i.e. ppopT, dTTP analogue, most efficient inhibitor of NTPase activity among nucleotide derivaties, inhibits the ATP-dependent helicase reaction and also the ATP-independent duplex unwinding, structure of nucleic base and ribose fragment of NTP molecule have a slight effects on inhibitory properties
i.e. supinoxin or RX-5902, intervenes in the phosphorylated p68-beta-catenin signaling pathway by interacting with Tyr593 in SK-MEL-28 (human melanoma), MDA-MB-231 (human metastatic breast cancer), and WI-38 (human normal fetal lung fibroblasts) cell lines
the small molecule reduces RHA helicase activity in a dose-dependent and enantiomeric manner without affecting intrinsic ATPase activity, the RHA kinetics indicate a complex model. Only (S)-YK-4-279 reverses the EWS-FLI1 inhibition of RHA helicase activity. YK-4-279 inhibition of RHA binding to EWS-FLI1 alters the RNA binding profile of both proteins. EWS-FLI1 modulates RHA helicase activity causing changes in overall transcriptome processing
maximal inhibitory activity among diphosphate analogues, non-catalytic and catalytic conditions, inhibits the ATP-dependent helicase reaction but no effect on the ATP-independent duplex unwinding, structure of nucleic base and ribose fragment of NTP molecule have a slight effects on inhibitory properties
DHX8 is an RNA-specific helicase by showing that a poly(dA)10 DNA strand cannot displace Cy5-poly(A)10 from DHX8 in the presence of ADP-AlFx. The displacement of the probe with poly(A)10, poly(C)10, poly(G)10 and poly(U)10 RNA indicates that DHX8 has a preference for binding adenine-rich sequences as the rank ascending order of IC50 values is poly (A)10, poly(U)10, poly(C)10, poly(G)10
the affinity for RNA is over 90fold weaker in the absence of nucleotide and in the presence of ADP, the RNA affinity is too weak to determine. These results indicate that DHX8-mediated disruption of RNA interactions occurs through a series of alternating strong and weak RNA binding events controlled by ATP hydrolysis. Both full-length fl-DHX8 and truncated DHX8DELAT547 preferentially bind the purine nucleotides ADP and GDP, but are also able to bind CDP, TDP and UDP. RNA binding triggers DEAH and P-loop movement and stimulates ADP release
RNA-dependent ATPase activity is sensitive to high salt concentrations. Maximal activity is obtained in the absence of KCl, and it is inhibited 50% at 0.1 M KC1, completely inhibited at 0.3 M KCl
the Jab1 domain of the Prp8 proten can inhibit Brr2 by intermittently inserting a C-terminal tail in the enzyme's RNA-binding tunnel or activate the helicase after removal of this tail. Binding of the Prp8 Jab1 C-terminal tail at the Brr2 RNA binding tunnel is evolutionarily conserved, Brr2-Jab1 binding structure and analysis, overview. Jab1-based inhibition of Brr2 presumably takes effect in all eukaryotes but is implemented via organism-specific molecular contacts. Brr2 autoinhibition can act in concert with Jab1-mediated inhibition. The NTR and the Jab1 tail cooperate in inhibiting RNA binding by Brr2; the Jab1 domain of the Prp8 proten can inhibit Brr2 by intermittently inserting a C-terminal tail in the enzyme's RNA-binding tunnel or activate the helicase after removal of this tail. Binding of the Prp8 Jab1 C-terminal tail at the Brr2 RNA binding tunnel is evolutionarily conserved, Brr2-Jab1 binding structure and analysis, overview. Jab1-based inhibition of Brr2 presumably takes effect in all eukaryotes but is implemented via organism-specific molecular contacts. Brr2 autoinhibition can act in concert with Jab1-mediated inhibition.The NTR and the Jab1 tail cooperate in inhibiting RNA binding by Brr2
the Jab1 domain of the Prp8 proten can inhibit Brr2 by intermittently inserting a C-terminal tail in the enzyme's RNA-binding tunnel or activate the helicase after removal of this tail. Binding of the Prp8 Jab1 C-terminal tail at the Brr2 RNA binding tunnel is evolutionarily conserved, Brr2-Jab1 binding structure and analysis, overview. Jab1-based inhibition of Brr2 presumably takes effect in all eukaryotes but is implemented via organism-specific molecular contacts. Brr2 autoinhibition can act in concert with Jab1-mediated inhibition.The NTR and the Jab1 tail cooperate in inhibiting RNA binding by Brr2
inhibitory potential of sequences of NTPase/helicase motifs VI derived peptides and their deleted derivatives analyzed, NTP-binding and hydrolyzing site not involved
domain 2 of wild-type NS3 protein and domain 2 devoid of the loop structure used for inhibition studies on functions of protein kinase C (PKC), inhibitory potential towards the majority of protein kinase C isoforms shown
domain 2 of wild-type NS3 protein and domain 2 devoid of the loop structure used for inhibition studies on functions of protein kinase C (PKC), inhibitory potential towards the majority of protein kinase C isoforms shown
Brr2 can be autoinhibited via a large N-terminal region folding back onto its helicase core and autoactivated by a catalytically inactive C-terminal helicase cassette
selectivity profiling indicated the allosteric inhibitor 6-benzyl-3-[(2R)-2-(3-fluoropyridin-2-yl)-6-methyl-3,4-dihydro-2H-1-benzopyran-7-yl]-4,6-dihydropyrido[4,3-d]pyrimidine-2,7(1H,3H)-dione is more Brr2-selective than the RNA site binder 3-[5-[(Z)-(2-cyclohexyl-5-imino-7-oxo-5H-[1,3,4]thiadiazolo[3,2-a]pyrimidin-6(7H)-ylidene)methyl]furan-2-yl]benzoic acid
Comparison of the ATPase activities of UPF1_1 and UPF1_2 shows that a longer regulatory loop does not inhibit the catalytic activity of the helicase. In fact, UPF1_1 shows a marginally higher ATPase activity than UPF1_2. ATP-dependent helicase assays with UPF11 and UPF12 also show that the unwinding activity of UPF1 is not inhibited by a longer regulatory loop
Brr2 can be autoinhibited via a large N-terminal region folding back onto its helicase core and autoactivated by a catalytically inactive C-terminal helicase cassette. Effects of NTR truncations on Chaetomium thermophilum Brr2NC variants. Binding of N-terminal Brr2NC truncations to U4/U6 di-snRNA monitored by electrophoretic mobility shift assays and time courses of U4/U6 unwinding by Brr2NC variants, overview