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UPF3B encodes a protein that is part of a post-splicing multiprotein complex involved in both mRNA nuclear export and mRNA surveillance. Additionally we are shipping UPF3B Antibodies (18) and many more products for this protein.
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UPF3B gene mutation is associated with Lujan-Fryns syndrome.
the neurodevelopmental phenotype of UPF3B missense mutation is caused by impairment of nonsense-mediated mRNA decay pathway function altering neuronal differentiation.
These findings indicate that SATB2 (show SATB2 Proteins) activates UPF3B expression through binding to its promoter.
Data indicate the mutation p.R430X of UPF3B gene as the genetic etiology in the mental retardation pedigree.
results demonstrate that the UPF3B-dependent NMD pathway is a major regulator of the transcriptome and that its targets have important roles in neuronal cells.
The two cases with renal dysplasia and developmental delay showed remarkable clinical variability despite having the same mutation in UPF3B.
Our results demonstrate that in addition to Lujan-Fryns and FG syndromes, UPF3B protein truncation mutations can cause also nonspecific XLMR (show DLG3 Proteins).
3.4 A resolution crystal structure of a minimal UPF3b-EJC assembly, consisting of the interacting domains of five proteins (UPF3b, MAGO (show MAGOHB Proteins), Y14 (show RBM8A Proteins), eIF4AIII (show EIF4A3 Proteins), and Barentsz (show CASC3 Proteins)) together with RNA and adenylyl-imidodiphosphate
A conserved domain of hUpf3b mediates an interaction with the EJC protein Y14 (show RBM8A Proteins). Y14 (show RBM8A Proteins) is required for nonsense-mediated decay induced by tethered hUpf3b.
The protein region that mediates this interaction and discriminates between hUpf3a (show UPF3A Proteins) and hUpf3b in NMD function is located in the C-terminal domain and fully contained within a small sequence that is highly conserved in Upf3b but not Upf3a (show UPF3A Proteins) proteins
Analysis revealed that UPF3A (show UPF3A Proteins) is a broadly acting nonsense-mediated RNA decay inhibitor. This discovery implies that UPF3A (show UPF3A Proteins) and UPF3B do not primarily work in a complementary or redundant manner as previously supposed; instead, they oppose each other, allowing this paralog pair to serve as a molecular rheostat to modulate the level of gene expression during development.
Evidence suggests Upf3b-dependent nonsense-mediated mRNA decay is regulated at multiple levels during development including regulation of expression and sub-cellular localization of Upf3b.
This gene encodes a protein that is part of a post-splicing multiprotein complex involved in both mRNA nuclear export and mRNA surveillance. The encoded protein is one of two functional homologs to yeast Upf3p. mRNA surveillance detects exported mRNAs with truncated open reading frames and initiates nonsense-mediated mRNA decay (NMD). When translation ends upstream from the last exon-exon junction, this triggers NMD to degrade mRNAs containing premature stop codons. This protein binds to the mRNA and remains bound after nuclear export, acting as a nucleocytoplasmic shuttling protein. It forms with Y14 a complex that binds specifically 20 nt upstream of exon-exon junctions. This gene is located on the long arm of chromosome X. Two splice variants encoding different isoforms have been found for this gene.
, nonsense mRNA reducing factor 3B
, regulator of nonsense transcripts 3B
, up-frameshift suppressor 3 homolog B
, up-frameshift suppressor 3 homolog on chromosome X