ライフサイエンスコーパス: apoptosis

1 maximum inhibition value mainly by inducing apoptosis.

2 creasing gluteal adipocyte susceptibility to apoptosis.

3 hanges followed a robust increase in stromal apoptosis.

4 ene (caspase-3) responsible for induction of apoptosis.

5 stress, FORCP depletion results in decreased apoptosis.

6 ng HMGI-C, which is known to protect against apoptosis.

7 e effects of FAM46C, inducing aggregates and apoptosis.

8 majority of cells died by treatment-induced apoptosis.

9 ltimately leading to an increase in cellular apoptosis.

10 agating complexes during the early stages of apoptosis.

11 ed-9/Bcl-2 implicating SEP-1 in execution of apoptosis.

12 es and upregulation of tumor suppressors and apoptosis.

13 ivation, which contributed to CXL146-induced apoptosis.

14 cell growth in vitro and in vivo and induces apoptosis.

15 f the DR-cell population may be regulated by apoptosis.

16 ation towards effector cells, glycolysis and apoptosis.

17 eta-cell dysfunction, dedifferentiation, and apoptosis.

18 pressed tumor cell proliferation and induced apoptosis.

19 (PARP) cleavage indicative of DNA damage and apoptosis.

20 ell fates such as quiescence, senescence, or apoptosis.

21 oxygen species (ROS), and the initiation of apoptosis.

22 C cells undergo double-strand DNA breaks and apoptosis.

23 t their original levels of proliferation and apoptosis.

24 cell growth, differentiation, migration, and apoptosis.

25 nsitizes to ischemic infarction by promoting apoptosis.

26 which is considered an irreversible step in apoptosis.

27 p/dt), decreased infarct size, and decreased apoptosis.

28 duces epithelial cell dysfunction leading to apoptosis.

29 stress fields that guide cell phenotype and apoptosis.

30 ing intracellular glutathione and activating apoptosis.

31 loid) cells and reduce the susceptibility to apoptosis.

32 cl2) confers resistance against drug-induced apoptosis.

33 s and related pathways such as autophagy and apoptosis.

34 infection is known to block the induction of apoptosis.

35 responses, loss of surfactant proteins, and apoptosis.

36 forming domain of Sarrah show an increase in apoptosis.

37 ferentiation, transient beta-catenin induces apoptosis.

38 ses the radiosensitivity of GBM by enhancing apoptosis.

39 feration, but also, at high levels, promotes apoptosis.

40 mIDH1 inhibition-related differentiation and apoptosis.

41 stress and potentiated beta cells to undergo apoptosis.

42 ven tumors by enhancing intrinsic MYC-driven apoptosis.

43 to mitochondrial membrane potential loss and apoptosis.

44 n of BAK1 proteins uniquely repress neuronal apoptosis.

45 analyses show that these compounds activate apoptosis.

46 ox, promoting double-stranded DNA breaks and apoptosis.

47 splatin/JH-RE-06 treatment does not increase apoptosis.

48 otrophins in modulating brain plasticity and apoptosis.

49 l cycle progression rather than induction of apoptosis.

50 ctivating unfolded protein response-mediated apoptosis.

51 NA recruitment and induced primary MCL cells apoptosis.

52 lls by enhancing EGFR/MEK inhibition-induced apoptosis.

53 myeloma cells from oxidative stress-induced apoptosis.

54 idly eliminated after radiation exposure via apoptosis.

55 t regulator of both cellular homeostasis and apoptosis.

56 s reduced in such cells, which were prone to apoptosis.

57 ess pro-apoptotic BMF, limiting drug-induced apoptosis.

58 sponse, causes oxidative stress, and induces apoptosis.

