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1 hrome c into the cytosol, which triggers the apoptotic cascade.
2 o an acute insult stimulus by activating the apoptotic cascade.
3 an the downstream events, which initiate the apoptotic cascade.
4 ropagation rather than the initiation of the apoptotic cascade.
5 ells, resulting in maximum activation of the apoptotic cascade.
6 us might activate the mitochondria-dependent apoptotic cascade.
7 hin 1 h) was a primary inciting event of the apoptotic cascade.
8 on and abolished activation of the caspase-3 apoptotic cascade.
9 h stimuli converge at a central point in the apoptotic cascade.
10 elevation of beta-catenin-Tcf signaling, and apoptotic cascade.
11 ptor level and triggering a caspase-mediated apoptotic cascade.
12 g step preceding cytochrome c release in the apoptotic cascade.
13 sential for initiation of a butyrate-induced apoptotic cascade.
14 ng or execution components of the endogenous apoptotic cascade.
15  or permissive for proper progression of the apoptotic cascade.
16 e hu MDR 1 protein alters progression of the apoptotic cascade.
17 iptionally regulating two key players in the apoptotic cascade.
18 n vivo, thereby curtailing the JNK3-mediated apoptotic cascade.
19 ory chain and as a signaling molecule in the apoptotic cascade.
20 ation, ROS generation, and activation of the apoptotic cascade.
21 organelles, consistent with the onset of the apoptotic cascade.
22 ter membrane of mitochondria, unleashing the apoptotic cascade.
23 y cytoprotective but also interfere with the apoptotic cascade.
24 llular signaling and activates the intrinsic apoptotic cascade.
25 lular mitochondria to activate the intrinsic apoptotic cascade.
26 se to the recruitment of mitochondria to the apoptotic cascade.
27 degradation resulting from activation of the apoptotic cascade.
28 st, DNA fragmentation, and activation of the apoptotic cascade.
29 Mcl-1-free Bim that mediates a Bax-dependent apoptotic cascade.
30 ues, which play a key role in initiating the apoptotic cascade.
31 hondrial membrane disruption, triggering the apoptotic cascade.
32  ligands and the activation of the extrinsic apoptotic cascade.
33 n part, to an increase of the E2F-1-mediated apoptotic cascade.
34 sting that VIAF functions to co-regulate the apoptotic cascade.
35 ion of Bax, a key component of the intrinsic apoptotic cascade.
36  mitochondrial translocation, preventing the apoptotic cascade.
37 ocalization in response to initiation of the apoptotic cascade.
38 of caspase-8, which initiates the downstream apoptotic cascade.
39 e nodal effector protein BAK to initiate the apoptotic cascade.
40 y that is capable of directly activating the apoptotic cascade.
41 and other agents that activate the extrinsic apoptotic cascade.
42 ral envelope and cell membranes triggers the apoptotic cascade.
43 ated Rac1 and downstream elements of the JNK apoptotic cascade.
44 and some of the key proteins involved in the apoptotic cascade.
45 against neurotoxicity, oxidative stress, and apoptotic cascades.
46  role in the initiation of erlotinib-induced apoptotic cascades.
47 e involvement of the intrinsic and extrinsic apoptotic cascades.
48 ls enter butyrate-mediated growth arrest and apoptotic cascades.
49 select cellular processes, including various apoptotic cascades.
50 ergy is a consequence and not a cause of the apoptotic cascade activated downstream of Bid.
51 tures of lineage commitment are reflected in apoptotic cascades activated in CD4(+) T effectors.
52 vel regulator of protein interactions in the apoptotic cascade and a therapeutically targetable contr
53 hare several components of the intracellular apoptotic cascade and are expressed by first trimester t
54         However, the connections between the apoptotic cascade and events leading to extrusion are no
55 rproduction of ceramide, an initiator of the apoptotic cascade and is induced by long-chain fatty aci
56 dence that O2*- facilitates an InsP3R-linked apoptotic cascade and may serve a critical function in I
57 es are integral to cellular inflammation and apoptotic cascades, and are commonly studied by cell bio
58 ite the paradigm that growth arrest triggers apoptotic cascades, apoptosis was detected before G2-M a
59 ation of downstream signaling, and effective apoptotic cascade are all factors that may affect the tu
60                    Various levels within the apoptotic cascade are being investigated as therapeutic
61  target(s) responsible for the mitochondrial apoptotic cascade are not known.
62                 Thus, while molecules of the apoptotic cascade are well represented in the CNS during
63 ly through a caspase-dependent pathway after apoptotic cascades are initiated.
