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1 T laser power (2 W/cm(2)) to achieve maximal induction of apoptosis.
2 ned by a surprising, concentration-dependent induction of apoptosis.
3 cellular defense mechanisms is essential for induction of apoptosis.
4 ll death through activation of caspase-3 and induction of apoptosis.
5 d redox ratio and ROS increased, followed by induction of apoptosis.
6 uced in deguelin-treated mice along with the induction of apoptosis.
7 sed DCs could be partially attributed to the induction of apoptosis.
8 nd an increase in cell death consistent with induction of apoptosis.
9 -driven apoptosis) support a mechanism-based induction of apoptosis.
10 s (PIV5DeltaSH and PIV5VDeltaC) that enhance induction of apoptosis.
11 cells and evaluated the mechanism[s] in the induction of apoptosis.
12 ion of DNA DSBs, G2-M cell-cycle arrest, and induction of apoptosis.
13 ibitors, trigger cellular stress and lead to induction of apoptosis.
14 f the proapoptotic protein, BIM, followed by induction of apoptosis.
15 ndent elevation of cytosolic Ca(2+) prior to induction of apoptosis.
16 bility to secondary bacterial infection, and induction of apoptosis.
17 killing leukemic cells through the forcible induction of apoptosis.
18 enhanced host protein synthesis shutoff and induction of apoptosis.
19 n to be hypersensitive to CPT with prominent induction of apoptosis.
20 se activity, malondialdehyde production, and induction of apoptosis.
21 , accumulation of unrepaired DNA damage, and induction of apoptosis.
22 o dephosphorylation of Akt at serine-473 and induction of apoptosis.
23 ulting from a differentiation defect and the induction of apoptosis.
24 kinase (AMPK), activation of caspase-3, and induction of apoptosis.
25 KT), because PI3K inhibitor results in early induction of apoptosis.
26 orrelate with protein kinase C inhibition or induction of apoptosis.
27 ICD target Hes1 gene in mouse brains without induction of apoptosis.
28 cells were then treated with doxorubicin for induction of apoptosis.
29 by RV metabolite treatments, as well as the induction of apoptosis.
30 cFLIP had been downregulated resulted in the induction of apoptosis.
31 lation of cytotoxic double-strand breaks and induction of apoptosis.
32 ulate Star-PAP control of BIK expression and induction of apoptosis.
33 promotes p53-dependent growth arrest and the induction of apoptosis.
34 a mechanism to promote BOK accumulation and induction of apoptosis.
35 , reduced colony formation in soft agar, and induction of apoptosis.
36 nockdown or inactivation were accompanied by induction of apoptosis.
37 gulation, modulation of differentiation, and induction of apoptosis.
38 nts, may also contribute to piperlongumine's induction of apoptosis.
39 tivation of PI3-kinase (PI3K) signaling, and induction of apoptosis.
40 r of apoptosis, activation of caspase 9, and induction of apoptosis.
41 ctly links ErbB receptor inactivation to the induction of apoptosis.
42 proliferation of pancreatic cancer cells and induction of apoptosis.
43 ion of gamma-tubulin protein levels leads to induction of apoptosis.
44 ing electron transfer, enzyme catalysis, and induction of apoptosis.
45 leading from ligation of the Fas receptor to induction of apoptosis.
46 otes ADAM17 activity in neutrophils upon the induction of apoptosis.
47 horylated on Tyr142, high levels of p53, and induction of apoptosis.
48 the MDA-MB-231 cell line via complement and induction of apoptosis.
49 motes the DNA damage response leading to the induction of apoptosis.
50 esting that kinase activity is essential for induction of apoptosis.
51 active state of the MST kinases and favoring induction of apoptosis.
52 d-type colon cultures respond similarly upon induction of apoptosis.
53 lls in sub-G(1) phase of the cell cycle, and induction of apoptosis.
54 s of the molecular processes involved in the induction of apoptosis.
55 some required EBV to prevent the inefficient induction of apoptosis.
56 iately activated by oncogenic events through induction of apoptosis.
57 ed multimeric IAP antagonist complex for the induction of apoptosis.
58 ibition of JAK-STAT activity, leading to the induction of apoptosis.
59 ression into the cell cycle, followed by the induction of apoptosis.
60 bose) polymerase and caspase cleavage and an induction of apoptosis.
61 asis mainly in the immune system through the induction of apoptosis.
62 of proliferation and survival pathways, and induction of apoptosis.
63 vo, including inhibition of tumor growth and induction of apoptosis.
64 oteins, reduction of cell proliferation, and induction of apoptosis.
65 ay involving cell surface GRP78 receptor for induction of apoptosis.