59 Drugging this target leads to cellular apoptosis accompanied by the formation of phase-separate

60 ulation of EZH2 or TET2 expression inhibited apoptosis, affected MAD2 and CDC20 expression, and promo

61 increased small intestinal inflammation and apoptosis after hepatic IR in intestinal TLR9 deficient

62 Klf10 also sensitized primary hepatocytes to apoptosis along with increased caspase 3 activation in r

63 Both BA caused cell necrosis and apoptosis, although the former was the main mode of acti

64 APIO-EE-07 inhibited cell growth and induced apoptosis and also increased expression of Bax as well a

65 Apoptosis and autophagy are two key elements involved in

66 influence of chronic ethanol consumption on apoptosis and autophagy following transient focal cerebr

67 Death receptors are known inducers of apoptosis and cell death that recruit death domain (DD)

68 LMP2A affected apoptosis and cell-cycle checkpoints by dysregulating th

69 as roles in key cellular processes including apoptosis and cellular proliferation.

70 carrying APOE epsilon4/epsilon4 show greater apoptosis and decreased synaptic integrity.

71 a, blunts PMN accumulation, and promotes PMN apoptosis and efferocytosis, thereby facilitating resolu

72 trophil granulocytes (PMNs), followed by PMN apoptosis and efferocytosis.

73 main, was endocytosed by podocytes to induce apoptosis and glomerular dysfunction kidney disease.

74 s, focusing on GRASP65 in cell migration and apoptosis and GRASP55 in unconventional protein secretio

75 olutin substantially decreased Abeta-induced apoptosis and inflammation in neuronal and glial cells.

76 the maintenance of Ab responses by promoting apoptosis and inhibiting necroptosis in B cells.

77 atly reduced lymphoma incidence by enhancing apoptosis and markedly decreasing premalignant B lymphoi

78 EBOV can induce satellite cell and neuronal apoptosis and microglial activation in infected ganglia.

79 rotein kinase 3 (RIPK3)-mediated pathways of apoptosis and mixed lineage kinase domain-like pseudokin

80 T-cell leukemia and TCL cell lines, induced apoptosis and modified the cell cycle.

81 enting with colitis characterized by colonic apoptosis and no identified known VEOIBD variants, to id

82 (-/-) mice was due to decreased cell loss by apoptosis and not enhanced proliferation.

83 odulates various cellular processes, such as apoptosis and proliferation, which has led to distinct c

84 Annexin A5 blocks immunosuppressive apoptosis and promotes immunostimulatory secondary necro

85 nhibition of FAK/Src signaling, induction of apoptosis and re-sensitization to chemotherapy.

86 rease in cell numbers could be attributed to apoptosis and reduced cell division.

87 lecular mechanisms underlying TRAIL-mediated apoptosis and resistance to TRAIL.

88 eutrophils by inhibiting caspase-8-dependent apoptosis and Ripk1-Ripk3-Mlkl-regulated necroptosis.

89 leading to reduced spinal cord neuronal cell apoptosis and smaller lesion area than in untreated anim

90 on but an up-regulation of genes involved in apoptosis and stress response to microbiomes.

91 ivity triggers FOA through DNA damage-driven apoptosis and the complement system of immunity.

92 beta, in Scx-lineage cells in mice increased apoptosis and the deposition of the matrix protein perio

93 ces the number of large lysosomes, decreases apoptosis, and activates autophagy, but it does not resc

94 expression decreases proliferation, induces apoptosis, and attenuates invasion.

95 ake by mitochondria regulates bioenergetics, apoptosis, and Ca(2+) signaling.

96 in the regulation of inflammatory cascades, apoptosis, and cancer.

97 Their importance in proliferation, apoptosis, and cell death ultimately renders them hot ta

98 xpression, DNA repair, chromatin remodeling, apoptosis, and cell proliferation; but it remains unclea

99 inical and clinical studies of TRAIL-induced apoptosis, and current attempts to overcome TRAIL resist

100 9/3 cascade and thereby suppress cancer cell apoptosis, and highlight the role of Trx/TrxR-mediated d

101 ganisms, such as the response to DNA damage, apoptosis, and homeostasis.

