ライフサイエンスコーパス: anti-apoptotic protein

1 IMP2) and down-regulation of BclII, a potent anti-apoptotic protein.

2 from apoptosis, suggesting that GIMAP6 is an anti-apoptotic protein.

3 tion of the DUSP4 gene that encodes Mkp2, an anti-apoptotic protein.

4 e that villin is an epithelial cell-specific anti-apoptotic protein.

5 ochondria that involves removal of the HAX-1 anti-apoptotic protein.

6 aggregates may deplete motor neurons of this anti-apoptotic protein.

7 es caspase-3-mediated proteolysis of FAK, an anti-apoptotic protein.

8 These cells up-regulate Bcl-X(L), an anti-apoptotic protein.

9 mia 2) homologue, is known to function as an anti-apoptotic protein.

10 vation and Bag-1 expression, a Bcl-2-binding anti-apoptotic protein.

11 membranes, instead contributes to binding to anti-apoptotic proteins.

12 ssion of both Bcl-2 and Survivin, two potent anti-apoptotic proteins.

13 teins impact the expression of oncogenes and anti-apoptotic proteins.

14 n's BH3 domain into the hydrophobic cleft of anti-apoptotic proteins.

15 y results from direct interaction with these anti-apoptotic proteins.

16 e canonical binding groove characterized for anti-apoptotic proteins.

17 ion of death receptors and neutralization of anti-apoptotic proteins.

18 poly(ADP-ribose) polymerase-1, caspases, and anti-apoptotic proteins.

19 y a consequence of downregulation of various anti-apoptotic proteins.

20 its substrates are transcription factors and anti-apoptotic proteins.

21 ing, but also primes cells for inhibitors of anti-apoptotic proteins.

22 ppaB) pathway that leads to up-regulation of anti-apoptotic proteins.

23 ncoding protein chaperones (e.g. iHsp70) and anti-apoptotic proteins.

24 e subverted by pathogens through use of host anti-apoptotic proteins.

25 ly in cancer cells by downregulating several anti-apoptotic proteins.

26 ics to derepress proapoptotic molecules from anti-apoptotic proteins.

27 iR-34a directly inhibits Bcl2 and XIAP, both anti-apoptotic proteins.

28 inducing apoptosis by reducing the levels of anti-apoptotic proteins.

29 and alphaB-crystallin act as chaperones and anti-apoptotic proteins.

30 lting in increased ratio of pro-apoptotic to anti-apoptotic proteins.

31 We show that the anti-apoptotic protein A20 is upregulated in hepatocytes

32 able to maintain the cellular homeostasis of anti-apoptotic proteins, Abcd1-deletion in B12 oligodend

33 e apoptosis through increasing expression of anti-apoptotic proteins, activation of NF-kappaB may con

34 cs detects production of only a few critical anti-apoptotic proteins against a background of general

35 eiotrophin-stimulated phosphorylation of the anti-apoptotic protein Akt.

36 survival functionality has been defined for anti-apoptotic proteins, an activation site has not been

37 These suggested that K7 is a new viral anti-apoptotic protein and survivin-DeltaEx3 is its like

38 the protein levels of survivin, a member of anti-apoptotic proteins and a known mediator of melanoma

39 erm sites of hnRNPA1 promotes translation of anti-apoptotic proteins and is indispensable for the pro

40 XIAP is member of the IAP family of anti-apoptotic proteins and is known for its ability to

41 or of apoptosis (PUMA) counters Bcl-2 family anti-apoptotic proteins and promotes apoptosis.

42 ogated the NF-kappaB activation, increase of anti-apoptotic proteins and protection against Apo2L/TRA

43 the first and second alpha-helices of these anti-apoptotic proteins and which were previously shown

44 ction of c-IAP2, a known NF-kappaB-dependent anti-apoptotic protein, and that the NF-kappaB inhibitor

45 stress resistant cells showed no increase in anti-apoptotic proteins, and released cytochrome c from

46 aperones, the protein degradation machinery, anti-apoptotic proteins, and transcription factors.

