFKBIZ. The cooperation requires RNA-binding by RC3H1 and the nuclease activity of ZC3H12A (PubMed:25282160). miRNA-binding protein that regulates microRNA homeostasis. Enhances DICER-mediated processing of pre-MIR146a but reduces mature MIR146a levels through an increase of 3' end uridylation. Both inhibits ICOS mRNA expression and they may act together to exert the suppression (PubMed:25697406). Acts as a ubiquitin E3 ligase. Pairs with E2 enzymes UBE2B, UBE2D2, UBE2E2, UBE2E3, UBE2G2, UBE2K and UBE2Q2 and produces polyubiquitin chains. Shows the strongest activity when paired with UBE2N:UBE2V1 or UBE2N:UBE2V2 E2 complexes and generate both short and long polyubiquitin chains. Involved in the ubiquitination of MAP3K5 (By similarity). Able to interact with double-stranded RNA (dsRNA). S-ubiquitinyl-[E2 ubiquitin-conjugating enzyme]-L-cysteine + [acceptor protein]-L-lysine = [E2 ubiquitin-conjugating enzyme]-L-cysteine + N(6)-ubiquitinyl-[acceptor protein]-L-lysine. Binding to dsRNA, but not CDE RNA, crosstalks with the E3 ubiquitin ligase activity and may inhibit ubiquitination. Protein modification; protein ubiquitination. Interacts with EDC4 (PubMed:23583643). Interacts with CCR4-NOT deadenylase complex (PubMed:23663784). Interacts with MAP3K5; the interaction is probably stimulus-dependent (By similarity). During stress, such as that induced by arsenite, localizes to cytosolic stress granules. Localization to stress granules, but not to P-bodies, depends upon the RING-type zinc finger. Highest levels in lymph node and thymus and slightly lesser amounts in brain, lung, and spleen (at protein level). Very weak expression in heart, muscle, and kidney (at protein level). Expressed in CD4(+) helper T-cells (at protein level). The RING-type zinc finger is required for proper localization to stress granules, but not to P-bodies. The ROQ region is required for CDE RNA-binding. Has 2 separate RNA-binding sites, one for CDE RNA and the other for dsRNA (PubMed:23663784). It may also be involved in localization to stress granules (By similarity). HEPN (higher eukaryotes and prokaryotes nucleotide-binding) are observed in both N- and C-terminal sides of ROQ domain with 3D structure even if they are poredcted on the basis of sequence. Proteolytically cleaved by MALT1 in activated CD4(+) T cells; cleavage at Arg-509 is critical for promoting RC3H1 degradation in response to T-cell receptor (TCR) stimulation, and hence is necessary for prolonging the stability of a set of mRNAs controlling Th17 cell differentiation. Mutant animals are born at Mendelian ratio, but very few reach adulthood, a large proportion die within the first days after birth. Lethality can be rescued by changing the genetic background from C57BL/6 to outbred NMRI, on which mutant animals appear healthy and fertile, although smaller. Immune cell homeostasis is normal (PubMed:23583643). However, Mice lacking both Rc3h1 and Rc3h2 genes in CD4(+) T-cells develop lymphadenopathy and splenomegaly with increased spleen weight and cellularity, already at young age. They show a prominent lung pathology with a progressive reduction in the alveolar space concomitant with inflammation. They show an average survival of 130 days. CD4(+) T-cells of these mutants show a pronounced bias toward Th17 differentiation (PubMed:23583643, PubMed:25282160).