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1 mor suppressor activity that is unrelated to protease inhibition.
2 preventive and/or therapeutic properties via protease inhibition.
3 Arg32 in the Kunitz-1 domain is critical for protease inhibition.
4 4-beta5 or beta5-beta6 loops are involved in protease inhibition.
5 ructures reveal a similar novel mechanism of protease inhibition.
6 atine-core unit, characteristic for aspartic protease inhibition.
7 nzymes as evidenced from their resilience to protease inhibition.
8  management, inhibition of inflammation, and protease inhibition.
9 ntermediate that may be populated during the protease inhibition.
10 de structural insight into antibody-mediated protease inhibition.
11 pathway (UPP), metallothionein function, and protease inhibition.
12  SBT propeptides with respect to its mode of protease inhibition.
13 nprecedented manner in the field of aspartyl protease inhibition.
14 ion does not involve the serpin mechanism of protease inhibition.
15 e optimal choice to study SLPI-based in vivo protease inhibition.
16  proteins involved in protein processing and protease inhibition.
17 s a functional motif characterized by serine protease inhibition activity in a number of whey acidic
18 ration, inflammation, matrix production, and protease inhibition, all critical to wound healing.
19 being shown to display functions beyond both protease inhibition and anti-infective activity, to whic
20 drophilic functionalities as P2' show potent protease inhibition and antiviral activities against HIV
21 s has been synthesized and evaluated for HIV protease inhibition and antiviral activity.
22 in domains, suggesting direct involvement in protease inhibition and axonal migration, respectively.
23 ng-based biomarker assay to assess real-time protease inhibition and disease progression in a preclin
24                    A tradeoff between serine protease inhibition and growth as well as an indirect tr
25                                              Protease inhibition and laser confocal microscopy associ
26  receptor class B-type I (SR-B1), HCV-NS3/4A protease inhibition, and anti-HBV polymerase activity we
27                  Na+/H+ exchange inhibition, protease inhibition, and Ca(2+)-free buffer did not decr
28 ics may dictate the rate of insertion during protease inhibition, and thus whether it behaves as an i
29 ses and proteases, whereas genes involved in protease inhibition, angiogenesis, cross-linking of base
30 ation involving the coagulation response and protease inhibition, as well as lipid transport and meta
31  that of beta-lactones in ClpP peptidase and protease inhibition assays and displayed unique target s
32             His-1084 did not improve A2ML1's protease inhibition at pH 5, indicating that A2ML1's hyd
33 epend on cysteine protease activity, because protease inhibition blocks egress but not poration, and
34 ) had modest adverse effects on the cysteine protease inhibition but conferred potent activity agains
35 gment of mature falcipain-2 and suggest that protease inhibition, but not the mediation of folding, i
36 nd in neutrophil granules) is the target for protease inhibition by alpha1-antitrypsin, and its unopp
37 hanced hydroxyl reactivity can contribute to protease inhibition by an alphaM protein.
38                                              Protease inhibition by Glu-Asp-Leu is dependent on a pro
39  key roles in determining the specificity of protease inhibition by plasma serpins.
40 evented by anti-CD18 mAb, R15.7, and also by protease inhibition by PMSF.
41                                              Protease inhibition by secretory leukocyte protease inhi
42                                              Protease inhibition by serpins requires a large conforma
43  thermophoresis and analyzed acceleration of protease inhibition by these molecules.
44 the molecular mechanisms that drive cysteine protease inhibition by vinyl sulfones, the binding speci
45 host lysosomal cathepsin L, S and K cysteine proteases (inhibition constants < 10 nM).
46                                              Protease inhibition did not affect the release of active
47                                              Protease inhibition did not increase BRCA1 synthesis, no
48 restoration of expression via proteasome and protease inhibition did not rescue activity.
49 helix and strand 5A must be displaced during protease inhibition, displacement of strand 1C is requir
50 bin A-sheet is crucial for the last steps of protease inhibition either by affecting the rate of RCL
51 on the interim analysis of the Evaluation of Protease Inhibition for COVID-19 in High-Risk Patients (
52 vir/ritonavir, 950 placebo) in Evaluation of Protease Inhibition for COVID-19 in High-Risk Patients (
53                In the Paxlovid Evaluation of Protease Inhibition for COVID-19 in High-Risk Patients t
54 gh-Risk Patients (EPIC-HR) and Evaluation of Protease Inhibition for COVID-19 in Standard-Risk Patien
55                                       Serine protease inhibition greatly reduces the severity of pers
56 f alternative linkers led to greatly reduced protease inhibition; however, further functionalization
57  mechanism of caspase inhibition, as well as protease inhibition in general.
58 p (RSL) suggests that the role of the RSL in protease inhibition is more complex than that of present
59 ver a novel mechanism whereby loss of serine protease inhibition leads to lung lymphocyte accumulatio
60                   We demonstrated that MALT1 protease inhibition led to a reduction in the expression
61 easome inhibition and not serine or cysteine protease inhibition, likely through positive changes lat
62                               Enteral serine protease inhibition may be a potential therapeutic inter
63 to the potent mitogen Con A, suggesting that protease inhibition may inhibit T cell activation in vit
64 erized with respect to inhibition of various proteases, inhibition mechanisms, membrane permeability,
65 oxomicin in restoring function suggests that protease inhibition might have therapeutic value for thi
66                     We describe a new serine protease inhibition motif in which binding is mediated b
67  bond-mediated, active site-directed, serine protease inhibition motifs is revealed in a set of over
68 njury and post-injury treatment with TTX and protease inhibition on proteolysis of the NaCh alpha-sub
69 on and was used to demonstrate the effect of protease inhibition on the quaternary structure of the e
70      The N-palmitoyl moiety is essential for protease inhibition; optimization of the peptide sequenc
71                 HBD2 did not show any direct protease inhibition or induce expression of known antipr
72 cules modulate the ER stress pathway through protease inhibition or lipid metabolism interference.
73                                       Either protease inhibition or MT1-MMP siRNA depletion moderatel
74 t the autophagic vacuoles accumulating after protease inhibition or prolonged vinblastine treatment s
75  57-kDa zymogens in the BHK media shared MMP protease inhibition patterns and MMP-2 immunoreactivitie
76                             Furthermore, the protease inhibition profile of Ced-3 was similar to the
77 ibition or off-target serine and/or cysteine protease inhibition remains unresolved.
78                                              Protease inhibition rescued the nuclear piston mechanism
79 D50 values of 0.32 and 0.75 microM for HIV-1 protease inhibition, respectively, and two other inhibit
80                             Results from the protease inhibition studies and the site-directed mutage
81                   We analyzed the effects of protease inhibition, substrate modification, and neurona
82        Here, we present a novel mechanism of protease inhibition that relies on active-site-directed
83 e findings extend our view on multicomponent protease inhibition that until now has mainly relied on
84 its tumor suppressor activity extends beyond protease inhibition to include direct modulation of tumo
85 he efficacy of remdesivir as well as TMPRSS2 protease inhibition, validating a putative mechanism use
86 revious research has revealed legumain (C13) protease inhibition via a carboxy-extended phytocystatin