47 Cells expressing high levels of the BCL-X(L) anti-apoptotic protein are preferentially killed by the

48 nd a diminution in the degree to which these anti-apoptotic proteins are down-modulated by sorafenib

49 the basal and TNFalpha-induced expression of anti-apoptotic proteins are normal in T2/5 DKO cells, ye

50 milarity of the BH3 binding domains of these anti-apoptotic proteins as well as recent evidence that

51 g cells may depend on enhanced expression of anti-apoptotic proteins as well as reduced expression an

52 ociated protein X-1 (HAX-1), a mitochondrial anti-apoptotic protein, as a specific Omi interactor tha

53 Caspase 3 levels with a parallel decrease in anti-apoptotic protein B-cell leukemia/lymphoma 2 levels

54 mplex in the mitochondria phosphorylates the anti-apoptotic protein B-cell lymphoma extra-large (Bcl-

55 ed by the intrinsic expression levels of the anti-apoptotic protein B-cell lymphoma-extra large (BCL-

56 ondria is inhibited by overexpression of the anti-apoptotic proteins B cell lymphoma/leukemia (Bcl)-2

57 ABT-737 inhibits the anti-apoptotic proteins B-cell lymphoma 2 (BCL-2) and BC

58 associated with increased expression of the anti-apoptotic protein Bag-1 and decreased expression of

59 Taken together, this study identifies the anti-apoptotic protein BAG-1 as a suppressor of the inhi

60 We have recently shown that the anti-apoptotic protein BAG-1, highly expressed in pre-ma

61 caspase 9 activation, or ratios of pro- and anti-apoptotic proteins (BAX, Bcl-2, and Bcl-X(L)).

62 We show that the anti-apoptotic protein Bcl-2 (either wild type or select

63 Inducing QLalpha12 led to degradation of the anti-apoptotic protein Bcl-2 (via the proteasome pathway

64 neonatal platelets had higher levels of the anti-apoptotic protein Bcl-2 and were more resistant to

65 h, we demonstrate that overexpression of the anti-apoptotic protein Bcl-2 attenuates both natural and

66 Overexpression of the anti-apoptotic protein Bcl-2 attenuates neurodegeneratio

67 The anti-apoptotic protein Bcl-2 binds to the pro-apoptotic

68 ers have reported that overexpression of the anti-apoptotic protein Bcl-2 can protect neurons both in

69 In contrast, overexpressing the anti-apoptotic protein Bcl-2 dramatically enhanced the s

70 erglycemia-induced anti-apoptotic effect and anti-apoptotic protein Bcl-2 expression in HASMCs.

71 Wnt3a increased the expression of the anti-apoptotic protein Bcl-2 in an ERK-dependent manner.

72 id receptors (GRs) formed a complex with the anti-apoptotic protein Bcl-2 in response to CORT treatme

73 The human anti-apoptotic protein Bcl-2 increased salt tolerance of

74 e transfer of T cells that overexpressed the anti-apoptotic protein Bcl-2 increased survival.

75 Overexpression of the anti-apoptotic protein Bcl-2 inhibited both the conforma

76 pase 3 activation, ectopic expression of the anti-apoptotic protein Bcl-2 is not sufficient to overco

77 Here, the anti-apoptotic protein Bcl-2 is shown to be highly sensi

78 Enforced expression of anti-apoptotic protein Bcl-2 or Bcl-X(L) inhibited TRAIL

79 The anti-apoptotic protein Bcl-2 protected NPC against nitri

80 3, HeLa, and NIH-3T3 cells, we show that the anti-apoptotic protein Bcl-2 significantly inhibits tran

81 c Alzheimer's mouse model overexpressing the anti-apoptotic protein Bcl-2 was generated.

82 nalysis indicated that the expression of the anti-apoptotic protein bcl-2 was greatly reduced in the

83 ce apoptotic markers, such as suppression of anti-apoptotic protein Bcl-2, activation of caspase-9 or

84 hat the Bak(72-87) peptide also binds to the anti-apoptotic protein Bcl-2, albeit with lower binding

85 s are generally N-myc amplified, express the anti-apoptotic protein Bcl-2, and do not express caspase

86 species, decreases expression levels of the anti-apoptotic protein Bcl-2, and reduces phosphorylatio

87 inhibitor of apoptosis protein survivin, the anti-apoptotic protein bcl-2, but not the pro-apoptotic

88 strate that both wt and mutant SOD1 bind the anti-apoptotic protein Bcl-2, providing evidence of a di

89 eins Bax and Bcl-x(L) and an increase in the anti-apoptotic protein Bcl-2, suggesting that decreased

90 was no change in the expression level of the anti-apoptotic protein Bcl-2, the pro-apoptotic protein

91 r of survival promoting factors, such as the anti-apoptotic protein bcl-2, to mesencephalic DA neuron

92 2) stimulation of JNK and degradation of the anti-apoptotic protein Bcl-2.

