As an RNA helicase, unwinds RNA and alters RNA structuresthrough ATP binding and hydrolysis. Involved in multiple cellularprocesses, including pre-mRNA splicing, alternative splicing, ribosomalRNA processing and miRNA processing, as well as transcriptionregulation. Regulates the alternative splicing of exons exhibitingspecific features. For instance, promotes the inclusion of AC-richalternative exons in CD44 transcripts. This functionrequires the RNA helicase activity. Affects NFAT5 and histone macro-H2A. 1/MACROH2A1 alternative splicing in a CDK9-dependent manner. In NFAT5, promotes the introductionof alternative exon 4, which contains 2 stop codons and may targetNFAT5 exon 4-containing transcripts to nonsense-mediated mRNA decay, leading to the down-regulation of NFAT5 protein. Affects splicing of mediators of steroid hormone signaling pathway, including kinases that phosphorylates ESR1, such as CDK2, MAPK1 andGSK3B, and transcriptional regulators, such as CREBBP, MED1, NCOR1 andNCOR2. By affecting GSK3B splicing, participates in ESR1 and ARstabilization. In myoblasts and epithelial cells, cooperates with HNRNPH1 to control the splicing of specific subsets ofexons. In addition to binding mature mRNAs, alsointeracts with certain pri-microRNAs, including MIR663/miR-663a, MIR99B/miR-99b, and MIR6087/miR-6087. Binds pri-microRNAs on the 3' segment flanking the stem loop via the 5'-[ACG]CAUC[ACU]-3' consensus sequence. Required forthe production of subsets of microRNAs, including MIR21 and MIR125B1. May be involved not only inmicroRNA primary transcript processing, but also stabilization. Participates in MYC down-regulation at high cell densitythrough the production of MYC-targeting microRNAs. Along with DDX5, may be involved in the processing of the 32Sintermediate into the mature 28S ribosomal RNA. Promoter-specific transcription regulator, functioning as a coactivatoror corepressor depending on the context of the promoter and thetranscriptional complex in which it exists. EnhancesNFAT5 transcriptional activity. Synergizes with TP53in the activation of the MDM2 promoter; this activity requiresacetylation on lysine residues. May also coactivate MDM2 transcription through aTP53-independent pathway. Coactivates MMP7transcription. Along with CTNNB1, coactivates MYC, JUN, FOSL1 and cyclin D1/CCND1 transcription. Aloneor in combination with DDX5 and/or SRA1 non-coding RNA, plays acritical role in promoting the assembly of proteins required for theformation of the transcription initiation complex and chromatinremodeling leading to coactivation of MYOD1-dependent transcription. This helicase-independent activity is required for skeletal musclecells to properly differentiate into myotubes. During epithelial-to-mesenchymal transition, coregulates SMAD-dependent transcriptional activity, directlycontrolling key effectors of differentiation, including miRNAs which inturn directly repress its expression. Plays a role inestrogen and testosterone signaling pathway at several levels. Mediatesthe use of alternative promoters in estrogen-responsive genes andregulates transcription and splicing of a large number of steroidhormone target genes. Contrary to splicing regulationactivity, transcriptional coregulation of the estrogen receptor ESR1 ishelicase-independent. Plays a rolein innate immunity. Specifically restricts bunyavirus infection, including Rift Valley fever virus (RVFV) or La Crosse virus (LACV), butnot vesicular stomatitis virus (VSV), in an interferon- and DROSHA-independent manner. Binds to RVFV RNA, likely viastructured viral RNA elements. Promotes mRNAdegradation mediated by the antiviral zinc-finger protein ZC3HAV1, inan ATPase-dependent manner. [1-5]

MPTGFVAPILCVLLPSPTREAATVASATGDSASERESAAPAAAPTAEAPPPSVVTRPEPQALPSPAIRAPLPDLYPFGTMRGGGFGDRDRDRDRGGFGARGGGGLPPKKFGNPGERLRKKKWDLSELPKFEKNFYVEHPEVARLTPYEVDELRRKKEITVRGGDVCPKPVFAFHHANFPQYVMDVLMDQHFTEPTPIQCQGFPLALSGRDMVGIAQTGSGKTLAYLLPAIVHINHQPYLERGDGPICLVLAPTRELAQQVQQVADDYGKCSRLKSTCIYGGAPKGPQIRDLERGVEICIATPGRLIDFLESGKTNLRRCTYLVLDEADRMLDMGFEPQIRKIVDQIRPDRQTLMWSATWPKEVRQLAEDFLRDYTQINVGNLELSANHNILQIVDVCMESEKDHKLIQLMEEIMAEKENKTIIFVETKRRCDDLTRRMRRDGWPAMCIHGDKSQPERDWVLNEFRSGKAPILIATDVASRGLDVEDVKFVINYDYPNSSEDYVHRIGRTARSTNKGTAYTFFTPGNLKQARELIKVLEEANQAINPKLMQLVDHRGGGGGGGGRSRYRTTSSANNPNLMYQDECDRRLRGVKDGGRRDSASYRDRSETDRAGYANGSGYGSPNSAFGAQAGQYTYGQGTYGAAAYGTSSYTAQEYGAGTYGASSTTSTGRSSQSSSQQFSGIGRSGQQPQPLMSQQFAQPPGATNMIGYMGQTAYQYPPPPPPPPPSRK