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1  spindle protein whose disruption results in nuclear fragmentation.
2 ackaged into a single mass, with no signs of nuclear fragmentation.
3 min-A/C and Lamin-B1 localization and causes nuclear fragmentation.
4 JNK (c-Jun N-terminal kinase) activation and nuclear fragmentation.
5 regation, lactate dehydrogenase release, and nuclear fragmentation.
6 ytochrome c release, caspase activation, 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 tion, most likely by promoting autophagy and nuclear fragmentation.
12  in association with morphologic evidence of nuclear fragmentation.
13  of telomeric association prior to apoptotic nuclear fragmentation.
14 olymerase cleavage, G2-M arrest, and DNA and nuclear fragmentation.
15  staining became weaker, and PI demonstrated nuclear fragmentation.
16 gh molecular weight (HMW) DNA (>/=50 kb) and nuclear fragmentation.
17 tion, condensation of nuclear chromatin, and nuclear fragmentation.
18 nt reduction of the formation of HMW DNA and nuclear fragmentation.
19 lines caused condensation of genomic DNA and nuclear fragmentation.
20 round up, detach from the plate, and undergo nuclear fragmentation.
21 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        NAM induced a significant increase in nuclear fragmentation (2.2-fold) and cleaved caspase-3,
23 lular proliferation, and increased apoptotic nuclear fragmentation after 1.4 kb anti-sense membrane t
24 es show defective G2-M checkpoint arrest and nuclear fragmentation after DNA damage, and contain supe
25 M2 cells undergo mitotic catastrophe-related nuclear fragmentation after they are released from the G
26    Using a distinct morphological pattern of nuclear fragmentation and an immunohistochemical method
27 synuclein showed signs of apoptosis, such as nuclear fragmentation and caspase 3 activation, both in
28 virus, as indicated by the induction of both nuclear fragmentation and caspase-mediated cleavage of D
29 apoptotic phenotype (chromatin condensation, nuclear fragmentation and cleavage of the nuclear membra
30 A by agarose gel electrophoresis, by finding nuclear fragmentation and condensation by electron micro
31                                 However, the nuclear fragmentation and condensation is completed only
32 tosis characterized by Annexin V positivity, nuclear fragmentation and condensation, and loss of clon
33 activation of the oxidative stress response, nuclear fragmentation and DNA degradation, and premature
34 lebs and nuclear condensation after 3 hours; nuclear fragmentation and DNA strand breaks after 4 hour
35  of ROCK I kinase, an enzyme that stimulates nuclear fragmentation and fragment distribution into ble
36 ), we observed loss of cells associated with nuclear fragmentation and increased expression of caspas
37 microscopy and electron microscopy indicates nuclear fragmentation and membrane disruption of C. neof
38 rastructural analysis, however, demonstrated nuclear fragmentation and mitochondrial alterations in a
39     Apoptotic cell death is characterized by nuclear fragmentation and oligonucleosomal DNA degradati
40              Compound 1a was found to induce nuclear fragmentation and PARP cleavage, as well as to a
41 ical apoptotic changes in neurons, including nuclear fragmentation and/or internucleosomal DNA fragme
42 esence of cytoplasm shrinkage, blebbing, and nuclear fragmentation, and (3) intact sarcolemma in the
43 s revealed by sarcolemmal membrane blebbing, nuclear fragmentation, and chromatin condensation (Hoech
44 o apoptosis, evidenced by loss of adherence, nuclear fragmentation, and chromosomal DNA degradation.
45      In Vero cells, limited multinucleation, nuclear fragmentation, and disruption of cytokinesis wer
46 companied by activation of caspases 3 and 8, nuclear fragmentation, and DNA laddering.
47 t, results in induction of sub-G1 phase DNA, nuclear fragmentation, and lethality.
48    Their deletion leads to nuclear bridging, nuclear fragmentation, and mitotic catastrophe, mirrorin
49 c changes evidenced by overt cell shrinkage, nuclear fragmentation, and specific immunostaining of na
50 ptosis as evidenced by cytochrome c release, nuclear fragmentation, and sub-G1 DNA content.
51 ies of biochemical changes that culminate in nuclear fragmentation, and that amyloid beta-peptide (Ab
52 easured using caspase-3 activation assays, a nuclear fragmentation assay, using fluorescence-activate
53 ne integrity, without the cell shrinkage and nuclear fragmentation associated with apoptosis.
