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1 s ConA/GalN induced apoptosis in addition to necrotic cell death.
2 the mice were resistant to apoptotic but not necrotic cell death.
3 th, and JNK contributes to apoptotic but not necrotic cell death.
4 Infected memory CD4+ T cells underwent rapid necrotic cell death.
5 ucella mutants induce macrophage oncotic and necrotic cell death.
6 eregulation, the first irreversible stage of necrotic cell death.
7 g components plays a key role in TNF-induced necrotic cell death.
8 l death, while other proteases are active in necrotic cell death.
9 assay demonstrated that BopC is required for necrotic cell death.
10 ochondria, which resulted in reduced ATP and necrotic cell death.
11 t subsequently promotes oxidative damage and necrotic cell death.
12 , a structure involved in both apoptotic and necrotic cell death.
13 gainst the loss of DeltaPsim and resulted in necrotic cell death.
14 (especially S-nitrosothiols) and subsequent necrotic cell death.
15 ritical role in mediating both apoptotic and necrotic cell death.
16 PT has been implicated in both apoptotic and necrotic cell death.
17 c release and caspase 3 cleavage, as well as necrotic cell death.
18 protein inhibited the loss of DeltaPsim and necrotic cell death.
19 in mediating ROS accumulation in TNF-induced necrotic cell death.
20 droxyanisole efficiently blocked TNF-induced necrotic cell death.
21 pattern of cell destruction consistent with necrotic cell death.
22 gp96 are released from cells as a result of necrotic cell death.
23 of NAD+/ATP energy stores and ultimately to necrotic cell death.
24 of the signaling cascade of this TNF-induced necrotic cell death.
25 f intracellular ATP depletion, a hallmark of necrotic cell death.
26 ors did not significantly affect TNF-induced necrotic cell death.
27 icular myocardium through both apoptotic and necrotic cell death.
28 ve oxygen species production, culminating in necrotic cell death.
29 n cleaved substrate, a marker of excitotoxic/necrotic cell death.
30 enated were the same as those that underwent necrotic cell death.
31 e modulation of other types of apoptotic and necrotic cell death.
32 etes cellular NAD+ and ATP stores and causes necrotic cell death.
33 oxygen species production, and apoptotic and necrotic cell death.
34 (LCLs) that had been subject to apoptotic or necrotic cell death.
35 h, we propose that CD91 acts as a sensor for necrotic cell death.
36 ath that has been described as distinct from necrotic cell death.
37 gnal downstream events such as apoptosis and necrotic cell death.
38 creases in chromosomal damage, apoptosis and necrotic cell death.
39 otective in an ischemia model of excitotoxic/necrotic cell death.
40 cells prevents apoptotic cell death but not necrotic cell death.
41 recognized as a major cause of apoptotic or necrotic cell death.
42 processes which result in both apoptotic and necrotic cell death.
43 ction of reactive oxygen species and massive necrotic cell death.
44 e event in apoptosis and also occurred after necrotic cell death.
45 the cell's earliest responses to inducers of necrotic cell death.
46 his swelling is, in many cases, a prelude to necrotic cell death.
47 ining uPAS cargo and leading to AIF-mediated necrotic cell death.
48 entiates MLKL phosphorylation/activation and necrotic cell death.
49 pecifically the role of Bax/Bak in regulated necrotic cell death.
50 mage in TEN through activation of programmed necrotic cell death.
51 X was accompanied by contractile failure and necrotic cell death.
52 ndrial calcium overload, MPTP formation, and necrotic cell death.
53 amics and participates in both apoptotic and necrotic cell death.
54 xygen species which can render apoptotic and necrotic cell death.
55 ependent mitochondrial swelling and restored necrotic cell death.
56 ing evidence regarding the immunogenicity of necrotic cell death.
57 stance to mitochondrial calcium overload and necrotic cell death.
58 dative stress and autophagic, apoptotic, and necrotic cell death.
59 water plays a critical role in apoptotic and necrotic cell death.
60 todynamic injury, resulting in predominantly necrotic cell death.
