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1 er neuronally or just axonally significantly impaired the ability of 24-h injury-conditioned sensory
2 nant interfering form of BimEL significantly impaired the ability of activated p75NTR to induce apopt
3 mediated suppression of BMPR-IB dramatically impaired the ability of ADAS to form bone in vitro.
4 und that loss of LKB1 in the liver partially impaired the ability of adiponectin to lower serum gluco
5       Loss of either G(z)alpha or G(i2)alpha impaired the ability of ADP and epinephrine to inhibit P
6                   Glucose deprivation, which impaired the ability of Akt to maintain mitochondrion-he
7 no acid residues (A76 and V77), dramatically impaired the ability of alpha-synuclein to polymerize in
8                           Each mutation also impaired the ability of alphaIIbbeta3 on affected platel
9                 Although bleomycin treatment impaired the ability of alveolar macrophages from wild-t
10 lation and phosphorylation by CKIepsilon and impaired the ability of APC to regulate beta-catenin.
11                                        Q386E impaired the ability of ASCT1 to bind acidic amino acids
12 in VDR at putative ATM phosphorylation sites impaired the ability of ATM to enhance VDR transactivati
13               Mutation of T74 only partially impaired the ability of Bcl-2 to block glucocorticoid-in
14  family members inhibited axis formation and impaired the ability of beta-catenin and XLef-1 to induc
15 uclear receptor corepressor motif (aa 86-95) impaired the ability of both truncated (aa 1-100) and fu
16      Furthermore, the downregulation of Cdk1 impaired the ability of both wild-type and mutant E6 to
17  lipid biosynthesis from acetate, perhaps by impairing the ability of CA to efficiently "trap" inorga
18  on the alpha3/switch II cleft of Galpha(i3) impaired the ability of Calnuc and NUCB2 to bind and act
19  in only one patch, P19K/I21E and Y22K/F84E, impaired the ability of calreticulin to suppress the the
20 ogation of the pSMAC formation significantly impaired the ability of CD8(+) but not CD4(+) CTL to lys
21 ic enzyme phosphoglycerate mutase-1 severely impaired the ability of CD8+ T cells to form long-term m
22                    Protein malnutrition also impaired the abilities of cells from vaccinated LP guine
23 xpression of the mutant BRG1 or BRM proteins impaired the ability of cells to activate the endogenous
24 and liposome-delivered blocking Ab, severely impaired the ability of cells to ingest IgG-opsonized ta
25 rm of RhoA, or in vitro ADP-ribosylated RhoA impaired the ability of cells to migrate.
26 ely, central antagonism of insulin signaling impaired the ability of circulating insulin to inhibit g
27      Point mutations affecting either domain impaired the ability of Cla4 to regulate cell morphogene
28 nish alveolar epithelial barrier function by impairing the ability of claudin-18 to interact with a s
29 ed cellular IL-6 and TNF-alpha responses and impaired the ability of co-stimulatory blockade to exten
30  kinase but not the VZV ORF47 protein kinase impaired the ability of coexpressed IE62 to transactivat
31  downstream synthesis of IL-6 and CCL-2, and impaired the ability of conditioned media from high gluc
32 easing MD activity during Pavlovian learning impaired the ability of conditioned stimuli to modulate
33                                         m138 impaired the ability of DC to activate CD8+ T cells.
34                      Moreover, EBOV and MARV impaired the ability of DCs to support T cell proliferat
35 f Cul-4A results in reduced p48 levels, thus impairing the ability of DDB in lesion recognition and D
36 oepithelin by siRNA and antisense strategies impaired the ability of DU145 cells to grow and migrate
37 nzyme IID subunit of this PTS, significantly impaired the ability of E. faecium to colonize the murin
38                            This substitution impaired the ability of echistatin to induce LIBS in alp
39                     CD98hc deletion markedly impaired the ability of embryonic stem cells to form ter
40 phorylation sites to phenylalanine partially impaired the ability of Ena to restore viability to ena
41 G protein subunit alpha13 (Galpha13) in mice impaired the ability of endothelial cells to develop int
42 of cell-surface integrin alpha(v)beta(3) and impaired the ability of endothelial cells to retain VWF
43  confirmed that infection with AdcaHIF1alpha impaired the ability of EPDCs to invade.
