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1 e dissociation rate of CP from the end (i.e. uncapping).
2 individual capped filaments, consistent with uncapping.
3 hat were associated with different levels of uncapping.
4 s free barbed ends generated by severing and uncapping.
5  high affinity, inhibits capping, and causes uncapping.
6 vely shorten, ultimately leading to telomere uncapping, a structural change at the telomere that acti
7                 To demonstrate this putative uncapping activity directly, we used total internal refl
8 a mechanistic explanation for the barbed end uncapping activity of CARMIL, and they identify the basi
9  during senescence and, at times of telomere uncapping, also can be induced by treatment of cells wit
10 pt the Stn1-Ten1 interaction induce telomere uncapping and abolish the telomere localization of Ten1.
11 s, PIP 5-kinase alpha induced actin filament uncapping and assembly.
12 olves ppI-mediated actin filament barbed end uncapping and de novo nucleation independently of surfac
13 more potent than TIN2-13 in causing telomere uncapping and eventual growth arrest.
14 ing and cancer, yet the precise mechanism of uncapping and its relationship to cell cycle remain to b
15 at low telomerase activity leads to telomere uncapping and senescence in proliferating primary cells.
16 l telomeric shortening can lead to telomere "uncapping" and may occur at the earliest recognizable st
17 lsolin/actin complexes consistent with actin uncapping, and increased F-actin levels, which were also
18 induce a rapid DNA damage response, telomere uncapping, and inhibition of cell proliferation in a var
19 tion of mutant telomeric sequences, telomere uncapping, and initiation of a DNA damage response, ulti
20  observations that V-1 had no activity in an uncapping assay and that the V-1.CP complex had no cappi
21 h as preferred branch orientations, filament uncapping at the obstacle, and preferential branching at
22 down in cancer cells does not cause telomere uncapping but rather induces changes in the global gene
23                        Thus, CARMIL promotes uncapping by binding to a freely accessible site on CP b
24 ractions of the mature pilus following their uncapping by the chaperone.
25                   A comparison with telomere uncapping caused by the absence of the double-stranded t
26  However, no evidence was found for telomere uncapping causing this cell death; chromosome spreads of
27 deficiency telomeres shorten to the point of uncapping, causing defects most pronounced in high-turno
28 nd capping by CP and why V-1 is incapable of uncapping CP-capped actin filaments, the two signature b
29 ucing its affinity for the barbed end and by uncapping CP-capped filaments, whereas the protein V-1/m
30 the time interval between mCAH3 addition and uncapping decreased as the concentration of mCAH3 increa
31 h short telomeres are vulnerable to telomere uncapping during or shortly after telomere replication.
32  the direction of the obstacle or barbed-end uncapping effects are included.
33                                              Uncapping effects cause the structures to have a few ver
34                               After telomere uncapping, Exo1 phosphorylation depends on components of
35 dly, suggesting the possible existence of an uncapping factor, for which the protein CARMIL (capping
36                                    To verify uncapping, filaments were capped with recombinant mouse
37 tion by small molecules can lead to telomere uncapping, followed by DNA damage response and senescenc
38        This is a mechanism whereby chaperone uncapping from a subunit is coupled with the simultaneou
39 partial alteration of shelterin through POT1 uncapping from telomeres in human HT1080 cancer cells an
40 lsolin actin filament severing, capping, and uncapping function upstream of Arp23 complex nucleation.
41                                     Telomere uncapping has been implicated in aging and cancer, yet t
42  embryonic and adult neurogenesis, but their uncapping has surprisingly no detectable consequences on
43                 Even small rates of filament uncapping have a large impact on the average filament le
44 he actin-capping activity of CP and promotes uncapping in biochemical experiments.
45 rin from the interior pores of MSN upon AuNP uncapping in response to disulfide-reducing antioxidants
46 s played by telomere shortening and telomere uncapping in the induction of senescence.
47 lomerase resulted in telomere shortening and uncapping in WT myocytes.
48 nding to telomeres, indicating that telomere uncapping is sufficient to initiate the telomere signali
49  inconsistent with the hypothesis suggesting uncapping is the dominant mechanism responsible for the
50         The mechanism by which Rac regulates uncapping is unclear, however.
51 , which is the major contributor to telomere uncapping, is stress dependent and largely caused by a t
52  between PAR-1 and actin filament barbed-end uncapping, leading to actin assembly.
53 the filament end, confirming the CAH3-driven uncapping mechanism.
54 pression profile changes induced by telomere-uncapping mutant template telomerase RNAs.
55                                     Telomere uncapping occurs transiently in every cell cycle in G2,
56 uces actin polymerization by stimulating the uncapping of actin filament barbed ends [2].
57 alternate involves phosphoinositide-mediated uncapping of actin filament barbed ends.
58 more strikingly, this interaction drives the uncapping of actin filaments previously capped with CP.
59 in-coupled receptors in neutrophils triggers uncapping of actin filaments, independently of PI 3-kina
60 3,4-P2, PtdIns 4,5-P2, and PtdIns 3, 4,5-P3, uncapping of barbed end actin, and actin filament format
61                                     Although uncapping of barbed ends by capping protein has been pro
62 e generated in response to cellular signals: uncapping of existing filaments; severing of existing fi
63 ids, including phosphatidic acid, results in uncapping of filament ends in vitro.
64 bed ends, which results from the severing or uncapping of pre-existing actin filaments [1] [2], or de
65 mutant DNA sequences into telomeres leads to uncapping of telomeres, manifested by dramatic telomere
66 hance Arp23 complex nucleation in vitro, but uncapping of the barbed ends of these actin filaments re
67                                              Uncapping of the chaperone-protected C terminus of PapA
68            Progressive telomere attrition or uncapping of the shelterin complex elicits a DNA damage
69 eased oxygen saturation values necessitating uncapping of the tracheal tube.
70                               Third, partial uncapping of the tubulin-GTP cap provides a possible mec
71 ated the effect of actin filament barbed end uncapping on Arp23 complex function both in vivo and in
72 oorly bound by Rap1, resulting in a telomere-uncapping phenotype and significant elongation of the te
73                            When the ter1-16T uncapping phenotype was repressed by overexpression of R
74                            Telomere loss and uncapping provokes progressive tissue atrophy, stem cell
75  is the deregulation resulting from telomere uncapping, rather than excessive telomere length per se,
76                                              Uncapping the 5-LOX active site by mutation of F177 and/
77                                     Telomere uncapping through either TRF2 shelterin protein knockdow
78  implicated for these compounds: 1) telomere uncapping with subsequent DNA damage response and senesc

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