93 iated apoptosis and prevents the loss of the anti-apoptotic protein Bcl-2.

94 -3 while simultaneously down-regulating the anti-apoptotic protein BCL-2.

95 nin adhesion complex to up-regulation of the anti-apoptotic protein Bcl-2.

96 nalogs induced apoptosis, with a loss of the anti-apoptotic protein Bcl-2.

97 of Rb and an indirect down-regulation of the anti-apoptotic protein bcl-2.

98 MECs) in vitro by inducing expression of the anti-apoptotic protein Bcl-2.

99 cleaved caspase-3, and downregulation of the anti-apoptotic protein Bcl-2.

100 Stat3, we investigated the regulation of the anti-apoptotic protein Bcl-x(L) and its role in cell sur

101 Ectopic expression of the anti-apoptotic protein Bcl-X(L) in HL-60 cells reduced a

102 ng approach to reengineer the multi-specific anti-apoptotic protein Bcl-x(L) to remove its interactio

103 We found that cells overexpressing the anti-apoptotic protein Bcl-X(L) were resistant to LPS an

104 t to determine if haploinsufficiency for the anti-apoptotic protein Bcl-x(L) would affect tumorigenes

105 ction between the Bak(72-87) peptide and the anti-apoptotic protein Bcl-x(L), the effect of both incr

106 on was performed for binding partners of the anti-apoptotic protein Bcl-X(L).

107 te T cell proliferation and induction of the anti-apoptotic protein Bcl-X(L).

108 h IL-6 cytokines increases expression of the anti-apoptotic protein Bcl-xL and induces activation of

109 ) signaling pathways and increased levels of anti-apoptotic protein Bcl-xL and Mcl-1, which are downs

110 ldamers that bind to a specific cleft on the anti-apoptotic protein Bcl-xL by mimicking an alpha-heli

111 Expression of the anti-apoptotic protein Bcl-XL declined during hyperoxia

112 ion was associated with up-regulation of the anti-apoptotic protein Bcl-XL in cells exposed to adriam

113 specifically and significantly increase the anti-apoptotic protein Bcl-XL in insulinoma cells and mo

114 Furthermore that the anti-apoptotic protein Bcl-xL is regulated by CLPTM1L in

115 Hydrated precipitates of the anti-apoptotic protein Bcl-xL show well-resolved (13)C-(

116 diverse helical BH3 ligands that bind to the anti-apoptotic protein Bcl-xL, a member of the Bcl-2 pro

117 e) polymerase activation, down-regulation of anti-apoptotic protein Bcl-XL, an arrest of the cell cyc

118 on of manganese superoxide dismutase and the anti-apoptotic protein Bcl-xL, and stabilizes mitochondr

119 Levels of the anti-apoptotic protein Bcl-xL, beta-catenin, connective

120 The anti-apoptotic protein bcl-xL, but not bcl-2, was decrea

121 ATA-1 strongly induces the expression of the anti-apoptotic protein bcl-xL, but not the related prote

122 sis by direct and indirect regulation of the anti-apoptotic protein BCL-xL.

123 ex that includes pancortin-2, WAVE1, and the anti-apoptotic protein Bcl-xL.

124 accompanied by an elevated expression of the anti-apoptotic protein Bcl-xL.

125 ription factor MYC and its downstream target anti-apoptotic protein BCL-XL.

126 des with respect to their affinities for the anti-apoptotic protein Bcl-xL.

127 We previously discovered that anti-apoptotic proteins Bcl-2 and Bcl-X(L) bind to and i

128 oviding insights into the mechanism by which anti-apoptotic proteins Bcl-2 and Bcl-X(L) inhibit NLRP1

129 s in association with phosphorylation of the anti-apoptotic proteins Bcl-2 and Bcl-X(L).

130 senolytic' agent, ABT263, which inhibits the anti-apoptotic proteins BCL-2 and BCL-xL and selectively

131 therefore assessed expression levels of the anti-apoptotic proteins BCL-2 and BCL-XL and the pro-apo

132 We show here that HBx interacts with the anti-apoptotic proteins Bcl-2 and Bcl-xL through a Bcl-2

133 entified ABT263 (a specific inhibitor of the anti-apoptotic proteins BCL-2 and BCL-xL) as a potent se

134 stration initially induced expression of the anti-apoptotic proteins Bcl-2 and Bcl-xL, correlating wi

135 s of potent small-molecule inhibitors of the anti-apoptotic proteins Bcl-2 and Bcl-xL.