102 in the ER, ii) ER Ca(2+) dyshomeostasis and apoptosis, and iii) altered ER Ca(2+) homeostasis in kid

103 escues LAT function in latency reactivation, apoptosis, and immune exhaustion, suggesting that LAT an

104 functions related to cellular proliferation, apoptosis, and inflammatory response.

105 ites, toxic aldehydes, steatosis, ER stress, apoptosis, and liver injury.

106 to stress causes impaired insulin secretion, apoptosis, and loss of cell identity, and a combination

107 et genes function in cell wall biosynthesis, apoptosis, and maintenance of xylem cell wall thickness

108 amlintide was associated with synaptic loss, apoptosis, and microglia activation.

109 ed cell death pathways including pyroptosis, apoptosis, and necroptosis (PANoptosis) and plays an ess

110 nduces cell death in the form of pyroptosis, apoptosis, and necroptosis (PANoptosis).

111 fects of IL2RA on AML cell proliferation and apoptosis, and on pertinent signaling pathways.

112 fferentially regulating cellular senescence, apoptosis, and other p53-mediated biological processes,

113 O inhibited cardiac pathological remodeling, apoptosis, and oxidative stress associated with both ons

114 protein trafficking, splicing, regulation of apoptosis, and prevention of amyloid cleavage pathways.

115 1 abundance to normal levels, decreases cDC1 apoptosis, and repairs cDC1 maturation to drive superior

116 that 16E6, but not 6E6, blocks AIF-mediated apoptosis, and that AIF may represent a novel therapeuti

117 ynergizes with MYC by suppressing MYC-driven apoptosis, and that it does so primarily by reducing the

118 ogramming, immune suppression, resistance to apoptosis, angiogenesis, metastasis, and invasion to sec

119 canonical p53 functions (i.e. senescence and apoptosis) are attributed to inflammation-associated met

120 ofibroblasts, rather than being resistant to apoptosis, are actually primed for apoptosis owing to co

121 of its slow retrotranslocation and mediated apoptosis as efficiently as WT BAX.

122 he 9-cis-retinal treatment decreased retinal apoptosis as shown by the terminal deoxynucleotidyl tran

123 we observe differences in proliferation and apoptosis as well as altered distribution of initiated t

124 mammary epithelial cells (MECs) and induced apoptosis, as determined by the terminal deoxynucleotidy

125 contrast, the CI+Txp group had tubular cell apoptosis associated with expression of caspase-8, TNFR1

126 li initiated by NOD-like receptor (NLR), and apoptosis-associated speck-like protein containing a cas

127 Ceramide-induced endothelial cell apoptosis boosts intestinal stem cell radiosensitivity.

128 Caspase proteases execute apoptosis but also function in development.

129 y meiotic pachytene arrest with accompanying apoptosis, but also apoptosis resulting from mitochondri

130 -negative bacterium Shigella flexneri stalls apoptosis by inhibiting effector caspase activity.

131 report for the first time that GNL1 inhibits apoptosis by modulating the expression of Bcl2 family of

132 Normal mitochondria can trigger intrinsic apoptosis by releasing cytochrome c into the cytosol.

133 in the cells and initiated caspase-dependent apoptosis cascade.

134 nd PKR and markedly increased DNA damage and apoptosis caused by dysregulation of TDP-43 localization

135 igands, many of which play critical roles in apoptosis, cell adhesion, signal transduction, or metabo

136 Physiologically, DJ34 induced apoptosis, cell cycle arrest, and cell differentiation.

137 vival effect through eight cancer hallmarks: apoptosis, cell cycle, cell death, cell motility, DNA re

138 These compounds induce significant PEL apoptosis, cell-cycle arrest, and intracellular ceramide

139 enetic program that intrinsically attenuates apoptosis competence in neurons.

