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Study showed that a genetic variant in the 5' UTR of DDX39B (show DDX39 Proteins) reduces translation of DDX39B (show DDX39 Proteins) mRNAs and increases multiple sclerosis (MS) risk. Importantly, this DDX39B (show DDX39 Proteins) variant showed strong genetic & functional epistasis with allelic variants in IL7R (show IL7R Proteins) exon 6; study establishes the occurrence of biological epistasis in humans & provides mechanistic insight into the regulation of IL7R (show IL7R Proteins) exon 6 splicing & its impact on MS risk.
DDX39B (show DDX39 Proteins) and its paralog DDX39A (show DDX39 Proteins) regulate androgen receptor (show AR Proteins) splice variant AR-V7 generation
Distinct features of RNA influence and ATPase efficiency between UAP56 and TcSub2 may reflect distinct structures for functional sites of TcSub2. For this reason, ligand-based or structure-based methodologies can be applied to investigate the potential of TcSub2 as a target for new drugs.
However, no significant association was observed between the DDX39B (show DDX39 Proteins) -22 G/C polymorphism in the cases and controls. Furthermore, it is clarified that the protective effect of IL-4 (show IL4 Proteins) -590 is independent from APOE (show APOE Proteins) protective genotypes
The G allele of DDX39B (show DDX39 Proteins)-22C > G was associated with absent or decreased manifestations of vivax malaria and the C allele was a risk factor for disease complications.
We unravel the role of unexplored immunologically important genes, BAT1 (show DDX39 Proteins) and BTNL2 (show BTNL2 Proteins), and the haplotypes of the significantly associated SNPs therein, to understand susceptibility to the disease, leprosy and its differential severity.
these data identify UAP56 as an important binding partner of Bcr (show BCR Proteins) and a novel target for inhibiting vascular smooth muscle cell proliferation.
UAP56 and URH49 (show DDX39 Proteins) exhibit an intrinsic CRM1 (show XPO1 Proteins)-independent nucleocytoplasmic shuttling
Mx proteins exert their antiviral activity against IAV by interfering with the function of the RNA helicases UAP56 and URH49 (show DDX39 Proteins)
In summary, these data demonstrate that UAP56 is utilized by influenza A viruses to prevent the formation of dsRNA and, hence, the activation of the innate immune response.
These results imply that murine leukemia virus requires UAP56, THOC5 (show THOC5 Proteins) and THOC7 (show THOC7 Proteins), in addition to NXF1 (show NXF1 Proteins), for nuclear export of viral transcripts.
This gene encodes a member of the DEAD box family of RNA-dependent ATPases that mediate ATP hydrolysis during pre-mRNA splicing. The encoded protein is an essential splicing factor required for association of U2 small nuclear ribonucleoprotein with pre-mRNA, and it also plays an important role in mRNA export from the nucleus to the cytoplasm. This gene belongs to a cluster of genes localized in the vicinity of the genes encoding tumor necrosis factor alpha and tumor necrosis factor beta. These genes are all within the human major histocompatibility complex class III region. Mutations in this gene may be associated with rheumatoid arthritis. Alternative splicing results in multiple transcript variants. Related pseudogenes have been identified on both chromosomes 6 and 11. Read-through transcription also occurs between this gene and the upstream ATP6V1G2 (ATPase, H+ transporting, lysosomal 13kDa, V1 subunit G2) gene.
56 kDa U2AF65-associated protein
, ATP-dependent RNA helicase p47
, HLA-B-associated transcript 1 protein
, nuclear RNA helicase (DEAD family)
, spliceosome RNA helicase BAT1
, spliceosome RNA helicase DDX39B
, DEAD box protein UAP56
, DEADD box protein
, HLA-B associated transcript 1
, HLA-B-associated transcript 1A
, nuclear RNA helicase Bat1
, spliceosome RNA helicase Bat1
, spliceosome RNA helicase Ddx39b
, HLA-B associated transcript 1A
, Nuclear RNA helicase