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1 motes efficient erythroblast enucleation and nuclear condensation.
2 These cells appeared to be undergoing nuclear condensation.
3 GE2- and cAMP-mediated DNA fragmentation and nuclear condensation.
4 loss of membrane phospholipid asymmetry, and nuclear condensation.
5 u at 24 h, when 20% of infected cells showed nuclear condensation.
6 mbrane leakage preceded the manifestation of nuclear condensation.
7 glycophorin A expression, and chromatin and nuclear condensation.
8 swellings, somal chromatolytic changes, and nuclear condensation.
9 -3 and PARP cleavage, DNA fragmentation, and nuclear condensation.
10 and caused mitochondrial depolarization and nuclear condensation.
11 substrate, poly(ADP-ribose) polymerase, and nuclear condensation.
12 of mitochondrial membrane potential, before nuclear condensation.
13 procaspase-7 activation, PARP cleavage, and nuclear condensation.
14 h-affinity binding to DNA and very efficient nuclear condensation.
15 -like activity, Annexin V incorporation, and nuclear condensation.
16 a reduction in cell size and an increase in nuclear condensation.
17 n phosphorylation, caspase-3 activation, and nuclear condensation.
18 terized by internucleosomal DNA cleavage and nuclear condensation.
19 within 30 min, before cellular shrinkage or nuclear condensation.
20 calculated as the fraction of cells showing nuclear condensation.
21 tive features such as cellular shrinkage and nuclear condensation.
22 11.8 +/- 0.50 vs. 3.3 +/- 0.26; p < 0.0001), nuclear condensation (10.9 +/- 0.58 vs. 3.4 +/- 0.20; p
24 al progenitors and other cell types leads to nuclear condensation accompanied by large-scale changes
26 sequence: formation of cytoplasmic blebs and nuclear condensation after 3 hours; nuclear fragmentatio
29 rapid externalization of phosphatidylserine, nuclear condensation and collapse, and single-stranded D
30 morphologic changes, histologic evidence of nuclear condensation and degeneration, and flow-cytometr
33 rous erythroid genes and is characterized by nuclear condensation and extrusion during terminal devel
36 both cell types, which was characterized by nuclear condensation and fragmentation and activation of
38 e potential (DeltaPsi), DNA degradation, and nuclear condensation and fragmentation characteristic of
41 ced by poly(ADP-ribose) polymerase cleavage, nuclear condensation and fragmentation, and hypodiploid
42 ormation of apoptotic bodies, detachment and nuclear condensation and fragmentation, in cells transfe
43 uced typical features of apoptosis including nuclear condensation and fragmentation, oligonucleosomal
44 SF-21 cell line induced apoptosis displaying nuclear condensation and fragmentation, oligonucleosomal
47 1 and caffeine, induced mitosis and abnormal nuclear condensation and increased the protein kinase ac
48 eath induced via CD95 (Fas), as evidenced by nuclear condensation and membrane blebbing, but did not
49 sequently undergo apoptosis, as indicated by nuclear condensation and poly(ADP-ribose) polymerase cle
50 ntiation associated with the onset of global nuclear condensation and reduced cell proliferation.
53 from the mitochondria, caspase-3 activation, nuclear condensation, and an orderly progression of hair
55 volume changes, intracellular acidification, nuclear condensation, and chromosomal digestion ("ladder
57 cell death involving cytoplasmic shrinkage, nuclear condensation, and DNA fragmentation characterist
60 hropoiesis include global gene inactivation, nuclear condensation, and enucleation to yield circulati
62 area, persistent ckit expression, incomplete nuclear condensation, and lower rates of enucleation.
63 apoptotic signs including membrane blebbing, nuclear condensation, and reduction of mitochondrial mem
64 th vacuolization and mitochondrial swelling, nuclear condensation, and sustained plasma membrane.
66 ructs were tested on cell toxicity using our nuclear condensation assay and on mitochondrial viabilit
68 de, we observed laddering of genomic DNA and nuclear condensation, both hallmarks of apoptotic cells.
69 antly protect from cell death as measured by nuclear condensation, caspase activation, PARP degradati
70 eath by apoptosis was confirmed by increased nuclear condensation, changes in membrane morphology, an
73 s demonstrated changes resembling apoptosis: nuclear condensation, chromatin fragmentation, and forma
74 plicing factors Sm and SC35 persisted during nuclear condensation, consistent with effective transcri
77 acrophages, which contrasted with the marked nuclear condensation displayed by control cells undergoi
78 through inducing cell apoptosis confirmed by nuclear condensation, DNA cleavage, and accumulation of
79 n was followed by apoptosis as determined by nuclear condensation, DNA fragmentation, and annexin V b
80 metry analyses were used to detect apoptotic nuclear condensation, DNA fragmentation, and changes in
82 ncer cell selective nuclear internalization, nuclear condensation, fragmentation, and eventually anti
83 , SNCEE did not induce caspase activation or nuclear condensation/fragmentation suggesting that PS ex
84 ptosis, characterized by caspase activation, nuclear condensation/fragmentation, and membrane blebbin
85 ells, including marked caspase-3 activation, nuclear condensation/fragmentation, but with swollen cyt
86 rial membrane potential, cell shrinkage, and nuclear condensation in a caspase-dependent fashion.
89 (1) peak in the attached cell population and nuclear condensation in the floating cell population.
90 nd propidium iodide staining showed profound nuclear condensation in the NMDA or QA-treated striatum.
92 is followed by caspase activation, apoptotic nuclear condensation, loss of membrane potential, and, f
93 jury in glutathione-depleted preOLs included nuclear condensation, margination of chromatin, and mito
94 classical hallmarks of apoptosis, including nuclear condensation, membrane blebbing, caspase activat
96 n (DCD) that is expressed as cytoplasmic and nuclear condensation, neuron shrinkage, and failure of p
98 Furthermore, the C127/508 cells did not show nuclear condensation or DNA fragmentation detected by in
101 such apoptotic markers as DNA fragmentation, nuclear condensation, poly(ADP-ribose) polymerase cleava
102 In apoptotic cells, DNA fragmentation and nuclear condensation result from caspase-3-mediated prot
103 sensory cells were dependent on the stage of nuclear condensation, suggesting a specific role for MMP
104 d caspase activation and activity along with nuclear condensation that occurs independent of actin cy
105 histones, HILS1 may participate in spermatid nuclear condensation through a mechanism distinct from t
106 eprivation; LY 294002-induced death included nuclear condensation, was blocked by cycloheximide, and
107 ntation and TUNEL-positive nuclei as well as nuclear condensation were abolished by the NMDA receptor
108 cells displayed irreversible cytoplasmic and nuclear condensation while maintaining intact membranes.
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