140 is important for development, attenuation of apoptosis competence through neural-specific splicing of

141 This P. zopfii GT-II driven apoptosis corresponded to mitochondrial pathways; mitoch

142 al fibroblast phenotype that is resistant to apoptosis, degrades normal stromal matrix and is replace

143 s were defective in their ability to undergo apoptosis due to the lack of LTB(4) -mediated down-regul

144 1 cells have abnormal morphology and undergo apoptosis, due to increased levels of active caspases 3

145 onally, a MT2A-dependent cellular evasion of apoptosis during cisplatin could be observed, leading to

146 ver, Batf3 (-/-) T cells underwent increased apoptosis during contraction to contribute to a substant

147 proteins play important roles in regulating apoptosis during homeostasis, tissue development, and in

148 o demonstrate that activated Dorsal triggers apoptosis during later developmental stages by up-regula

149 The result was demonstrated improved apoptosis efficiency in HeLa cells.

150 yclase with SQ 22,536 restored BLT1(-/-) BMN apoptosis, FasL and CD36 expression, and clearance by ma

151 lular signal-regulated kinase, and increased apoptosis following serum deprivation or chemotherapy.

152 X3 plays a pivotal role in the inhibition of apoptosis found in the beta-catenin S45F mutants.

153 levated expression of proliferation and anti-apoptosis genes such as BCL2L1 and CCND1.

154 lysosomal dysfunction, inflammatory cascade, apoptosis, genotoxicity, and ultimately necrosis of neur

155 ked to an increase in inflammatory response, apoptosis, glycolytic process and decrease in myocardial

156 al program employed by tumor cells to escape apoptosis, hence developing more aggressive and metastat

157 MCB-613 decreases infarct size, apoptosis, hypertrophy, and fibrosis while maintaining s

158 dexamethasone-induced cell-cycle arrest and apoptosis, illuminating a new possible driver of myeloma

159 Mitotic defects often trigger apoptosis, impairing cell viability as a tradeoff for tu

160 ta-induced impairments on autophagy flux and apoptosis in a calcium-dependent manner.

161 ed CHOP nuclear translocation and downstream apoptosis in a T4SS-dependent manner.

162 sm that fully compensates for the absence of apoptosis in antiviral host defense.

163 observed increases in both proliferation and apoptosis in beta-cells of betaeIF4G1KO.

164 chondrial calcium and mitochondria-dependent apoptosis in cardiac myocytes.

165 he development of T cells, and PRRSV-induced apoptosis in CD4(pos)CD8(pos) thymocytes modulates cellu

166 d apoptosis-inducing ligand (TRAIL) triggers apoptosis in cells by signaling through the O-glycosylat

167 The enhanced monocyte apoptosis in CMH-treated mice was paralleled by increase

168 class-I HDAC inhibitor) efficiently promoted apoptosis in colorectal cancer cells in response to Nutl

169 platin treatment with strongest induction of apoptosis in each of the MPM cell lines, but in differen

170 Fgl2 induced caspase-3/7-mediated apoptosis in Fcgr2b(+), but not Fcgr2b(-/-), CD8(+) T ce

171 sion in blocking homeostatic epithelial cell apoptosis in gastric cancer pathogenesis, suggesting a m

172 ic insight into H. pylori's ability to delay apoptosis in gastric epithelial cells by actively drivin

173 meric DNA damage response (DDR) and cellular apoptosis in highly permissive SupT1 cells, followed by

174 rates DNA damage, telomere erosion, and cell apoptosis in HIV-infected individuals on antiretroviral

175 urkat cells, consistent with higher rates of apoptosis in HLA-E(high) T cells in the presence of NKG2

176 ration and cell-cycle activity and inhibited apoptosis in human AML cell lines and primary cells.

177 Furthermore, HVT blocks apoptosis in infected cells but activates apoptosis in n

178 al JAK inhibition, YBX1 inactivation induces apoptosis in JAK2-dependent mouse and primary human cell

179 enhancer suppresses cell growth by inducing apoptosis in leukemia cell lines.

