Associated Papers
UPF3B modulates endoplasmic reticulum stress through interaction with inositol-requiring enzyme-1α.
Sun X et al.
Cell Death & Disease, 2024
Expanding the phenotype of UPF3B-related disorder: Case reports and literature review.
Romano F et al.
American Journal of Medical Genetics. Part A, 2024
Nonsense-Mediated mRNA Decay Factor Functions in Human Health and Disease.
Sun L et al.
Biomedicines, 2023
Structures of nonsense-mediated mRNA decay factors UPF3B and UPF3A in complex with UPF2 reveal molecular basis for competitive binding and for neurodevelopmental disorder-causing mutation.
Bufton JC et al.
Nucleic Acids Research, 2022
No-nonsense: insights into the functional interplay of nonsense-mediated mRNA decay factors.
Mailliot J et al.
The Biochemical Journal, 2022
Functional roles of human Up-frameshift suppressor 3 (UPF3) proteins: From nonsense-mediated mRNA decay to neurodevelopmental disorders.
Deka B et al.
Biochimie, 2021
Systematic analysis of the intersection of disease mutations with protein modifications.
Simpson CM et al.
Bmc Medical Genomics, 2019
31345222 (PubMed )
Supplement: 12920_2019_543_MOESM6_ESM.xlsx › S5A
15 years of PhosphoSitePlus®: integrating post-translationally modified sites, disease variants and isoforms.
Hornbeck PV et al.
Nucleic Acids Research, 2019
30445427 (PubMed )
Supplement: gky1159_supplemental_files.xlsx › SupplT1
Full UPF3B function is critical for neuronal differentiation of neural stem cells.
Alrahbeni T et al.
Molecular Brain, 2015
Reproducible Analysis of Post-Translational Modifications in Proteomes--Application to Human Mutations.
Holehouse AS et al.
Plos One, 2015
26659599 (PubMed )
Supplement: pone.0144692.s002.xlsx › suppTable_2.txt
Genome-wide analysis to predict protein sequence variations that change phosphorylation sites or their corresponding kinases.
Ryu GM et al.
Nucleic Acids Research, 2009
19139070 (PubMed )
Supplement: gkn1008_nar-01723-s-2008-File009.xls › TypeI-
Mutations in UPF3B, a member of the nonsense-mediated mRNA decay complex, cause syndromic and nonsyndromic mental retardation.
Tarpey PS et al.
Nature Genetics, 2007
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