136 showed that 9-2 can indeed interact with the anti-apoptotic proteins Bcl-2 and Bclx(L) in vivo and in

137 observed down-regulation of c-Myc and of the anti-apoptotic proteins Bcl-2 and Bfl-1 as well as high

138 gulated the expression genes that encode the anti-apoptotic proteins Bcl-2 and Xiap by a mechanism th

139 Anti-apoptotic proteins Bcl-2 and XIAP were up-regulated

140 death pathways, including over-expression of anti-apoptotic proteins Bcl-2 or Bcl-X(L) and genetic ab

141 ibition up-regulated Bax; down-regulated the anti-apoptotic proteins Bcl-2, A1, and cIAP-2; and induc

142 nd was blocked by caspase inhibitors and the anti-apoptotic proteins Bcl-2, and Bcl-x(L), suggesting

143 d ABT-737, a small-molecule inhibitor of the anti-apoptotic proteins Bcl-2, Bcl-X(L) and Bcl-w, with

144 is a potent small molecule inhibitor of the anti-apoptotic proteins Bcl-2/Bcl-X(L)/Bcl-w.

145 We observed that transduction of the anti-apoptotic proteins Bcl-X(L) and PEA-15 fused to TAT

146 Here we report a reduction in the anti-apoptotic proteins Bcl-X(L), Mcl-1, and Bcl-2 in HS

147 contains two distinct binding sites for the anti-apoptotic proteins Bcl-XL and Bcl-2.

148 rimarily from differential expression of the anti-apoptotic proteins Bcl-xL and Mcl-1 relative to Bak

149 However, the basal levels of anti-apoptotic proteins Bcl-xL and Mcl-1 were 4 - 8-fold

150 g proteins Bax and Bak and by inhibiting the anti-apoptotic proteins Bcl-XL, Bcl-2 and Mcl-1.

151 (P < 0.05) increased expression of p-Akt and anti-apoptotic proteins (Bcl-2 and Bcl-xL), while reduce

152 increasing NF-kappaB-mediated expression of anti-apoptotic proteins (Bcl-2 and Survivin) and intrace

153 er the levels of pro-apoptotic protein, Bax, anti-apoptotic protein, Bcl-2, caspase-3 and cytochrome

154 The anti-apoptotic protein, Bcl-2, interacts with the evolut

155 Here we demonstrate that the anti-apoptotic protein, Bcl-2, is highly expressed in RA

156 The anti-apoptotic protein, Bcl-2, promotes the survival of

157 d was not inhibited by overexpression of the anti-apoptotic protein, Bcl-2.

158 -2 mRNA and decreased cellular levels of the anti-apoptotic protein, bcl-2.

159 cally promote the phosphorylation of the key anti-apoptotic protein, Bcl-xL.

160 Also, levels of the anti-apoptotic proteins, Bcl-2 and Bcl-xL were elevated

161 part mediated by expression of either of the anti-apoptotic proteins, BCL-2 and BCL-XL.

162 spase 9 and PARP, with the downregulation of anti-apoptotic protein Bcl2 in HepG2 cells.

163 In circumstances where expression of the anti-apoptotic protein BCL2 is high, Casp8p41 instead bi

164 Overexpression of the anti-apoptotic protein Bcl2, but not the oncoprotein Myc

165 the systemic delivery of siRNA that targets anti-apoptotic protein Bcl2.

166 The levels of anti-apoptotic proteins Bcl2 and Bcl-X(L) were increased

167 p-regulation of heme oxygenase 1, COX-2, and anti-apoptotic proteins (BCL2, BCL2-A1, and MCL-1) and i

168 P (inhibitor of apoptosis protein) family of anti-apoptotic proteins because the levels of XIAP, surv

169 apoptosis that correlated with inhibition of anti-apoptotic proteins being sufficient to permeabilize

170 ciated with an increase in expression of the anti-apoptotic protein Bfl-1 and a decrease in expressio

171 suppressor TP53; mutated genes encoding the anti-apoptotic protein BIRC3 and Toll-like receptor 2 (T

172 HIV also upregulates the anti-apoptotic protein BIRC5, which when blocked promote

173 a 5-fold decrease in phosphorylated Bad, an anti-apoptotic protein, but an increase in Bcl-2 express

174 that in the salivary glands, sens acts as an anti-apoptotic protein by repressing reaper and possibly

175 selective inhibition of NF-kappaB-dependent anti-apoptotic proteins, bypassing potential mitochondri

176 ctor(s) increased the baseline levels of the anti-apoptotic protein c-FLIP in all cell lines tested.