180 ly inhibited protein prenylation and induced apoptosis in MESN cells, while having little effect in M

181 ks apoptosis in infected cells but activates apoptosis in noninfected bystander cells.IMPORTANCE B ce

182 nscriptionally up-regulated by p53), induced apoptosis in Nutlin-3A-treated, FLIP(L)-depleted cells,

183 OR inhibition restores autophagy and induces apoptosis in p27(-/-) cells.

184 Functionally, UBR5 suppressed MYC-mediated apoptosis in p53-mutant breast cancer cells with UBR5/MY

185 hibits cancer cell proliferation and induces apoptosis in part by blocking the MDM2-p53 feedback loop

186 ed by YAP, which, when suppressed, prevented apoptosis in response to nutrient deprivation in vitro a

187 egeneration of photoreceptors and a role for apoptosis in secondary degeneration of cones, highlighti

188 ger ceramide at plasma membranes, triggering apoptosis in specific cells, such as hematopoietic cells

189 ood cytopenia, bone marrow damage as well as apoptosis in sternum was observed in mice pre-treated wi

190 dle-regulating genes, Shot knockdown induces apoptosis in the absence of Jun kinase (JNK) activation,

191 Consequently, capsaicin induced apoptosis in the cancer cells, but not in the less glyco

192 ucible factor-1 alpha expression and reduced apoptosis in the terminal ileum via Fas-associated prote

193 Protecting ECs from apoptosis in this model did not prevent capillary closur

194 s commonly overexpressed in TMEs and induces apoptosis in tumor-infiltrating, Fas receptor-positive l

195 synthesis and promotes oxidative stress and apoptosis in tumors when administered in combination wit

196 ereby sensitizing CD8 T cells to DEX-induced apoptosis in vitro and significantly reducing tissue imm

197 ensitized them to temozolomide (TMZ)-induced apoptosis in vitro Likewise, in in vivo human GBM xenogr

198 To test the effect of C674 oxidation on apoptosis in vivo, SERCA knock-in mice were subjected to

199 inhibitors promote mitochondrial fission and apoptosis in vivo.

200 TFEB potently inhibits apoptosis in VSMCs, and transcriptome analysis revealed

201 h concentration dependent cell migration and apoptosis, independent of the morphogen transport mechan

202 s to sheer stress inhibited YK-4-279-induced apoptosis, indicating that low-flow vessels may be uniqu

203 nt effects on elevation of ceramide level or apoptosis, indicating that the increases in lung ceramid

204 LIP in pancreatic cancer models and enhanced apoptosis induced by alphaDR5-NPs.

205 tearic acids were able to suppress beta-cell apoptosis induced by proinflammatory cytokines, increasi

206 g the pro-apoptotic genes reaper and hid The apoptosis induced by Reaper and Hid was probably the und

207 Apoptosis induces cell death through mitochondrial outer

208 S13 in CRC cell lines increased tolerance to apoptosis-inducing agents, including paclitaxel and HA14

209 Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induces apoptosis sele

210 The TNF-related apoptosis-inducing ligand (TRAIL) triggers apoptosis in

211 y that targets tumor necrosis factor-related apoptosis-inducing ligand receptor 2, as heavy chains to

212 c-Myc inhibition and apoptosis induction were additionally shown in hematolog

213 pound, 3 n, was significantly more active in apoptosis induction, activation of caspase 3/7, and form

214 ect against hepatic IR injury and intestinal apoptosis/inflammation in intestinal TLR9 deficient mice

215 that vNr-13 is unequivocally involved in the apoptosis inhibition, and it is associated with an incre

216 tes apoptotic signaling pathways, especially apoptosis inhibitor B-cell lymphoma 2.