66 s as well as the JNK1/2/c-Jun pathway to the induction of apoptosis.
67 ibition of soft agar clonogenic capacity and induction of apoptosis.
68 limits both FasL and ceramide analogs in the induction of apoptosis.
69 rowth of the cell line A427, which is due to induction of apoptosis.
70 s results in irreversible DNA damage and the induction of apoptosis.
71 ions in the morphology of this organelle and induction of apoptosis.
72 lular trap formation, bacterial killing, and induction of apoptosis.
73 mediated by both G0/G1 cell cycle block and induction of apoptosis.
74 chondria represents a critical signal in the induction of apoptosis.
75 vity and annexin V-positive cell number upon induction of apoptosis.
76 ells causes G1 cell cycle arrest followed by induction of apoptosis.
77 on cell cycle regulation is followed by the induction of apoptosis.
78 due to cell-cycle regulation leading to the induction of apoptosis.
79 the onset of irreversible DNA damage and the induction of apoptosis.
80 g of gene expression, cell cycle arrest, and induction of apoptosis.
81 d SHP-1 activity, inhibition of p-STAT3, and induction of apoptosis.
82 by immune cells to kill cancer cells through induction of apoptosis.
83 erlying mechanism for this by using H2O2 for induction of apoptosis.
84 alpha, other interferon-stimulated genes and induction of apoptosis.
85 a mechanism of inhibiting metastasis via the induction of apoptosis.
86 ading to cessation of cell proliferation and induction of apoptosis.
87 3 activation and either cell cycle arrest or induction of apoptosis.
88 believed to result directly or indirectly in induction of apoptosis, a better understanding of the bi
90 r-bearing mice with LV-tSMAC resulted in the induction of apoptosis, activation of antitumor immunity
93 least partially associated with an enhanced induction of apoptosis although triggered by distinct ap
94 mpairment of granule neuron differentiation, induction of apoptosis and abnormal localization of Purk
98 o control OS tumor growth which involved the induction of apoptosis and cell cycle arrest, supporting
100 degradation by PS-341 occurred early before induction of apoptosis and could not be inhibited by a p
101 BP2 had reduced viability and proliferation, induction of apoptosis and cytotoxicity, and up-regulati
102 testing of their biological activity such as induction of apoptosis and evaluation of anti-cancer eff
104 downregulation of MYC expression, as well as induction of apoptosis and induces differentiation of pr
106 y small-interfering (si) RNA caused a strong induction of apoptosis and inhibition of cell-cycle prog
107 stress and p53 activation, resulting in the induction of apoptosis and inhibition of proliferation,
113 eckpoint both contributed to the synergistic induction of apoptosis and proliferation inhibition in A
114 gh PERK-eIF2alpha-dependent pathways, of the induction of apoptosis and reduction of autophagy by Sub
116 lective DNA damage at telomeric level and to induction of apoptosis and senescence on tumor cells is
117 A] and its downstream substrate FOXO1 in the induction of apoptosis and the synthesis of catalase.
118 nteracts with E2F1, and is required for E2F1 induction of apoptosis and transcription of a number of
119 cytotoxic effect appeared to be mediated by induction of apoptosis and was inhibited in a concentrat
120 GI-1776 results in a concentration-dependent induction of apoptosis and we investigated its effect on
121 DCP inhibitory effects were attributed to induction of apoptosis and/or increased production of in
123 ell-based assays to evaluate cell viability, induction of apoptosis, and accumulation of ROS followin
124 on of Sp-regulated genes, growth inhibition, induction of apoptosis, and antiangiogenic responses.
125 inhibition of cancer cell and tumor growth, induction of apoptosis, and antiangiogenic responses.
126 alization along with osteonectin expression, induction of apoptosis, and cytotoxicity assays were per
127 cells by RNAi resulted in aberrant mitoses, induction of apoptosis, and decreased ability of human b
128 he most potent effects on growth inhibition, induction of apoptosis, and delay of acquired resistance
129 DO or CDDO-Me resulted in growth inhibition, induction of apoptosis, and down-regulation of cyclin D1
130 The mechanism of action of IAD is largely induction of apoptosis, and each mechanism of resistance
132 4 results in efficient degradation of Mcl-1, induction of apoptosis, and inhibition of tumor growth i
133 ulting in a shut-off of general translation, induction of apoptosis, and inhibition of virus replicat
134 al dysfunction, generation of peroxynitrite, induction of apoptosis, and oxidative stress due to disr
135 ociated with the inhibition of angiogenesis, induction of apoptosis, and reduction in keloid phenotyp
136 rosurvival Bcl-2 proteins leads to effective induction of apoptosis, and strongly support the concept
137 d cells, which were also associated with the induction of apoptosis, and these results were consisten
138 ibition-induced down-regulation of c-Myc and induction of apoptosis are mitigated when the cells are
139 correction of mitochondrial dysfunction and induction of apoptosis are promising strategies in cance
140 e main function ascribed so far has been the induction of apoptosis as a crucial mediator of KRAS-dri
141 the cytotoxic effect may be associated with induction of apoptosis as evidenced by increased percent
142 an intrinsic innate immune response and the induction of apoptosis as mechanisms to restrict viral r
145 An opposite pattern was observed regarding induction of apoptosis, as studied by Western blotting f
146 osphocholine, inhibition of cell growth, and induction of apoptosis at low micromolar concentrations.