177 ote unconventional polyubiquitination of the anti-apoptotic protein c-FLIP(L) and demonstrate that de

178 We have identified two known endothelial anti-apoptotic proteins, c-FLIP and Mcl-1, the expressio

179 that the mechanism involves induction of an anti-apoptotic protein called ITA.

180 We demonstrate for the first time that two anti-apoptotic proteins can enable tumorigenesis equally

181 pathways or of altered expression of pro- or anti-apoptotic proteins can thus be compared.

182 ed with down-regulation of cyclin D1 and the anti-apoptotic proteins cFLIP, BCL-XL, and MCL-1.

183 total BAD concentration level and the total anti-apoptotic protein concentration level (usually Bcl-

184 Both pro- and anti-apoptotic proteins containing DEDs have been identi

185 BCL-X(L), an anti-apoptotic protein, contains potential BCL-6 target

186 B substrates and the validation of Hip as an anti-apoptotic protein contribute to understanding the i

187 The expression of both anti-apoptotic proteins correlates with the enhanced res

188 cumulating pro-apoptotic signal arising from anti-apoptotic protein degradation, generation of a swit

189 we examined the critical role of Bcl-xL, an anti-apoptotic protein, during brain development.

190 A number of pro- and anti-apoptotic proteins exhibit their effects by modulat

191 and increases the ratio of the apoptotic to anti-apoptotic protein expression.

192 In contrast, the expression of several known anti-apoptotic proteins (FLIP, XIAP, Bcl-x(L)) was not a

193 was associated with a down-regulation of the anti-apoptotic protein, FLIP.

194 differentiation stimuli, stabilizes another anti-apoptotic protein fortilin maximizing the prosurviv

195 The Golgi anti-apoptotic protein (GAAP) is a hydrophobic Golgi pro

196 Golgi anti-apoptotic proteins (GAAPs) are hydrophobic proteins

197 Golgi anti-apoptotic proteins (GAAPs) are multitransmembrane p

198 A2 overexpression degraded the mitochondrial anti-apoptotic protein HAX-1, an effect attenuated by Uc

199 a yeast two-hybrid screen, we identified the anti-apoptotic protein HAX1 to interact with RNF217.

200 e p23 to Hsp90 and induced overexpression of anti-apoptotic proteins Hsp70 and Hsp27 are thought to c

201 striking induction by severe hypoxia of the anti-apoptotic protein IAP-2.

202 We have previously shown that the HSV-2 anti-apoptotic protein ICP10PK is delivered by the repli

203 lpains and induce proteasomal degradation of anti-apoptotic proteins, if and how PARC is regulated by

204 Survivin, an overexpressed anti-apoptotic protein in cancer, represents a pharmacol

205 he Bcl-2 family member Mcl-1 is an important anti-apoptotic protein in the development of multiple ce

206 ecific actin-binding protein functions as an anti-apoptotic protein in the gastrointestinal epitheliu

207 (hVDAC-2) functions primarily as the crucial anti-apoptotic protein in the outer mitochondrial membra

208 udy to elucidate the involvement of pro- and anti-apoptotic proteins in alkylating drug resistance of

209 ) and B cell leukemia/lymphoma 2 (BCL-2) are anti-apoptotic proteins in the BCL-2 protein family ofte

210 though the basal and inducible expression of anti-apoptotic proteins in TRAF2-DeltaR-expressing TRAF2

211 a decrease in the level of Bcl-2, a primary anti-apoptotic protein, in Id1(-/-) endothelial cells, s

212 actor; upregulates a series of intracellular anti-apoptotic proteins including FLIP, survivin, cIAP-2

213 kappaB-dependent expression of both pro- and anti-apoptotic proteins including TRAIL and its death re

214 treated group modulated several key pro- and anti-apoptotic proteins, including Bax, Bad, Bcl-xL, and