217 Apoptosis is an ancient and evolutionarily conserved cel

218 Ultimately, apoptosis is an important innate mechanism by which cell

219 Although apoptosis is important for development, attenuation of a

220 However, we show that, when apoptosis is inhibited, severe DNA damage is corrected v

221 Furthermore, the effect of GABA on apoptosis is mediated by inputs from medial ganglionic e

222 ism by which HFD/obesity induces chondrocyte apoptosis is not clearly understood.

223 ropose that, upon telomere shortening, early apoptosis leads to cell depletion and insufficient compe

224 esponse to a parasite antigen that initiates apoptosis-like cell death of parasites, adding fascinati

225 sphamide-induced intermediate and basal cell apoptosis, likely by phosphorylated AKT, and drives phos

226 uding ATP production, cofactor biosyntheses, apoptosis, lipid synthesis, and steroid metabolism.

227 ve described for miRNAs, including acting on apoptosis, M. leprae recognition and engulfment, Schwann

228 matory cytokine interleukin (IL) 10, and the apoptosis markers caspase 3 and TUNEL as well as insulin

229 Carcinogen-induced apoptosis may trigger escape from dormancy of microtumor

230 The G2/M arrest was accompanied by apoptosis, mitochondrial depolarization, generation of r

231 IncuCyte S3 real-time apoptosis monitoring demonstrated that vNr-13 is unequiv

232 Activation of RIPK1 controls TNF-mediated apoptosis, necroptosis and inflammatory pathways(1).

233 -mediated programmed cell death (pyroptosis, apoptosis, necroptosis) is an integral part of host defe

234 ce lacking one of the genes of interest, the apoptosis/necroptosis gene RIPK3, show disturbed bone mi

235 ntify the cell detachment process induced by apoptosis, necrosis or cell lysis substances, respective

236 CIm cytotoxicity was evaluated by MTT assay, apoptosis/necrosis and phosphorylated-cAbl (cAbl-p).

237 d DR5), but the sensitivity to TRAIL-induced apoptosis of cells varies, and the attributes of this ph

238 (2)/M cell-cycle arrest and caspase-mediated-apoptosis of CRC cells.

239 es (TNF-alpha, IL-1beta and Cxcl-1) and also apoptosis of epithelial cells.

240 whereas overexpression of miR-181c promoted apoptosis of HCV-infected hepatocytes and can be inhibit

241 We screened drugs for those that prevent apoptosis of in cells with TTC7A deficiency and tested t

242 enhanced vascular integrity and accelerated apoptosis of infiltrated monocytes.

243 Further, canagliflozin prevents ISO-induced apoptosis of kidney cells by inhibiting Bax protein upre

244 w that loss of Atg7 induces the p53-mediated apoptosis of Lgr5(+)ISC.

245 on in Peyer's Patches is associated with the apoptosis of multiple B cell subsets.

246 uppresses leukemogenic potential and induces apoptosis of primary LSCs from MLL-rearranged AML patien

247 romote degeneration of optic nerve axons and apoptosis of retinal ganglion cells (RGCs), however, the

248 val of LEE-negative STEC as well as inducing apoptosis of the host cells.

249 lization of TP73 protein, which mediated the apoptosis of the neuroblastoma cells upon irradiation tr

250 t not short-chain, Vi conjugate induced late apoptosis of Vi-specific B cells in spleen and early dep

251 n, cell-cycle arrest, and execution phase of apoptosis on treatment.

252 e loss, premature cell aging, and CD4 T-cell apoptosis or depletion via dysregulation of the PI3K/ATM

253 s)-dependent inflammation, caspase-dependent apoptosis, or necroptosis in response to extracellular s

254 istant to apoptosis, are actually primed for apoptosis owing to concomitant activation of cell death

255 nflammation and pyroptosis, necroptosis, and apoptosis (PANoptosis) by activating receptor-interactin

256 on of the intrinsic (mitochondrial mediated) apoptosis pathway in these cells under starvation condit

257 ression of the immune system, autophagy, and apoptosis pathway transcripts, indicating that the DAP1

258 The BAD-BAX-caspase-3 cascade is a canonical apoptosis pathway.

259 eads to cell death through necrotic and late apoptosis pathways.

