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1 the HSV-1 protein gamma34.5 for reversal of translational arrest.
2 o stress-granules (SGs), known sites of mRNA translational arrest.
3 -functional ribosomal components and undergo translational arrest.
4 t ribosome pauses, but responds to prolonged translational arrest.
5 sting that increased recoding alleviates the translational arrest.
6 RNA production and promotes arsenite-induced translational arrest.
7 hibits arsenite-induced tiRNA production and translational arrest.
8 iRNAs promotes phospho-eIF2alpha-independent translational arrest.
9 ion by means of targeted RNA degradation and translational arrest.
10 reonine kinases that regulate stress-induced translational arrest.
11 isense ORNs is mediated through a process of translational arrest.
12 nt deprivation through a mechanism involving translational arrest.
13 therefore unrestricted by their concomitant translational arrest.
14 slation elongation (No-Go), which results in translational arrest.
15 control mechanism that evolved to cope with translational arrests.
16 red rapidly (<15 min) and resulted in modest translational arrest, a fundamental homeostatic response
19 tain amino acid sequences induce very strong translational arrest and provide a toolbox of APs of var
21 type-dependent induction of stress granules, translational arrest, and growth impairment in a manner
22 d otherwise stimulate the cell's autophagic, translational-arrest, and type I interferon responses to
24 lly target messenger RNAs for degradation or translational arrest are the best-understood class of sR
25 a local storage compartment for mRNAs under translational arrest but are poised for release to activ
26 regulates autophagy, it is the prevention of translational arrest by ICP34.5 rather than its control
27 f certain polypeptides that initially bypass translational arrest can be stopped at later stages of e
29 c communication within the ribosomal tunnel, translational arrest, chaperone interaction, folding, an
30 e receptor activation failed to liberate the translational arrest conferred by the 3'-UTR of TNF-alph
31 bility to MCMV infection, demonstrating that translational arrest dependent on GCN2 contributes to th
32 uld regulate the duration of stress- induced translational arrest in cells recovering from environmen
37 l for viral pathogenesis, where it precludes translational arrest mediated by double-stranded-RNA-dep
38 t leads to stress granule (SG) formation and translational arrest mediated by the phosphorylation of
41 lly predisposed persons could lead to global translational arrest of physiologically relevant enzymes
45 conserved homeostatic response that mediates translational arrest through phosphorylation of eukaryot
46 .5-null virus to counteract the induction of translational arrest through the PKR antiviral pathway,
47 modulate the rate of translation and induce translational arrest to regulate expression of downstrea
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