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1 ackaged into a single mass, with no signs of nuclear fragmentation.
2 min-A/C and Lamin-B1 localization and causes nuclear fragmentation.
3 JNK (c-Jun N-terminal kinase) activation and nuclear fragmentation.
4 regation, lactate dehydrogenase release, and nuclear fragmentation.
5 ytochrome c release, caspase activation, and nuclear fragmentation.
6 tion, most likely by promoting autophagy and nuclear fragmentation.
7 pase-3 activity, chromatin condensation, and nuclear fragmentation.
8 apoptosis before chromatin condensation and nuclear fragmentation.
9 ncrease in annexin V binding, and subsequent nuclear fragmentation.
10 ), as detected by chromatin condensation and nuclear fragmentation.
11 in association with morphologic evidence of nuclear fragmentation.
12 of telomeric association prior to apoptotic nuclear fragmentation.
13 olymerase cleavage, G2-M arrest, and DNA and nuclear fragmentation.
14 staining became weaker, and PI demonstrated nuclear fragmentation.
15 gh molecular weight (HMW) DNA (>/=50 kb) and nuclear fragmentation.
16 tion, condensation of nuclear chromatin, and nuclear fragmentation.
17 nt reduction of the formation of HMW DNA and nuclear fragmentation.
18 lines caused condensation of genomic DNA and nuclear fragmentation.
19 round up, detach from the plate, and undergo nuclear fragmentation.
20 11.9 +/- 0.44 vs. 3.5 +/- 0.28; p < 0.0001), nuclear fragmentation (11.8 +/- 0.50 vs. 3.3 +/- 0.26; p
22 lular proliferation, and increased apoptotic nuclear fragmentation after 1.4 kb anti-sense membrane t
23 es show defective G2-M checkpoint arrest and nuclear fragmentation after DNA damage, and contain supe
24 M2 cells undergo mitotic catastrophe-related nuclear fragmentation after they are released from the G
25 Using a distinct morphological pattern of nuclear fragmentation and an immunohistochemical method
26 synuclein showed signs of apoptosis, such as nuclear fragmentation and caspase 3 activation, both in
27 virus, as indicated by the induction of both nuclear fragmentation and caspase-mediated cleavage of D
28 apoptotic phenotype (chromatin condensation, nuclear fragmentation and cleavage of the nuclear membra
29 A by agarose gel electrophoresis, by finding nuclear fragmentation and condensation by electron micro
31 tosis characterized by Annexin V positivity, nuclear fragmentation and condensation, and loss of clon
32 activation of the oxidative stress response, nuclear fragmentation and DNA degradation, and premature
33 lebs and nuclear condensation after 3 hours; nuclear fragmentation and DNA strand breaks after 4 hour
34 of ROCK I kinase, an enzyme that stimulates nuclear fragmentation and fragment distribution into ble
35 ), we observed loss of cells associated with nuclear fragmentation and increased expression of caspas
36 microscopy and electron microscopy indicates nuclear fragmentation and membrane disruption of C. neof
37 rastructural analysis, however, demonstrated nuclear fragmentation and mitochondrial alterations in a
38 Apoptotic cell death is characterized by nuclear fragmentation and oligonucleosomal DNA degradati
40 ical apoptotic changes in neurons, including nuclear fragmentation and/or internucleosomal DNA fragme
41 esence of cytoplasm shrinkage, blebbing, and nuclear fragmentation, and (3) intact sarcolemma in the
42 s revealed by sarcolemmal membrane blebbing, nuclear fragmentation, and chromatin condensation (Hoech
43 o apoptosis, evidenced by loss of adherence, nuclear fragmentation, and chromosomal DNA degradation.
47 Their deletion leads to nuclear bridging, nuclear fragmentation, and mitotic catastrophe, mirrorin
48 c changes evidenced by overt cell shrinkage, nuclear fragmentation, and specific immunostaining of na
50 ies of biochemical changes that culminate in nuclear fragmentation, and that amyloid beta-peptide (Ab
51 easured using caspase-3 activation assays, a nuclear fragmentation assay, using fluorescence-activate
53 - to 5.5-mm-diameter laser capsulotomies and nuclear fragmentation) at the Singapore National Eye Cen
54 hology, revealing chromatin condensation and nuclear fragmentation; (b) flow cytometry, showing chang
55 ity, internucleosomal DNA fragmentation, and nuclear fragmentation but not the shrinkage and condensa
56 in purified cholangiocytes by assessment of nuclear fragmentation by 4, 6-diamidino-2-phenylindole (
57 se cells displayed apoptotic markers such as nuclear fragmentation, chromatin condensation, and accum
59 s exhibited a fivefold increase in apoptotic nuclear fragmentation compared to Id3-GFP-negative cells
60 ed enhanced radiation-induced polyploidy and nuclear fragmentation, consistent with the consequences
61 f apoptosis including cytoplasmic shrinkage, nuclear fragmentation, DNA laddering, and caspase activa
63 ted increases in reactive oxygen species and nuclear fragmentation, eventually leading to apoptosis.
64 changes such as swelling, vacuolization, and nuclear fragmentation following treatment with ATP and t
65 ive mutant or survivin antisense cDNA causes nuclear fragmentation, hypodiploidy, cleavage of a 32-kD
66 cks caspase activation, DNA degradation, and nuclear fragmentation in both cases but only prevents lo
69 infection, induced caspase 3 activation and nuclear fragmentation in LLC-MK2 cells, identifying the
70 with Id3 significantly suppressed apoptotic nuclear fragmentation, indicating that caspase-9 activat
71 s is associated with chromatin condensation, nuclear fragmentation, induction of sub-G1 phase DNA and
72 ulted in myocyte apoptosis, as determined by nuclear fragmentation, internucleosomal cleavage of DNA,
73 ced degree of chromatin condensation, absent nuclear fragmentation, intranuclear cytoplasmic invagina
75 We describe a novel phenotype, designated nuclear fragmentation (NF), that occurs following replic
77 his assay reflects the relative frequency of nuclear fragmentation observed in transfections using th
78 st is non-lethal and unlike the catastrophic nuclear fragmentation phenotype of smc6(ts) mutants, the
79 ration, as well as fluorescent microscopy of nuclear fragmentation revealed that apoptotic activity w
81 f cytochrome c, activation of caspase-9, and nuclear fragmentation that was prevented by the overexpr
82 ceded TAM-induced chromatin condensation and nuclear fragmentation, the typical apoptotic morphologie
88 pecific stain 4',6-diamidino-2-phenylindole, nuclear fragmentation was observed in a time-dependent m
89 y evolving apoptotic death, characterized by nuclear fragmentation, was not attenuated by MK-801 but
90 ic features such as cytoplasmic blebbing and nuclear fragmentation were seen within 6 hr, but neither
91 as a JNK inhibitor attenuated Abeta-induced nuclear fragmentation, which followed the changes in ROS
92 er technology to perform the capsulotomy and nuclear fragmentation, with successful preservation of t
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