64 of Abeta in neuroblastoma IMR-32 cells after apoptotic cascades are initiated.
65 K3beta prosurvival pathway and activates the apoptotic cascade, as demonstrated in vivo and in vitro.
66 rcurials and organoleads, alkyltins activate apoptotic cascades at low concentrations.
67          Mitochondrial damage initiated this apoptotic cascade, because overexpression of Bcl-X(L), a
68  cells were isolated at the beginning of the apoptotic cascade, before the activation of caspase 3 fa
69 ty and subsequent activation of an intrinsic apoptotic cascade beginning with a loss of mitochondrial
70 catalytic center of caspase proteases of the apoptotic cascade but no region characteristic of the ca
71 xidative stress, inflammatory cytokines, and apoptotic cascades, but its molecular mechanisms have no
72 uced SM-dependent virus fusion initiates the apoptotic cascade by inducing SM degradation and ceramid
73  in the initiation of the bortezomib-induced apoptotic cascade by mediation of the disruption of Delt
74                         The initiation of an apoptotic cascade by NMDA or QA appears to be mediated b
75 t cell lines, presumably acts at the apex of apoptotic cascade by preventing the activation of caspas
76  unfolded protein response (UPR) triggers an apoptotic cascade by the co-activation of Caspase 12 and
77 er AMPK is a molecular target mediating this apoptotic cascade by utilizing PCa cell lines stably ove
78 leads to activation of the receptor-mediated apoptotic cascade (caspase-8-mediated) and ultimately to
79 perate to engage the intrinsic and extrinsic apoptotic cascades, culminating in pronounced mitochondr
80  Thus, cleaved caspase 3 could stimulate the apoptotic cascade further, and lack of its activation li
81 the initially cytoprotective UPR triggers an apoptotic cascade if ER stress is not corrected, called
82 initially cytoprotective UPR will trigger an apoptotic cascade if the cellular insult is not correcte
83 eam players could initiate a self sustaining apoptotic cascade in breast cancer cells.
84 nslocation from the nucleus may initiate the apoptotic cascade in colon cancer cells by stimulating o
85 s show an increase in the stimulation of the apoptotic cascade in hepatocytes, the magnitude of which
86 L-265-treatment did reduce entrance into the apoptotic cascade in in vitro and in vivo models of oute
87 ic anti-Fas antibody (Ab), the tumor-induced apoptotic cascade in Jurkat cells is significantly ampli
88 necessary for the induction of the intrinsic apoptotic cascade in mammalian cells.
89 ged cells by analyzing the activation of the apoptotic cascade in p21(Cip1)-deficient HCT116 colorect
90 f caspase-8 activation and initiation of the apoptotic cascade in response to SKI-I, a pan-sphingosin
91 report here that activation of the caspase-3 apoptotic cascade in spinal cord injury is regulated, in
92 ase (SMAC)/Diablo and trigger the subsequent apoptotic cascade in spite of concomitant Mcl-1 increase
93 amide, which can initiate the lipid-mediated apoptotic cascade in susceptible cells, failed to either
94     Therefore, we have identified a distinct apoptotic cascade in SW620 cells that was induced indepe
95 city of herpes simplex virus to initiate the apoptotic cascade in the absence of de novo protein synt
96            ROS initiates an inflammatory and apoptotic cascade in the cochlea by activating STAT1 tra
97 of the Fas/FasL system and activation of the apoptotic cascade in the epithelial cells that line the
98 cell death signal to trigger a BAX-dependent apoptotic cascade in the murine blastocyst.
99      Endotoxin induces a TNF-alpha-dependent apoptotic cascade in the myocardium, which contributes t
100 actor contributes to NMDA receptor-triggered apoptotic cascades in vivo, rats were given the NMDA rec
101 interfering RNA in primary cells triggers an apoptotic cascade, in contrast to treatment with a MAPK/
102 sp9), the initiator caspase of the intrinsic apoptotic cascade, in murine fetal and adult hematopoies
103 oduction of Abeta-(1-42) after initiation of apoptotic cascades, indicating factors regulating apopto
104            Granzyme B activates a ubiquitous apoptotic cascade induced by caspase cleavage, but the g
105 indings, we propose a model of the intrinsic apoptotic cascade induced by DNA damage where proapoptot
106            We have identified an alternative apoptotic cascade induced in SW620 human colonic carcino
107              These findings demonstrate that apoptotic cascades induced in Jurkat T lymphocytes by an
108                              Early events in apoptotic cascades initiated by ceramides or by activati
109 om these cells but also the pressure-induced apoptotic cascade intrinsic to RGCs.
