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1 demonstrate that alpha1s haploinsufficiency renders cells and mice more resistant to infection by th
2 ion in specific resistance settings, RB loss rendered cells completely independent of these kinases.
3 chemical composition of the environment, it renders cells completely autonomous in their locomotive
4 s p53 for the stress response, but this also renders cells dependent on PEPD for survival, as it supp
5 s induced changes in cellular morphology and rendered cells growth-factor independent by upregulating
8 usly reported that loss of function of TORC2 renders cells highly sensitive to DNA replication stress
11 repair by homologous recombination (HR) and renders cells hypersensitive to poly (ADP-ribose) polyme
12 , Stat1 inhibits cell proliferation but also renders cells increasingly resistant to antiproliferativ
15 ISRIB, a potent drug-like small molecule, renders cells insensitive to eIF2alpha phosphorylation a
16 viability in constant light conditions, but renders cells inviable in cycling conditions when light
17 vacuolar morphogenesis and loss of function renders cells largely insensitive to auxin-dependent gro
18 ed cellular movement and invasion, moreover, rendered cells less stem cell-like through reducing mito
19 growth-promoting cell signaling pathways and rendering cells metabolically vulnerable, making it an e
20 5b (a critical effector of the Fgf pathway), rendering cells more responsive to dynamic changes in Fg
22 he high-altitude variant of CDT1 (Ala537Val) renders cells more resistant to UV irradiation, and the
23 nduces a global relaxation of chromatin that renders cells more susceptible to DSB formation, while c
24 ART-18 function in an EBV(+) tumor cell line renders cells more susceptible to IFN-mediated effects.
25 e show that differential ER stress induction renders cells more susceptible to Salmonella enterica se
26 antiapoptotic genes upon TNF stimulation and renders cells partially resistant to TNF-induced apoptos
28 elevates RS by upregulating c-Myc activity, rendering cells reliant on the ATR/CHK1 axis for surviva
29 Genetic ablation of the HLA-DR alpha-chain rendered cells resistant to infection by bat influenza A
31 hthamide prevented ADP ribosylation of eEF2, rendered cells resistant to PE and DT, but does not affe
34 inding partner beta 2 microglobulin (beta2M) renders cells resistant to infection by a panel of echov
38 iability, simultaneous deletion of all genes renders cells sensitive to cell wall interfering compoun
40 diated NHEJ of tyrosine blocked termini, and renders cells sensitive to the anticancer agent etoposid
41 members, SWS1 and SWSAP1, using CRISPR/Cas9, renders cells specifically sensitive to the replication
44 rt in BTSCs with high EAAT1/EAAT2 expression rendered cells susceptible to GLS inhibition, triggering
46 ten considered a pro-survival mechanism that renders cells viable in stressful conditions and thus mi
47 sease mutations compromise ATP synthesis and render cells vulnerable to nutrient and oxidative stress
48 n cancers show increased replication stress, rendering cells vulnerable to ATR inhibition because of
50 tors abrogates GNA13-induced TIC phenotypes, rendering cells vulnerable to standard-of-care cytotoxic