protein
| interacting with DCP2 |
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interacting with SMG6 |
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binding to ERF1 and to the GTPase domain of ERF3 both in its GTP- and GDP-bound states |
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in the UPF trimeric complex, UPF2 and UPF3B cooperatively stimulate both ATPase and RNA helicase activities of UPF1 (pMID: 18066079) |
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association with the cap-binding protein, NCBP1, promotes nonsense-mediated mRNA decay at two distinct steps |
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upon binding to UPF2, the regulatory CH domain of UPF1 undergoes a large conformational change, causing the catalytic helicase domain to bind RNA less extensively and triggering its helicase activity |
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association with telomeres is stimulated by the phosphoinositide 3-kinase (PI3K)-related protein kinase ataxia telangiectasia mutated and Rad3-related (ATR) and by telomere elongation |
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physically interacts with the telomeric factor TPP1 and with telomerase |
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recruitment of STAU2 alone or in combination with UPF1 differentially affects the fate of mRNAs |
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similarly to UPF1 and UPF2, PTBP3 is required for the destabilization of a known nonsense-mediated mRNA decay (NMD) substrate |
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also interacts with proteins associated with nuclear RNA degradation and transcription termination |
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MARVELD1 promotes the dissociation of SMG1 from UPF1, resulting in the repression of serine phosphorylation of UPF1 |
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MOV10 functions in UPF1-mediated mRNA degradation as an RNA clearance factor to resolve structures and displace proteins from 3prime UTRs |
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SMG1C (a complex containing SMG1, SMG8, and SMG9) contributes to regulate NMD by recruiting UPF1 and UPF2 to distinct sites in the vicinity of the kinase domain |
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endonuclease SMG6, which cleaves mRNA near the premature translation-termination codons (PTCs), is one of the three known NMD factors thought to be recruited to nonsense mRNAs via an interaction with P-UPF1, leading to eventual mRNA degradation |
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DHX34 is recruited to the SURF complex via its preferential interaction with hypophosphorylated UPF1 |
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UPF1 is recruited to the SMG1 kinase domain and C-terminal insertion domain, inducing an opening of the head domain that provides access to the active site |
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ability of UPF1 to impinge on premature termination, moreover, requires ATP-binding, RNA-binding and NMD cofactors UPF2 and UPF3 |
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UPF1 and ribosomes are new interaction partners of UPF3B |
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mRNA repressor TRIM71 cooperates with Nonsense-Mediated Decay factors SMG1, SMG7, UPF1 to destabilize the mRNA of CDKN1A |
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SMG8 and SMG9 act, in addition to serving as a scaffold for the interaction between SMG1 and UPF1, to negatively regulate SMG1 kinase activity and maintain UPF1 in the unphosphorylated (inactive) form within the SURF complex |