110 hese results suggest that Abeta activates an apoptotic cascade involving AP-1 DNA binding, subsequent
111 the presence of Gadd45 beta, the Fas-induced apoptotic cascade is halted at mitochondria.
112                                          The apoptotic cascade is initiated either by mitochondrial d
113  Fas binds its ligand, Fas ligand (FasL), an apoptotic cascade is initiated in the cell bearing the F
114                          When this fails, an apoptotic cascade is initiated so that the affected cell
115 These results suggest that a stress-mediated apoptotic cascade is involved in the mechanism of action
116 location and subsequent amplification of the apoptotic cascade is not by providing a physical barrier
117 ee competing protein families regulating the apoptotic cascade is subverted in tumor cells is incompl
118                      A critical event in the apoptotic cascade is the proteolytic activation of proca
119                                       Normal apoptotic cascade kinetics are partially restored by pre
120 ctive cycle, play a key role in blocking the apoptotic cascade leading to cell death.
121 ore DNA repair is complete, can activate the apoptotic cascade, leading to cell death.
122                  Therapies that activate the apoptotic cascade may have potential for use in RA; howe
123 t therapeutic approaches targeting the Par-4 apoptotic cascade may prove beneficial in preventing neu
124 ivity levels of Caspase-3, a protease in the apoptotic cascade, measured in outflow tract homogenates
125 ed cytochrome c, the form that activates the apoptotic cascade of cell death.
126  an apoptotic effector activated late in the apoptotic cascade, PKCdelta also activates upstream comp
127              To establish if proteins of the apoptotic cascades [pro-apoptotic: active caspase 3, 8,
128                    Mechanistically, among 35 apoptotic cascade-related proteins tested, the apoptosis
129 de, which normally initiate and suppress the apoptotic cascade, respectively.
130 ein is toxic in cell culture and triggers an apoptotic cascade resulting in activation of caspase-3.
131 e nucleus to the mitochondria, initiating an apoptotic cascade resulting in caspase activation within
132  in hair follicle SCs (HFSCs) attenuates the apoptotic cascade, resulting in significant temporal del
133                      However, PS-341-induced apoptotic cascade(s) are not yet fully defined.
134  proteins affected are integral parts of the apoptotic cascade such as pro- and antiapoptotic members
135 up-regulation of molecules implicated in pro-apoptotic cascades such as p53, p21(Waf1), and p27(Kip1)
136  have investigated the critical steps in the apoptotic cascade that are affected by hypoxia and have
137 ctivates a p53-mediated, caspase-independent apoptotic cascade that contributes to suppression of col
138 teracts with Bax and suppresses the caspase6 apoptotic cascade that fosters axonal degeneration.
139 hibition of PtdCho biosynthesis activates an apoptotic cascade that is a causative event in pathogene
140  BAD to mitochondria, thereby inhibiting the apoptotic cascade that leads to apoptosis.
141 studied Bax, an intracellular protein of the apoptotic cascade, the Bax antagonist and anti-apoptotic
142               To investigate its role in the apoptotic cascade, the U(S)3 open reading frame was clon
143 xtent to which cells enter growth arrest and apoptotic cascades, these data establish a role for the
144 del in which Bax insertion amplifies the Fas apoptotic cascade through cytochrome c release and compl
145 noma cell death depends on the nature of the apoptotic cascade (TNF or Fas) and on the availability o
146 stitutively activates the Akt/NF-kappaB anti-apoptotic cascade to confer resistance to TNF on cancer
147  signal(s) that is an essential component of apoptotic cascades triggered by diverse stimuli.
148 ctivation of mitochondrial caspase-dependent apoptotic cascades, up-regulation of cyclin-dependent ki
149 to the cytosol, where they contribute to the apoptotic cascade upstream of mitochondria.
150 n in Nurr1 +/- mice led to the activation of apoptotic cascade via the differential alterations in th
151                             The block in the apoptotic cascade was in the mitochondrial mechanism for
152          The significance of Bim in this GrB apoptotic cascade was indicated by the marked protection
153 for essential components of the Fas-mediated apoptotic cascade, we isolated a Jurkat T lymphocyte cel
154                  We previously discovered an apoptotic cascade wherein cytochrome c binds to IP3R ear
155 tivation of survivin, two key players in the apoptotic cascade, which normally initiate and suppress
156 n trigger in T lymphocytes caspase-dependent apoptotic cascades, which are not effectively protected
157 milarly, inhibition of the receptor-mediated apoptotic cascade with a caspase-8 dominant-negative mut

 
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