61 cate serglycin in promoting apoptotic versus necrotic cell death.
62 and nuclear DNA fragmentation, resulting in necrotic cell death.
63 oduction of interleukin-1beta and programmed necrotic cell death.
64 sing SV40 large T antigen completely rescued necrotic cell death.
65 APAP hepatotoxicity in humans, resulting in necrotic cell death.
66 ibly by suppressing JNK-dependent programmed necrotic cell death.
67 key RIP3 downstream component of TNF-induced necrotic cell death.
68 yers in COR signaling and disease-associated necrotic cell death.
69 (DISC) and is required for the induction of necrotic cell death.
70 s as the quintessential framework underlying necrotic cell death.
71 tic of C. elegans programmed cell deaths and necrotic cell deaths.
72 eyond the simple view of 'apoptotic' versus 'necrotic' cell death.
75 l permeability transition (MPT) can initiate necrotic cell death after reperfusion, but the MPT is al
76 ed molecular pattern that is released during necrotic cell death and also secreted from activated mac
77 eficient (PARP(-/-)) mice are protected from necrotic cell death and ATP depletion but not from apopt
78 ificantly affected the extent of UVA-induced necrotic cell death and ATP depletion in all the cell li
79 ore, hematoxylin and eosin staining revealed necrotic cell death and cell loss in Pgc-1(c) livers and
80 echanism of IFN-induced RIP kinase-dependent necrotic cell death and identify FADD and caspases as ne
83 eptide cancer therapeutic because it induces necrotic cell death and not apoptosis, which is uncommon
84 an and deferoxamine to UW solution inhibited necrotic cell death and preserved mitochondrial structur
85 his swelling is, in many cases, a prelude to necrotic cell death and the dye trypan blue was used to
87 actor receptor (TNFR) I mediates TNF-induced necrotic cell death, and that RIP, FADD, and TRAF2 are c
89 mitochondrial respiratory chain defects and necrotic cell death are mutually dependent on and obliga
92 DNA damage-induced necrosis, thus assigning necrotic cell death as a form of "programmed cell death.
93 Myocardial infarction is a manifestation of necrotic cell death as a result of opening of the mitoch
94 The mechanism of neutrophil impairment was necrotic cell death as determined by morphological analy
97 classification model specified apoptotic and necrotic cell death based on single cell Raman spectra.
98 to I/R increased reactive oxygen species and necrotic cell death, both of which were mitigated by ATF
99 to I/R increased reactive oxygen species and necrotic cell death, both of which were mitigated by ATF
100 Reperfusion with glycine alone prevented necrotic cell death but did not induce apoptosis and onl
101 APAP-induced phosphorylase a activation and necrotic cell death, but failed to inhibit phosphorylase
102 rned by signals associated with apoptotic or necrotic cell death, but is an intrinsic feature of the
103 herefore serine hydrolase inhibitors prevent necrotic cell death by blocking mitochondrial calcium up
104 -mediated proteolysis; caspases also subvert necrotic cell death by cleaving and inactivating poly AD
105 so required for mitochondrial pore-dependent necrotic cell death by facilitating outer membrane perme
106 tuberculosis inhibits apoptosis and promotes necrotic cell death by inhibiting production of prostagl
107 have been shown to suppress cell damage and necrotic cell death by moderating the amount of labile i
108 psulotomy specimens most likely results from necrotic cell death caused by damage during or soon afte
113 scription and affected genes associated with necrotic cell death, chromosome condensation, and mRNA p
114 apoptotic-competent conditions or a type of necrotic cell death dependent on RIP1 kinase, termed nec
117 -associated caspase-8 activity and increased necrotic cell death following antigenic stimulation, imp
120 )-NC(Ca-ATP) channel plays a central role in necrotic cell death in central nervous system (CNS) inju
123 Virulent M. tuberculosis strains induce necrotic cell death in macrophages by an obscure molecul
125 a CD44/ITGA4 containing complex and triggers necrotic cell death in multiple myeloma cell lines.
