1 ppaB pathway caused IFN-I hyperinduction and rendered cells and mice substantially more resistant to
2 s p53 for the stress response, but this also renders cells dependent on PEPD for survival, as it supp
3 ptotic Bcl-2 family member ratio by acidosis renders cells exquisitely sensitive to the Bcl-2/Bcl-xL
4 s induced changes in cellular morphology and rendered cells growth-factor independent by upregulating
5 mpaired the accuracy of mRNA translation and rendered cells highly sensitive to oxidative stress.
6 usly reported that loss of function of TORC2 renders cells highly sensitive to DNA replication stress
7 the UPR, but the resulting protein overload rendered cells hypersensitive to ER stress induced by ei
8 In consequence, loss of diphthamide rendered cells hypersensitive toward TNF-mediated apopto
9 utation) imparts a dominant negative effect, rendering cells hypersensitive to agents that cause DNA
10 NA2, in mutp53-R273H-expressing cancer cells renders cells hypersensitive to cisplatin.
11 , Stat1 inhibits cell proliferation but also renders cells increasingly resistant to antiproliferativ
12 on, block production of the Prg adhesins and render cells insensitive to pheromone.
13 onserved cysteine residues to serine in Ssa1 rendered cells insensitive to Hsf1 activation and subseq
14 ISRIB, a potent drug-like small molecule, renders cells insensitive to eIF2alpha phosphorylation a
15 viability in constant light conditions, but renders cells inviable in cycling conditions when light
16 vacuolar morphogenesis and loss of function renders cells largely insensitive to auxin-dependent gro
17 -of-function study showed that MTP depletion rendered cells less responsive to alpha interferon (IFN-
18 he recruitment of 53BP1, and decreases NHEJ, rendering cells more sensitive to DSBs.
19 gion to lower Cyclin D synthesis rates, thus rendering cells more susceptible to cycling.
20 Noise in gene expression renders cells more adaptable to changing environment by
21 he high-altitude variant of CDT1 (Ala537Val) renders cells more resistant to UV irradiation, and the
22 Interestingly, UVRAG(FS) expression renders cells more sensitive to standard chemotherapy re
23 oxia, whereas stable silencing of the enzyme renders cells more susceptible to apoptosis.
24 nduces a global relaxation of chromatin that renders cells more susceptible to DSB formation, while c
25 ART-18 function in an EBV(+) tumor cell line renders cells more susceptible to IFN-mediated effects.
26 Finally, knockdown renders cells more susceptible to the Hsp90 inhibitor 17
27 ciency reduces antiviral gene expression and renders cells more susceptible to viruses.
28 redicted N-glycosylated asparagines of FlgA1 renders cells nonmotile, providing direct evidence for t
29 ion, and reveal the critical role of InlB in rendering cells permissive to InlA-mediated invasion.
30 NA to inhibit PY-STAT1 nuclear transport and render cells refractory to IFNs.
31 similarly activated the Surivin promoter and rendered cells refractory to further promoter activation
32 e likely by stabilizing the Myc protein, and rendered cells resistant to dexamethasone, which was rev
33 hthamide prevented ADP ribosylation of eEF2, rendered cells resistant to PE and DT, but does not affe
34 reatment or silencing Epac-1 gene expression rendered cells resistant to viral infection.
35 upts proximal Fas signaling events, but also renders cells resistant to Fas-mediated apoptosis.
36 AIL)-induced apoptosis, and knockdown of CAS renders cells resistant to TRAIL.
37 (G12V)-induced mitochondrial dysfunction and renders cells resistant to transformation.
38 ond signal such as IFN-gamma was required to render cells responsive to exogenous IL-32gamma; importa
39 mpromised DNA DSB repair in human cells, and rendered cells sensitive toward a radiomimetic agent, ne
40 is possible, but results in slow growth and renders cells sensitive to DNA damaging agents.
41 Disruption of complex III renders cells sensitive to H(2)O(2) but not to the super
42 diated NHEJ of tyrosine blocked termini, and renders cells sensitive to the anticancer agent etoposid
43 ccessibility and nucleosome positioning that render cells susceptible to lineage transition.
44 es, and DARC overexpression is sufficient to render cells susceptible to toxin-mediated lysis.
45 F2K-mediated inhibition of protein synthesis renders cells susceptible to apoptosis and functions to
46 Loss of Lto1 function renders cells susceptible to hydroperoxide pro-oxidants,
47 ten considered a pro-survival mechanism that renders cells viable in stressful conditions and thus mi
48 activation, metabolic stress represses HSF1, rendering cells vulnerable to proteotoxic stress.
49 tors abrogates GNA13-induced TIC phenotypes, rendering cells vulnerable to standard-of-care cytotoxic
50 Here we show that lack of arginylation renders cells vulnerable to purine nucleotide synthesis
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