147 e mediated by the block of autophagy and the induction of apoptosis; (b) decreased metastatic potenti
148 r fate by regulating both cytoprotection and induction of apoptosis based on the metabolic state.
150 v toxin is linked to V. vulnificus dependent induction of apoptosis, but the region of the large mult
151 e inhibition of tumor cell proliferation and induction of apoptosis, but their effect on tumor cell i
152 x and decreased Bcl-2 expression, indicating induction of apoptosis by 48 hours after SP treatment.
153 t significantly affect AcMNPV replication or induction of apoptosis by a mutant of AcMNPV lacking the
154 signaling to AMPK, making them resistant to induction of apoptosis by adenosine 3',5'-cyclic monopho
155 cells transfected with miR-K10a showed less induction of apoptosis by annexin V staining and termina
156 n of Caspase3 at 200muM at 48h confirmed the induction of apoptosis by apigenin and quercetagetin.
160 we examined and quantitatively evaluated the induction of apoptosis by drug combination therapies.
162 Early L3 animals are highly resistant to induction of apoptosis by expression of IAP-antagonists,
174 vity of elephant cells to DNA damage and the induction of apoptosis by regulating activity of the TP5
177 small cell lung cancer cell lines toward the induction of apoptosis by the DNA-damaging agent etoposi
178 us, mutation of cleavage sites inhibited the induction of apoptosis by treatment with tumor necrosis
181 AKT2-amplified PDAC, was able to bypass the induction of apoptosis caused by KRAS* ablation, highlig
182 is demonstrates that BIM is critical for the induction of apoptosis caused by potentially oncogenic D
183 time-dependent inhibition of proliferation, induction of apoptosis, cell-cycle arrest, and terminal
184 showed the largest inhibition of growth and induction of apoptosis compared with the double combinat
186 ed to significant inhibition of cell growth, induction of apoptosis, decreased invasiveness and decre
187 on (that resulted in loss of nuclear CK2 and induction of apoptosis) demonstrated dynamic modulation
189 as a scaffold for pro-caspase-8 binding and induction of apoptosis downstream of induced-proximity a
191 crease in LC3 levels that was accompanied by induction of apoptosis, evidenced by increases in cleave
192 Usp9x in myeloma cells resulted in transient induction of apoptosis, followed by a sustained reductio
196 ough mostly cytosolic in healthy cells, upon induction of apoptosis, IBRDC2 accumulates in mitochondr
197 MV-4-11 human leukemia cells, showed potent induction of apoptosis (IC(50)'s approximately 20 muM) w
199 lence functions for P. aeruginosa, including induction of apoptosis in a variety of target host cells
202 genes, decreased dendritic spine density and induction of apoptosis in astrocytes may contribute to t
203 function of WT p53 is directly linked to the induction of apoptosis in both cancer cells and tumor xe
204 domain protein Miz-1 restricts p53-dependent induction of apoptosis in both pro-B and DN3a pre-T cell
205 imary myoblasts and C2C12 cultures, chemical induction of apoptosis in C2C12 cells results in indiscr
209 tion protects stalled forks from collapse or induction of apoptosis in CHK1 inhibited cells during re
210 us in response to altered growth stimuli and induction of apoptosis in cultured prostate cells and in
211 , irreversible DNA damage, and ATM-dependent induction of apoptosis in cytokine-treated beta cells.