126 and neurobehavioral deficits; apoptotic and necrotic cell death in neurons were reduced by Rapamycin
127 d orchestrate the induction of apoptotic and necrotic cell death in neurons, a VDAC1siRNA and an acti
128 sine triphosphate depletion, and the ensuing necrotic cell death in skin fibroblasts, and this effect
129 tal cytokeratin 18 suggested the presence of necrotic cell death in TASH and may be a useful serologi
130 e, Leu-Leu-OMe, mimics the alum-like form of necrotic cell death in terms of cathepsin dependence and
133 n of the suicide program of myocytes exceeds necrotic cell death in the pathologic heart of ischemic
134 s oxidative burst, mitochondrial damage, and necrotic cell death in TSC-deficient cells in a highly s
139 eases (HD) selectively induces a new form of necrotic cell death, in which endoplasmic reticulum (ER)
141 ess both mec-4(d)-induced cell death and the necrotic cell death induced by expression of a constitut
144 ELLigence technology and AFM have shown that necrotic cell death induced the expansion of the cell ad
147 BNIP3 has been linked to both apoptotic and necrotic cell death involving mitochondrial permeability
149 gical and genetic analyses revealed that the necrotic cell death is distinct from the RIP1/3 pathway-
150 onfirming that protection from apoptotic and necrotic cell death is independent of the stage of hiber
153 tion with RBCs, lung ECs underwent regulated necrotic cell death (necroptosis) and released the essen
154 very high concentrations, leukotoxin caused necrotic cell death of bovine peripheral leukocytes.
156 te that the intracellular LIP and subsequent necrotic cell death of human skin fibroblasts is signifi
158 exacerbated ATP depletion, cytotoxicity, and necrotic cell death of LLCPK(1) cells subjected to hypox
160 ic ischemia followed by reperfusion leads to necrotic cell death (oncosis), which often occurs within
161 rane potential, leading to ATP depletion and necrotic cell death or to cytochrome c release and apopt
163 mpound 1 concentration-dependently inhibited necrotic cell death pathway activation and 2.5 mM compou
168 strate that PARP-1 activation and consequent necrotic cell death play an important role in the pathog
170 physiological (apoptotic) and pathological (necrotic) cell deaths reflects mechanistic differences i
171 cellular molecules associated with regulated necrotic cell death, replicating the characteristics of
175 predominance of ultrastructural features of necrotic cell death suggest a switch from apoptosis to n
176 ibitors of NF-kappaB facilitated TNF-induced necrotic cell death, suggesting that NF-kappaB suppresse
178 ating and suppressing two regulated forms of necrotic cell death, termed pyroptosis and necroptosis,
179 s are much more susceptible to apoptotic and necrotic cell death than CNS microglia, which is mirrore
180 l injury, there is an immediate induction of necrotic cell death that is seen only in GAG-depleted ex
181 n, and peroxynitirte), induced apoptotic and necrotic cell death that was RONS-mediated (cell death p
182 on, lactate dehydrogenase (LDH) release, and necrotic cell death that were blocked by cyclosporin A (
185 mitochondrial respiratory chain defects and necrotic cell death to the BH3-only protein Bcl-2-like 1
187 intestinal Caco-2 cells undergo nonapoptotic necrotic cell death triggered by inositol 1,4,5-trisphos
189 amage caused by UVA to mitochondria leads to necrotic cell death via adenosine triphosphate depletion
191 ed, particularly in T cells, and the rate of necrotic cell death was increased in patients with SLE.
193 cluding apoptosis, which relies on caspases, necrotic cell death, which depends on receptor-interacti
194 (TG) have been used to study the process of necrotic cell death, which involves mitochondria in the
195 iving increased generation of superoxide and necrotic cell death, which was rescued by genetic inhibi
196 ffect of purines, hypoxanthine has prevented necrotic cell death while increasing caspase activity an
197 lin showed enhanced apoptosis, yet decreased necrotic cell death with associated increased caspase-3
200 icin concentrations >/=10 micromol/L induced necrotic cell death within 24 hours, with no changes cha
202 n either case, activated glia caused 75-100% necrotic cell death within 48 hr, which was completely p
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