215 aster regulator of numerous antioxidants and anti-apoptotic proteins, including HO-1, also accumulate

216 The target gene was survivin, an anti-apoptotic protein induced by chemotherapy and assoc

217 rgoing apoptosis, it is likely that MCL1, an anti-apoptotic protein inducible by growth and different

218 er with computational modeling and selective anti-apoptotic protein inhibitors, uncovers new mechanis

219 efficient system of transiently transferring anti-apoptotic proteins into pancreatic islets, thus ope

220 The increased cap-independent translation of anti-apoptotic proteins is involved in the development o

221 e report that both TNF and IL-1 activate the anti-apoptotic protein kinase Akt in growth factor and s

222 eatment blocks EGF-induced activation of the anti-apoptotic protein kinase Akt suggesting that Src ma

223 also reduced v-Src-induced activation of the anti-apoptotic protein kinase Akt.

224 cade, because overexpression of Bcl-X(L), an anti-apoptotic protein localized to mitochondria, blocke

225 ommunications define a critical role for the anti-apoptotic protein MCL-1 as a driver of adaptive sur

226 suppressing apoptosis and, accordingly, the anti-apoptotic protein Mcl-1 is one target of both phosp

227 report, we show that the level of the human anti-apoptotic protein Mcl-1 is regulated during the cel

228 ed that L. donovani exploited the macrophage anti-apoptotic protein MCL-1 to prevent BAK-mediated mit

229 t in HaCaT cells triggers a reduction in the anti-apoptotic protein Mcl-1, similar to UV radiation.

230 apoptosis by reducing concentrations of the anti-apoptotic protein Mcl-1.

231 ctor NOXA, thus creating a dependence on the anti-apoptotic protein MCL-1.

232 2 family member Noxa only interacts with the anti-apoptotic proteins Mcl-1 and A1 but not Bcl-2.

233 NBK/BIK activated BAK by displacing it from anti-apoptotic proteins MCL-1 and BCL-X(L) that sequeste

234 xa- and caspase-dependent degradation of the anti-apoptotic protein, Mcl-1.

235 Overexpression of anti-apoptotic proteins MCL1 and Bcl-xL are frequently o

236 pproaches, we documented that the macrophage anti-apoptotic protein myeloid cell leukemia 1 (MCL-1) i

237 The anti-apoptotic protein myeloid cell leukemia 1 (Mcl-1) p

238 d this was associated with the activation of anti-apoptotic protein NF-kappaB, a downstream target of

239 t PPAN is a novel interaction partner of the anti-apoptotic protein nucleophosmin (NPM).

240 se-12 were dramatically decreased, while the anti-apoptotic proteins of Bcl-2 and NF-kappaB were sign

241 ling expression of the anti-inflammatory and anti-apoptotic protein, PI-9.

242 udies in vitro and in vivo, we show that the anti-apoptotic protein poly(ADP-ribose) polymerase (PARP

243 TUNEL positive cells, and increase of Bcl-2 (anti-apoptotic protein) positive cells in the ischemic a

244 pounds show selectivity for Mcl-1 over other anti-apoptotic proteins, possess cytotoxicity to cancer

245 ndotoxemia-associated elevation of Mcl-1, an anti-apoptotic protein primarily under the transcription

246 The IAP (inhibitor of apoptosis) family of anti-apoptotic proteins regulates programmed cell death.

247 ither inactivation or activation of pro- and anti-apoptotic proteins, respectively.

248 atic beta-cell line, indicating that TAT/PTD anti-apoptotic proteins retained their biological activi

249 Analysis of several anti-apoptotic proteins revealed that Bcl-x(L) levels an

250 ficant increase in mRNA levels for the known anti-apoptotic protein serum and glucocorticoid-regulate

251 This suggests that an anti-apoptotic protein such as Bcl-2 should be minimally

252 Anti-apoptotic proteins such as BCL-2 counteract BAX-med

253 This is commonly due to overexpression of anti-apoptotic proteins such as Bcl-2, Bcl-X(L), and Mcl

254 oresistant cells that express high levels of anti-apoptotic proteins such as BCL-XL is thought to res

255 to the up-regulation of NF-kappaB-dependent anti-apoptotic proteins, such as BCL2, c-FLIPS, XIAP, an

256 The anti-apoptotic protein survivin (Sur) plays an important

257 We found that the expression of the anti-apoptotic protein survivin correlated positively wi

258 ild-type APC in the colon down-regulates the anti-apoptotic protein survivin, and APC mutation up-reg

259 n vivo and that STAT3 activation induces the anti-apoptotic protein survivin.