44 or a dominant negative ras mutant profoundly impaired the ability of EWS/FLI-1 to transform NIH3T3 ce
45                          Serotonin depletion impaired the ability of exendin-4, a clinically used GLP
46             Disruption of migR and fevR also impaired the ability of F. tularensis to prevent neutrop
47 ed that RNAi knockdown of GPAT significantly impaired the ability of females to attract males.
48 B, and complete ablation of the AOBs further impaired the ability of females to discriminate between
49    Mutations at this channel binding surface impaired the ability of FHFs to co-localize with Navs at
50                     RMTg lesions drastically impaired the ability of foot shock to suppress operant r
51 n of a dominant-negative PKCbetaII, markedly impaired the ability of FUS to bind DNA.
52 ion of intact cells with CD also drastically impaired the ability of galanin to activate intracellula
53 ations in either acetylation motif partially impaired the ability of GATA-1 to induce differentiation
54      Knockdown of EB1 expression using siRNA impaired the ability of GFP-MCAK to localize to MT tips
55   Furthermore, we found that Abeta treatment impaired the ability of GPCs from HC subjects to generat
56 r, depletion of Xena/XVASP proteins severely impaired the ability of growth cones to form branches wi
57         Prephosphorylating tau with cdk5/p25 impaired the ability of GSK3beta-R96A to phosphorylate t
58                   At ~10 microM all four APs impaired the ability of HBMECs to reduce MTT which was f
59 61 or siRNA in HBx-expressing cells severely impaired the ability of HBx to modulate the endogenous l
60 ound that the absence of c-Rel significantly impaired the ability of Helicobacter hepaticus to induce
61 CSF, but the removal of this region severely impaired the ability of hGM-CSF to support cell survival
62 tiomerization or linearization significantly impaired the ability of HNP1 and HD5 to kill Staphylococ
63 etin bound the C-terminal region of hnRNPA1, impairing the ability of hnRNPA1 to shuttle between the
64 f PD-L1 with programmed cell death protein 1 impaired the ability of HSCs to inhibit B cells.
65 that abolished binding to USP7 significantly impaired the ability of HSV-1 to replicate.
66           Only mutations in Phos 1, however, impaired the ability of ICP0 to complement the replicati
67 t became clear that the mutations identified impaired the ability of IDH1 and IDH2 to catalyze the co
68 set of cell-mediated immunity by selectively impairing the ability of infected macrophages to produce
69     Moreover, inhibition of RASSF1A by shRNA impaired the ability of K-Ras to activate Bax.
70              Lack of PLCgamma2 significantly impaired the ability of lineage-committed NK precursor c
71 nge with Escherichia coli endotoxin markedly impaired the ability of LMBO to reduce QLPA/QPA in wild-
72 nd mutations in or adjacent to this sequence impaired the ability of LMP1 or CD40 to induce NF-kappaB
73 dimethylated arginines within the RGG domain impaired the ability of Lsm4 to promote PB accumulation.
74 ion of ARF1 expression and activity markedly impaired the ability of M.D. Anderson-metastatic breast-
75 , the authors found that fornix transections impaired the ability of macaque monkeys (Macaca mulatta)
76         Interestingly, the blocking of VLA-4 impaired the ability of MBP-primed T cells to induce mic
77 rins on T cells or PDGF-Rbeta on glial cells impaired the ability of MBP-primed Th2 cells to induce g
78 ions targeting area 14, but not areas 11/13, impaired the ability of monkeys to learn to stop respond
79 mutation of Tyr188 to phenylalanine severely impaired the ability of mouse CD28 to deliver a costimul
80  mitochondria mediates insulin resistance by impairing the ability of muscle to oxidize fatty acids (
81 se of -1 frameshifting without substantially impairing the ability of mutant tRNA(Gly)(2) variants to
82 bet specifically in NKp46(+) ILCs profoundly impaired the ability of myelin-reactive TH17 cells to in
83 tidylinositol-3-kinase (PI3K), significantly impaired the ability of Nef to promote vIL-6-induced tum
84 substitution of E160 with uncharged residues impaired the ability of Nef to up-regulate the expressio
85 tamine 231 (Q231) by PEDV, and this cleavage impaired the ability of NEMO to activate downstream IFN
86        Importantly, down-regulation of Bmi-1 impaired the ability of neuroblastoma cells to grow in s
87 ertain mutations lethal to virus replication impaired the ability of nsp2 to inhibit NF-kappaB activa
88 eased expression of caveolin-2 significantly impaired the ability of P. aeruginosa to invade MLE-12 c
89 PRAK, disrupted the PRAK-p38 interaction and impaired the ability of p38alpha and p38beta to redistri