54 - to 5.5-mm-diameter laser capsulotomies and nuclear fragmentation) at the Singapore National Eye Cen
55 hology, revealing chromatin condensation and nuclear fragmentation; (b) flow cytometry, showing chang
56 ity, internucleosomal DNA fragmentation, and nuclear fragmentation but not the shrinkage and condensa
57  in purified cholangiocytes by assessment of nuclear fragmentation by 4, 6-diamidino-2-phenylindole (
58 se cells displayed apoptotic markers such as nuclear fragmentation, chromatin condensation, and accum
59                                  Evidence of nuclear fragmentation colocalized to cells with expressi
60 s exhibited a fivefold increase in apoptotic nuclear fragmentation compared to Id3-GFP-negative cells
61 ed enhanced radiation-induced polyploidy and nuclear fragmentation, consistent with the consequences
62 f apoptosis including cytoplasmic shrinkage, nuclear fragmentation, DNA laddering, and caspase activa
63 D), resulting in an absence of chromatin and nuclear fragmentation during apoptotic cell death.
64 ted increases in reactive oxygen species and nuclear fragmentation, eventually leading to apoptosis.
65 changes such as swelling, vacuolization, and nuclear fragmentation following treatment with ATP and t
66 ive mutant or survivin antisense cDNA causes nuclear fragmentation, hypodiploidy, cleavage of a 32-kD
67 cks caspase activation, DNA degradation, and nuclear fragmentation in both cases but only prevents lo
68 ear condensation in dying wt or E7 cells but nuclear fragmentation in E6 cells.
69  c release, caspase activation and apoptotic nuclear fragmentation in extracts of Xenopus eggs.
70  infection, induced caspase 3 activation and nuclear fragmentation in LLC-MK2 cells, identifying the
71  with Id3 significantly suppressed apoptotic nuclear fragmentation, indicating that caspase-9 activat
72 s is associated with chromatin condensation, nuclear fragmentation, induction of sub-G1 phase DNA and
73 ulted in myocyte apoptosis, as determined by nuclear fragmentation, internucleosomal cleavage of DNA,
74 ced degree of chromatin condensation, absent nuclear fragmentation, intranuclear cytoplasmic invagina
75                                              Nuclear fragmentation is a common feature in many neurod
76 on depth (P < 0.05), possibly indicating the nuclear fragmentation lethality potential of the carbon-
77    We describe a novel phenotype, designated nuclear fragmentation (NF), that occurs following replic
78            Loss of PPP1R12A or PPP1CB causes nuclear fragmentation, nuclear envelope rupture, nuclear
79 his assay reflects the relative frequency of nuclear fragmentation observed in transfections using th
80 st is non-lethal and unlike the catastrophic nuclear fragmentation phenotype of smc6(ts) mutants, the
81 ration, as well as fluorescent microscopy of nuclear fragmentation revealed that apoptotic activity w
82 akage, activation of family of caspases, and nuclear fragmentation studies.
83 f cytochrome c, activation of caspase-9, and nuclear fragmentation that was prevented by the overexpr
84 ceded TAM-induced chromatin condensation and nuclear fragmentation, the typical apoptotic morphologie
85  characterized by chromatin condensation and nuclear fragmentation (type II nuclear morphology).
86 rocytes exhibited enlarged size and elevated nuclear fragmentation upon SARS-CoV-2 infection.
87  hallmarks of lysigenous-type PCD, including nuclear fragmentation, vacuolation and lysis.
88 poptotic assay, it was demonstrated that the nuclear fragmentation was caused by apoptosis.
89                                              Nuclear fragmentation was detected using the Hoechst Blu
90 ng apoptotic assay, we demonstrated that the nuclear fragmentation was due to apoptosis.
91 pecific stain 4',6-diamidino-2-phenylindole, nuclear fragmentation was observed in a time-dependent m
92 y evolving apoptotic death, characterized by nuclear fragmentation, was not attenuated by MK-801 but
93 ic features such as cytoplasmic blebbing and nuclear fragmentation were seen within 6 hr, but neither
94  as a JNK inhibitor attenuated Abeta-induced nuclear fragmentation, which followed the changes in ROS
95 er technology to perform the capsulotomy and nuclear fragmentation, with successful preservation of t