| Genetic compensation response could exist in colorectal cancer: UPF3A upregulates the oncogenic homologue gene SRSF3 expression corresponding to SRSF6 to promote colorectal cancer metastasis. | Genetic compensation response could exist in colorectal cancer: UPF3A upregulates the oncogenic homologue gene SRSF3 expression corresponding to SRSF6 to promote colorectal cancer metastasis.
Xu W, Ou W, Feng Y, Xu Q, Yang Y, Cui L, Du P. | 04/21/2023 |
| 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. | 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, Powers KT, Szeto JA, Toelzer C, Berger I, Schaffitzel C., Free PMC Article | 06/18/2022 |
| Mammalian UPF3A and UPF3B can activate nonsense-mediated mRNA decay independently of their exon junction complex binding. | Mammalian UPF3A and UPF3B can activate nonsense-mediated mRNA decay independently of their exon junction complex binding.
Yi Z, Arvola RM, Myers S, Dilsavor CN, Abu Alhasan R, Carter BN, Patton RD, Bundschuh R, Singh G., Free PMC Article | 05/21/2022 |
| Human UPF3A and UPF3B enable fault-tolerant activation of nonsense-mediated mRNA decay. | Human UPF3A and UPF3B enable fault-tolerant activation of nonsense-mediated mRNA decay.
Wallmeroth D, Lackmann JW, Kueckelmann S, Altmüller J, Dieterich C, Boehm V, Gehring NH., Free PMC Article | 05/21/2022 |
| (Phospho)proteomic Profiling of Microsatellite Unstable CRC Cells Reveals Alterations in Nuclear Signaling and Cholesterol Metabolism Caused by Frameshift Mutation of NMD Regulator UPF3A. | (Phospho)proteomic Profiling of Microsatellite Unstable CRC Cells Reveals Alterations in Nuclear Signaling and Cholesterol Metabolism Caused by Frameshift Mutation of NMD Regulator UPF3A.
Michalak M, Katzenmaier EM, Roeckel N, Woerner SM, Fuchs V, Warnken U, Yuan YP, Bork P, Neu-Yilik G, Kulozik A, von Knebel Doeberitz M, Kloor M, Kopitz J, Gebert J., Free PMC Article | 02/20/2021 |
| Study observed that CHERP and its binding partner SR140 are significantly upregulated in human clinical colorectal cancer tissues (CRC) and clarified how CHERP/SR140 exert an oncogenic role in CRC development partially through regulating expression of UPF3A variants. | U2-related proteins CHERP and SR140 contribute to colorectal tumorigenesis via alternative splicing regulation.
Wang Q, Wang Y, Liu Y, Zhang C, Luo Y, Guo R, Zhan Z, Wei N, Xie Z, Shen L, Wu G, Wu W, Feng Y. | 02/22/2020 |
| Results suggest that UPF3A levels are tightly regulated by a post-transcriptional switch to maintain appropriate levels of NMD substrates in cells containing different levels of UPF3B. | A UPF3-mediated regulatory switch that maintains RNA surveillance.
Chan WK, Bhalla AD, Le Hir H, Nguyen LS, Huang L, Gécz J, Wilkinson MF. | 01/21/2010 |
| The Upf complex communicates with the exon-junction complex and triggers nonsense-mediated decay in the cytoplasm. | Communication with the exon-junction complex and activation of nonsense-mediated decay by human Upf proteins occur in the cytoplasm.
Singh G, Jakob S, Kleedehn MG, Lykke-Andersen J. | 01/21/2010 |
| hUpf3a is much less active than hUpf3b to induce NMD and to stimulate translation | Functions of hUpf3a and hUpf3b in nonsense-mediated mRNA decay and translation.
Kunz JB, Neu-Yilik G, Hentze MW, Kulozik AE, Gehring NH., Free PMC Article | 01/21/2010 |
| The complex between the interacting domains of human UPF2 and UPF3b at a 1.95 A resolution. | The structural basis for the interaction between nonsense-mediated mRNA decay factors UPF2 and UPF3.
Kadlec J, Izaurralde E, Cusack S. | 01/21/2010 |
| binds to spliced mRNAs upstream of exon-exon junctions; is part of mRNP complexes that are ready for nuclear export and that participate in nonsense-mediated mRNA decay | Role of the nonsense-mediated decay factor hUpf3 in the splicing-dependent exon-exon junction complex.
Kim VN, Kataoka N, Dreyfuss G. | 09/27/2001 |