260 s (P1 to P3), we observed cell cycle arrest, apoptosis, progressive change to a glial morphology and

261 The strain Merlin viral inhibitor of apoptosis pUL36 was necessary and sufficient both to deg

262 f autophagy markers, leading to an increased apoptosis rate following arsenic trioxide treatment.

263 MSTO-211H cells showed lower apoptosis rates at an increased expression level of MT2A

264 t ventricle cardiac function, inhibited cell apoptosis, reduced MI scar size, and promoted post-MI ne

265 ae, with an increased occurrence of cellular apoptosis, reduced neuronal connection, and reduced opto

266 red and modulation of mitochondrion-mediated apoptosis regulating genes changed (increased transcript

267 eckpoints by dysregulating the expression of apoptosis regulators such as BCl-xL and the tumor suppre

268 inguished on the basis of cell signaling and apoptosis-related ions [fatty acids (341.2100 and 382.37

269 activity, dienone compounds are cytotoxic to apoptosis-resistant tumor cells and show activity in ani

270 arrest with accompanying apoptosis, but also apoptosis resulting from mitochondrial morphology and fu

271 The apoptosis seen at 43 degrees C and at 39 degrees C with

272 ed apoptosis-inducing ligand (TRAIL) induces apoptosis selectively via its interaction with the death

273 ppaB-mediated pathways for cell survival and apoptosis signaling in cancer remain to be elucidated.

274 e permeabilization (MOMP) is a core event in apoptosis signaling.

275 Reducing apoptosis signalling via in situ vaccination could be a

276 bind BAK, permeabilize membranes and induce apoptosis, suggesting a potential role for this BH3-bind

277 During apoptosis, these phospholipids move to the cell's outer

278 erase ST6Gal-I is known to block homeostatic apoptosis through alpha2,6-linked sialylation of the dea

279 as maintained for a day longer by countering apoptosis through BCL2 overexpression.

280 F in the mitochondrial genome and inhibiting apoptosis through interactions with the pro-apoptotic BC

281 ER stress initiates apoptosis through intracellular activation of death rece

282 Kynurenine precipitates cardiomyocyte apoptosis through reactive oxygen species production in

283 concentration dependent manner and to induce apoptosis through the mitochondrial pathway.

284 cl-2 protein family also mediate a number of apoptosis-unrelated functions.

285 AIP8 or TIPE) acts as a negative mediator of apoptosis via inhibition of caspase-3 activation, promot

286 r, DSBs were not detected after therapy when apoptosis was inhibited, supporting a framework in which

287 Apoptosis was preceded by an increase of intracellular a

288 genes associated with increased p53 mediated apoptosis was replicated in bronchial biopsies of COPD p

289 Although reduced proliferation and increased apoptosis were observed in alpha3beta1-deficient tumor c

290 ed with cell adhesion, the cytoskeleton, and apoptosis, were increased.

291 ed renal tubular necrosis, inflammation, and apoptosis when compared to P2X4 wild-type (WT) mice subj

292 The observation of apoptosis, which is characterized by the binding of Anne

293 Islet cultures at 20 mm glucose increased apoptosis, which was further amplified when UDP-G was pr

294 Loss of beta-PIX promoted podocyte apoptosis, which was mediated by the reduced activity of

295 on is that hypertrophic chondrocytes undergo apoptosis, while invading vasculature with osteoprogenit

296 out (KO) mice in association with increased apoptosis with no change in proliferation.

297 e biomarker of response to treatment-induced apoptosis with two MYCN-targeted small-molecule inhibito

298 t given BPTPE's delayed induction of UPR and apoptosis, with a higher probability of tumor clonal evo

299 combined experiments of cell proliferation, apoptosis, wound healing assay, as well as reverse-phase

300 thin a defined time window results in B cell apoptosis, yet the mechanisms that enforce dependence on