90 BRAF dependent phosphorylation sites in PAX3 impaired the ability of PAX3 to promote migration of C2C
91 alanine, serine, or asparagine significantly impaired the ability of PCNA to (i) support the RFC/PCNA
92                            In addition, they impaired the ability of PP1 to bind neurabin-I, the neur
93 ereas siRNA-mediated silencing of CD44v8-v10 impaired the ability of prostate cancer cells to form co
94 inding loop and C-terminal prenylation motif impaired the ability of R-Ras to regulate integrin funct
95  indicated that exposure to MA significantly impaired the ability of rats to use negative outcomes ef
96                     Finally, whole OSPW also impaired the ability of RAW 264.7 cells to perform phago
97 that c.202G > A and c.679G > A significantly impaired the ability of RHOXF2/2B to regulate downstream
98 ne/histidine-rich, putative E3 ligase domain impaired the ability of RTA to induce RelA ubiquitinatio
99 f Cys81 with serine or alanine significantly impaired the ability of S100A4 to promote myosin-IIA fil
100 regions, but not each region alone, markedly impaired the ability of Ski and SnoN to repress TGF-beta
101 or 474-494, either singly or in combination, impaired the ability of spinophilin to coprecipitate PP1
102                                         This impaired the ability of subjects to remember a face and
103 A (Toa2) at residue Y69 or W76 significantly impaired the ability of TFIIA to stimulate TBP-promoter
104 tivation of vPS cortex by cooling profoundly impaired the ability of the cats to recall the differenc
105                        Improper localization impaired the ability of the E1B 19K protein to inhibit a
106  of the PHD finger, but not the bromodomain, impaired the ability of the enzyme to acetylate histones
107  of M(1)dG in the EcoRI recognition sequence impaired the ability of the enzyme to cleave DNA, result
108 utations that reduced ssDNA or Rad51 binding impaired the ability of the fusion proteins to function
109 tions in Rab3a were identified that strongly impaired the ability of the GTP-bound form to interact w
110 block association of GCN2 with ribosomes and impaired the ability of the kinase to stimulate translat
111 se production, indicating that elevated FFAs impaired the ability of the liver to autoregulate.
112 E) greatly reduced MAT activity and severely impaired the ability of the MAT(alpha)1 subunits to form
113  of 200-fold and 480-fold, respectively, and impaired the ability of the mutant enzymes to stabilize
114 , showing that NS1 mutations D189N and V194I impaired the ability of the NS1 protein to inhibit gener
115                NS1 mutations D189N and V194I impaired the ability of the NS1 protein to inhibit gener
116 tation into a pem1Delta pem2Delta background impaired the ability of the resulting strain to grow wit
117 teractions between the VDR and LEF1 but also impaired the ability of the VDR to enhance Wnt signaling
118 f or the lysine required for kinase activity impaired the ability of the virus to stabilize and phosp
119 tes the sigma(W) stress response, perhaps by impairing the ability of the cell wall biosynthetic mach
120 rce production increased with walking speed, impairing the ability of the muscle to produce high peak
121  of Ca2+ extrusion/sequestration mechanisms, impairing the ability of the neuron to restore resting [
122 re conformationally altered at the NPT, thus impairing the ability of the protein to activate transcr
123 s with antago-205 increased SHIP2 levels and impaired the ability of these cells to seal linear scrat
124 e-binding function of CD3 zeta significantly impaired the ability of this invariant chain to accumula
125 ne 1006 of VEGFR-2 to phenylalanine severely impaired the ability of this receptor to stimulate endot
126                               NAPQI strongly impaired the ability of topoisomerase IIalpha to reseal
127                         Fibulin-2 deficiency impaired the ability of tumor cells to migrate and invad
128 our blocks within the W region substantially impaired the ability of UhpA to bind to this region, to
129      However, disruption of IF significantly impaired the ability of uninjured small-sized DRG neuron
130   Specifically, deletion of the cpxRA operon impaired the ability of UTI89 to colonize the murine bla
131 e of functional tumor-reactive T cells, thus impairing the ability of vaccines to elicit effective an
132 rved metal ion-dependent adhesion site motif impaired the ability of VWA to potentiate TMEM16A activi
133 l OM due to NTHi, whereas a CCL3-blocking Ab impaired the ability of wild-type mice to recover from O

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