1 or in the biosynthesis of PPhiB, and thereby render cells accumulating BVR phytochrome deficient.
2 ppaB pathway caused IFN-I hyperinduction and rendered cells and mice substantially more resistant to
3 ne c-Myc stimulates glutamine metabolism and renders cells dependent on glutamine to sustain viabilit
4 ptotic Bcl-2 family member ratio by acidosis renders cells exquisitely sensitive to the Bcl-2/Bcl-xL
5 athway can promote this metabolic program to render cells glucose dependent.
6 Mutational inactivation of TolC renders cells highly susceptible to antibiotics and lead
7 ncated protein that is not secreted, thereby rendering cells hyperresponsive to interleukin-1beta sti
8 ed on upregulation of several receptors that render cells hypersensitive to angiogenic stimuli.
9 omologous recombination-mediated repair, and render cells hypersensitive to IR.
10 the UPR, but the resulting protein overload rendered cells hypersensitive to ER stress induced by ei
11 utation) imparts a dominant negative effect, rendering cells hypersensitive to agents that cause DNA
12 ryo fibroblasts affects S-phase progression, rendering cells hypersensitive to replication poisons.
13 onserved cysteine residues to serine in Ssa1 rendered cells insensitive to Hsf1 activation and subseq
14 and -independent routes, and ablation of p16 renders cells insensitive to an Hh inhibitor and increas
15 Replacement of total eIF2Bdelta with V1 renders cells insensitive to eIF2alpha phosphorylation;
16 In addition, the network renders cells insensitive to fluctuations in signaling a
17 the expense of ISGF3-mediated transcription, rendering cells less resistant to infection.
18 this approach, we demonstrate that soft ECMs render cells maximally sensitive to changes in RhoA acti
19 utations in DNA binding domains of ERCC1-XPF render cells more sensitive to the crosslinking agent mi
20 KT, stimulate cell growth and migration, and rendered cells more resistant to PDK1 and PI3K inhibitio
21 phenotype, delayed tumor growth in mice, and rendered cells more sensitive to EGFR-TKI.
22 Further, disruption of IGF1R rendered cells more susceptible to anoikis.
23 ing maturation of the autophagosome, thereby rendering cells more sensitive to nutrient deprivation o
24 gion to lower Cyclin D synthesis rates, thus rendering cells more susceptible to cycling.
25 ciency reduces antiviral gene expression and renders cells more susceptible to viruses.
26 redicted N-glycosylated asparagines of FlgA1 renders cells nonmotile, providing direct evidence for t
27 for establishment of spindle bipolarity and renders cells partially resistant to Eg5 inhibitors.
28 I-like receptor innate immune signaling that rendered cells permissive to secondary virus infection.
29 similarly activated the Surivin promoter and rendered cells refractory to further promoter activation
30 ogated cell migration in response to HGF but rendered cells resistant to apoptosis by cisplatin.
31 Expression of a triple-Glu zwint-1 mutant rendered cells resistant to AurB inhibition during prome
32 Notably, overexpression of IKKepsilon rendered cells resistant to cisplatin, whereas knockdown
33 screened in fission yeast for mutations that rendered cells resistant to overexpressed chk1(+).
34 reatment or silencing Epac-1 gene expression rendered cells resistant to viral infection.
35 stance and acts by sequestering antifungals, rendering cells resistant to their action.
36 cer cell lines, and genetic knockout of CTR1 renders cells resistant to cisplatin in vivo.
37 Absence of Bax/Bak renders cells resistant to mPTP opening and necrosis, ef
38 ion increases with increasing viral load and renders cells resistant to TRAIL-induced death.
39 TR) and sortilin receptor complex formation, rendering cells responsive to proneurotrophins.
40 retinoids and because epigenetic changes can render cells retinoid resistant.
41 gative breast cancer cells was sufficient to render cells susceptible to the PARP inhibitors ABT-888
42 rentially affect mitochondrial functions and render cells susceptible to the perturbation of cellular
43 ls of DeltaNp63alpha can be reduced, thereby rendering cells susceptible to cell death in the face of
44 F2K-mediated inhibition of protein synthesis renders cells susceptible to apoptosis and functions to
45 Loss of Lto1 function renders cells susceptible to hydroperoxide pro-oxidants,
46 , proximal to the Fe-S cluster domain, which renders cells temperature sensitive, closely mimics the
47 ultiple agents, whereas knockdown of miR-155 renders cells to apoptosis and enhances chemosensitivity
48 reduction in the rate of envelope growth and renders cells unable to regulate cell size properly in r
49 Autophagy is a protective mechanism that renders cells viable in stressful conditions.
50 activation, metabolic stress represses HSF1, rendering cells vulnerable to proteotoxic stress.
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