260 L at least in part by reducing levels of the anti-apoptotic protein survivin: ectopic expression of s

261 Infected AmEpCs up-regulated anti-apoptotic proteins survivin and Bcl-xL by mechanism

262 Extracts decreased expression of anti-apoptotic proteins (survivin, cIAP-2, XIAP), induce

263 d to screen 157 compounds in 6 h against the anti-apoptotic protein target Bcl-x(L).

264 recently identified as a bcl-2-interacting, anti-apoptotic protein that binds to the ATPase domain o

265 of FLICE-like inhibitory protein (FLIP), an anti-apoptotic protein that has previously been shown to

266 Bcl-2 is an anti-apoptotic protein that has recently been shown to r

267 PEA-15 is a small anti-apoptotic protein that is enriched in astrocytes, b

268 essor with Caspase recruitment domain) is an anti-apoptotic protein that is found abundantly in termi

269 Survivin is a novel anti-apoptotic protein that is highly expressed in cance

270 Survivin is an anti-apoptotic protein that is overexpressed in most hum

271 Mcl-1 is an anti-apoptotic protein that is particularly important fo

272 Myeloid cell leukemia 1 protein (MCL1) is an anti-apoptotic protein that is structurally related to B

273 inhibitor of apoptosis (ML-IAP) is a potent anti-apoptotic protein that is upregulated in a number o

274 , we investigated Bax inhibitor 1 (BI-1), an anti-apoptotic protein that primarily resides in the ER

275 Galectin-3 is an anti-apoptotic protein that protects T cells, macrophage

276 cytoplasmic C terminus of Kv3.3 to Hax-1, an anti-apoptotic protein that regulates actin nucleation t

277 vival dependence on individual or subsets of anti-apoptotic proteins that could be effectively target

278 creased expression of both pro-oncogenic and anti-apoptotic proteins that result in increased cell pr

279 ocalized at the mitochondria functions as an anti-apoptotic protein, the function of Bcl-2 at the nuc

280 The gene encoding the anti-apoptotic protein TNFAIP8 (tumor necrosis factor al

281 ies, which become dependent on expression of anti-apoptotic proteins to counter expression of pro-apo

282 ll death, due to the impaired recruitment of anti-apoptotic proteins to the TNFR1 complex in the abse

283 ts TNFalpha-induced cell death by recruiting anti-apoptotic proteins to the TNFR1 complex rather than

284 to BH3 mimetics reflects the identity of the anti-apoptotic proteins to which BAK is constitutively b

285 nding and recruiting Bcl-2 and Bcl-X(L), two anti-apoptotic proteins, to mitochondria.

286 ing partners we found that HOXA5 binds to an anti-apoptotic protein, Twist.

287 d CD4(+) T cells facilitated the transfer of anti-apoptotic proteins via nanotubes, resulting in incr

288 6-day treatment gene expression of bcl-2, an anti-apoptotic protein, was down-regulated, whereas casp

289 d PLGA-NP were internalized in HCC cells and anti-apoptotic proteins were down regulated with apoptos

290 ation, even when both Bcl-xL- and Mcl-1-type anti-apoptotic proteins were inhibited.

291 itive to TNFalpha-induced cell death because anti-apoptotic proteins were not recruited to the TNFR1

292 Notably, the same anti-apoptotic proteins were previously found to reduce

293 l differentiation protein (Mcl-1), two major anti-apoptotic proteins, were present within the nanotub

294 rgins were characterized by pro-survival and anti-apoptotic proteins, whereas perinecrotic regions we

295 Amounts of A1, A20, and Bcl-x(L), anti-apoptotic proteins whose transcription is dependent

296 Bcl-xL, is an anti-apoptotic protein with a high degree of homology to

297 m FKBP38 facilitates the association of this anti-apoptotic protein with the pro-apoptotic protein Ba

298 on-influenced expression of several pro- and anti-apoptotic proteins within CFSE-labeled cultures.

299 SW480 cells increased the expression of the anti-apoptotic protein XIAP.

300 D is also prevented by overexpression of the anti-apoptotic proteins XIAP or Bcl-xL, and by a mutant