214 e importance of hnRNP A1 was demonstrated by induction of apoptosis in eIF2alpha phosphorylation-defi
218 ection gonorrhea, protects against exogenous induction of apoptosis in human cervical epithelial cell
220 lpain, CAPN1, which were requisite steps for induction of apoptosis in MDS cells and in acute myeloid
223 ensory epithelium (OSE) in hamsters and that induction of apoptosis in olfactory receptor neurons (OR
225 ment of multiple oncogenic processes and the induction of apoptosis in pancreatic and breast cancer c
226 on causes reduction in adipogenesis, through induction of apoptosis in pre-adipocytes, by inhibition
228 cept in cancer therapy, coiled-coil mediated induction of apoptosis in Raji B cells, for treatment of
230 ied the molecular mechanisms involved in the induction of apoptosis in response to cisplatin, and fou
232 activation plays a major regulatory role in induction of apoptosis in response to ER stress and indi
234 these two microRNAs in mediating p16-related induction of apoptosis in response to this genotoxic str
235 sclerosis (RRMS) is not well understood, but induction of apoptosis in specific leukocyte subsets is
236 s revealed that Dicer1 deficiency led to the induction of apoptosis in T-ALL cells, whereas cell cycl
238 ERK phosphorylation and the late response of induction of apoptosis in the human prostatic carcinoma
239 , attenuation of cell survival pathways, and induction of apoptosis in the ischemic territory, which
240 depletion causes impaired proliferation and induction of apoptosis in the OP9 cell line and in prima
241 ly demonstrated that Heme is involved in the induction of apoptosis in vascular endothelial cells.
242 nducing ligand (TRAIL) for markedly enhanced induction of apoptosis in VHL-null 786-O cells but not i
243 ulting in viral RNA replication and a potent induction of apoptosis in vitro and antitumor effects in
244 inical Akt and CDK inhibitors, demonstrating induction of apoptosis in vitro and providing a preclini
246 siParp1 inhibits cell growth, primarily by induction of apoptosis, in Brca1-deficient cells both in
247 c protein that forms a complex with Bax upon induction of apoptosis, in the presence of gamma-secreta
248 ents that require BID activation for maximal induction of apoptosis, including topoisomerase inhibito
251 tinoblastoma and current models propose that induction of apoptosis is a key p53 tumor suppressive fu
253 The regulation of neutrophil lifespan by induction of apoptosis is critical for maintaining an ef
254 in the activation of Bid, and the consequent induction of apoptosis is inhibited by Noxa silencing.
257 impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in meth
259 ificant inhibition of cell proliferation and induction of apoptosis, making it an attractive target f
260 R (PKR) was blocked in EBOV-infected cells, induction of apoptosis mediated by dsRNA was not suppres
261 in orchestrating various pathologies via the induction of apoptosis, necroptosis, and nuclear factor-
262 blood-brain barrier integrity during ECM by induction of apoptosis of brain vascular endothelial cel
263 e capacity to help GC-B cells because of the induction of apoptosis of GC-B cells through the FAS/FAS
264 B-ALL development, which was accompanied by induction of apoptosis of leukemic B-lymphoid progenitor
265 : (i) inhibition of cell proliferation, (ii) induction of apoptosis of tumor xenograft cells, (iii) d
266 receptor, death receptor 5 (DR5), leading to induction of apoptosis, offers a promising anticancer st
267 lthough p53 limits tumorigenesis through the induction of apoptosis or cell cycle arrest, its molecul
269 f c-Jun N terminal kinases (JNK)1/2, but not induction of apoptosis or the JAK/STAT pathway that is n
272 70alpha is AR-dependent and mediated through induction of apoptosis rather than cell cycle arrest.
273 f breast cancer cells, which correlated with induction of apoptosis, reduced expression of SOX2 but e
274 ation of oxidant and antioxidant levels, and induction of apoptosis-related proteins in the lung tiss
275 , including cell activation, protection from/induction of apoptosis, release of inflammatory cytokine
276 ppression of TWIST in stroma interfered with induction of apoptosis sensitivity in cocultured CD34(+)
277 Degradation of FAT10 is accelerated after induction of apoptosis, suggesting that it plays a role
278 lts in loss of MCL-1 expression prior to the induction of apoptosis, suggesting that MCL-1 may be an
279 Combination treatment resulted in rapid induction of apoptosis that coincided with increased DNA
283 um by down-regulation of XIAP expression and induction of apoptosis through specific targeting of a S
286 Independent cell cycle arrest and increased induction of apoptosis underlies the synergistic effect
289 previously unidentified role of ISG54 in the induction of apoptosis via a mitochondrial pathway and s
290 BID and BIM have nonoverlapping roles in the induction of apoptosis via BAK and BAX, affecting chemot
291 t that cellular levels of PPARgamma regulate induction of apoptosis via caspase-8 activation, whereas
293 rimary epidermal keratinocytes, photodynamic induction of apoptosis was elicited by the combined acti
296 served that, in clade B infected astrocytes, induction of apoptosis was significantly higher than in
297 ynthesis inhibition, cell cycle effects, and induction of apoptosis were determined for two character
298 or, significant reduction in cell viability, induction of apoptosis were observed when treated with a
300 5q inhibits tumor cell growth through the induction of apoptosis, with detailed mechanism of its s
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