抗Human DDX39B 抗体:
抗Rat (Rattus) DDX39B 抗体:
抗Mouse (Murine) DDX39B 抗体:
Human Monoclonal DDX39B Primary Antibody for CyTOF, ELISA - ABIN4363868
Boehringer, Garcia-Mansfield, Singh, Bakkar, Pirrotte, Bowser: ALS Associated Mutations in Matrin 3 Alter Protein-Protein Interactions and Impede mRNA Nuclear Export. in Scientific reports 1970
DDX39B promotes proliferation and colony forming potential of cells and its levels are significantly elevated in diverse cancer types.DDX39B regulates the pre-ribosomal RNA levels.
Study showed that a genetic variant in the 5' UTR of DDX39B reduces translation of DDX39B mRNAs and increases multiple sclerosis (MS) risk. Importantly, this DDX39B variant showed strong genetic & functional epistasis with allelic variants in IL7R exon 6; study establishes the occurrence of biological epistasis in humans & provides mechanistic insight into the regulation of IL7R exon 6 splicing & its impact on MS risk.
DDX39B and its paralog DDX39A regulate androgen receptor 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 -22 G/C polymorphism in the cases and controls. Furthermore, it is clarified that the protective effect of IL-4 -590 is independent from APOE protective genotypes
The G allele of DDX39B-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 and BTNL2, 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 and a novel target for inhibiting vascular smooth muscle cell proliferation.
UAP56 and URH49 exhibit an intrinsic CRM1-independent nucleocytoplasmic shuttling
Mx proteins exert their antiviral activity against IAV by interfering with the function of the RNA helicases UAP56 and URH49
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 findings demonstrate that replication of the inlfuenza virus genome is followed by its encapsidation by NP in collaboration with its chaperone UAP56.
UAP56 binding was shown to represent a unique characteristic of members of the genus Cytomegalovirus that is required for efficient replication of HCMV and required for nuclear mRNA export.
Data show that the two closely related RNA helicases UAP56 and URH49 have evolved to form distinct mRNA export machineries, which regulate mitosis at different steps.
Using a UL69 viral mutant that is unable to bind UAP56 and URH49, the authors demonstrated that UL69's interaction with UAP56 or URH49 does not contribute to the growth phenotype associated with the UL69 deletion mutant.
UAP56 is an important regulator of protein synthesis and plays an important role in the regulation of cardiomyocyte growth.
BAT1 transcription on the 7.1 AH (diabetes-resistant ancestral haplotype)is modified by interactions involving DNA flanking positions -22 and -348 in the promotor
The structures of UAP56/Sub2(BAT1) reveal a unique spatial arrangement of the two conserved helicase domains, and ADP-binding induces significant conformational changes of key residues in the ATP-binding pocket
recruitment of the human TREX complex to spliced mRNA is not directly coupled to transcription, but is instead coupled to transcription indirectly through splicing
UAP56 provides a herpesviral regulatory protein with access to a conserved cellular transport system in order to promote nuclear export of unspliced RNA.
Ectopic UAP56 upregulated HSF4-controlled HSP25 and alpha B-crystallin proteins expression, while knocking down UAP56 by shRNA reversed it.
These results imply that murine leukemia virus requires UAP56, THOC5 and THOC7, in addition to NXF1, 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
, HLA-B associated transcript 1
, HLA-B associated transcript 1A
, HLA-B-associated transcript 1A
, Nuclear RNA helicase
, spliceosome RNA helicase Bat1
, spliceosome RNA helicase Ddx39b
, DEADD box protein
, nuclear RNA helicase Bat1
, DEAD (Asp-Glu-Ala-Asp) box polypeptide 39B