ライフサイエンスコーパス: antiapoptotic

1 and, PDGF may exert vascular stabilizing and antiapoptotic actions through endothelial-pericyte and e

2 rier stabilization and anti-inflammatory and antiapoptotic actions; and (3) a regenerative on the bas

3 P in such a way that cellular IAP levels and antiapoptotic activities are maintained.

4 nd it was recently suggested that AAT exerts antiapoptotic activities, we aimed to explore whether ad

5 Here we report that ATR has an antiapoptotic activity at mitochondria in response to UV

6 This antiapoptotic activity in E. faecalis-infected cells was

7 he F1L N-terminal region does not impede F1L antiapoptotic activity in the context of a viral infecti

8 Thus, the antiapoptotic activity of AnkG is controlled by p32-medi

9 that immune exhaustion is not caused by the antiapoptotic activity of the LAT.

10 cellular pathogen Coxiella burnetii displays antiapoptotic activity which depends on a functional typ

11 n to provide the Mcl-1 protein with enhanced antiapoptotic activity, thereby highlighting the clinica

12 lated by growth factor signals that manifest antiapoptotic activity.

13 ins their unusual stability and their potent antiapoptotic activity.

14 his relationship, due to insulin's mitogenic/antiapoptotic activity.

15 ephosphorylation of Bcl-2 and inhibiting its antiapoptotic activity.

16 ells, indicating that a T4SS effector(s) has antiapoptotic activity.

17 These results define a novel function of the antiapoptotic, adenoviral E1B 19K protein that may limit

18 Our results define a new function of the antiapoptotic, adenoviral protein E1B 19K, which we have

19 at extend to nonerythroid tissues, including antiapoptotic and anti-inflammatory effects.

20 More importantly, the antiapoptotic and antiautophagic functions of vBcl-2 wer

21 cation but showed little or no effect on the antiapoptotic and antiautophagic functions of vBcl-2.

22 eplication is genetically separated from its antiapoptotic and antiautophagic functions, suggesting t

23 Furthermore, the Nrf2 protein levels and antiapoptotic and antioxidant enzyme levels are higher i

24 we found that this pathway is important for antiapoptotic and cell proliferation signaling.

25 dent susceptibility include higher levels of antiapoptotic and innate immune factors in mature neuron

26 wth factor (VEGF)-B activates cytoprotective/antiapoptotic and minimally angiogenic mechanisms via VE

27 The LPA2 GPCR mediates antiapoptotic and mucosal barrier-protective effects in

28 phorylation of CREB, increased expression of antiapoptotic and neurotrophic molecules and reduced apo

29 leading to cancer involve the activation of antiapoptotic and proliferation programs, as well as eva

30 ve capacity, acquiring angiogenic, invasive, antiapoptotic and survival properties, becoming free fro

31 ation, NO production, and anti-inflammatory, antiapoptotic, and antioxidant effects.

32 Erythropoietin exerts anti-inflammatory, antiapoptotic, and cytoprotective effects in addition to

33 C)-induced cytoprotective effects, including antiapoptotic, anti-inflammatory, and barrier stabilizat

34 ely, we present a new mechanism of action of antiapoptotic ARC by which ARC regulates PGE2 production

35 myeloid cell leukemia 1 (Mcl1) but not other antiapoptotic B cell leukemia/lymphoma 2 (Bcl2) family m

36 ree major classes of antiapoptotic proteins: antiapoptotic B cell lymphoma 2 (BCL-2) proteins, inhibi

37 Although lowering the levels of the antiapoptotic B-cell lymphoma (BCL)2 family proteins, BA

38 COPD AMs had elevated levels of Mcl-1, an antiapoptotic B-cell lymphoma 2 family member, with sele

39 e PROTACs a first step toward a new class of antiapoptotic B-cell lymphoma 2 family protein degraders

40 high-dose pre-BCR/BCR stimulation as well as antiapoptotic Bcl(xL) overexpression in pre-B cells.

41 umbers of apoptotic cells but high levels of antiapoptotic Bcl-2 expression, some dividing cells, and

42 can even promote Treg expansion by enhancing antiapoptotic Bcl-2 expression.

43 aved-caspase-3 expression, and downregulated antiapoptotic Bcl-2 expression; while overexpression (OE

44 Bcl-xL, an antiapoptotic Bcl-2 family member, undergoes conformatio

45 These results demonstrate that the antiapoptotic Bcl-2 family members do not directly inhib

46 Unlike other antiapoptotic Bcl-2 family members, Mcl-1 also mediates

47 n tumor cell growth as well as expression of antiapoptotic BCL-2 family members.

48 Cs (cDCs) and their dependence on individual antiapoptotic BCL-2 family members.

49 Several reports suggested that the antiapoptotic Bcl-2 family protein Bcl2a1/Bfl-1/A1 plays

50 tial resistance mediated by induction of the antiapoptotic Bcl-2 family proteins Bcl-xL and Bfl-1.

51 Accordingly, BCL2 mutations can affect antiapoptotic Bcl-2 function, are associated with increa

52 strated that proapoptotic Bim interacts with antiapoptotic Bcl-2 members in a sequential manner: Bcl-

53 im or, to a lesser extent, overexpression of antiapoptotic Bcl-2 or Mcl-1, significantly accelerated

54 tor signaling leads to overexpression of the antiapoptotic BCL-2 protein and is implicated in the pat

55 Accordingly, strategies to antagonize the antiapoptotic Bcl-2 proteins have largely focused on the

56 The prosurvival function of the antiapoptotic Bcl-2 proteins is manifested by capturing

57 between the transmembrane domains of Bax and antiapoptotic Bcl-2 proteins represent a previously unap

58 Overexpression of antiapoptotic Bcl-2 proteins such as Bcl-2, Bcl-xL, and

59 establish latency by modulating or mimicking antiapoptotic Bcl-2 proteins to promote survival of carr

60 unresponsive to antagonistic effects of the antiapoptotic BCL-2 proteins.

61 lecule BH3 mimetic, inhibits the function of antiapoptotic Bcl-2 proteins.

62 here that Emicro-directed expression of the antiapoptotic Bcl-B protein in mice drives an MM phenoty

63 rotein PUMA induces significant unfolding of antiapoptotic Bcl-xL at the interface, which in turn dis

64 Furthermore, JUNB and BCL2L1 (which encodes antiapoptotic BCL-xL) mRNA levels were markedly reduced

65 y microenvironmental signals that upregulate antiapoptotic Bcl-xl, Mcl-1, and A1, which can be counte

66 and functionality of the complex represents antiapoptotic Bcl-XL.Bax complexes in the MOM.

67 ormal and malignant lymphocytes, whereas the antiapoptotic BCL2 confers resistance.

68 The abundance of antiapoptotic BCL2 family members based on immunoblottin

69 ff cell survival by increasing expression of antiapoptotic BCL2 family members but instead acts by pr

70 Mcl-1 is a unique antiapoptotic Bcl2 family protein that functions as a ga

71 Expression of the antiapoptotic BCL2 protein or inactivation of the p53 pr

72 expression signature, hairy morphology, and antiapoptotic behavior.

73 ome mutant Bcl-2 proteins exhibited enhanced antiapoptotic capacity in vitro.

74 y by down-regulating the expression of vital antiapoptotic cellular proteins and inhibiting the genet

75 nd can trigger important proinflammatory and antiapoptotic changes in latently infected cells.

76 plasmacytomas highlight the significance of antiapoptotic changes in multiple myeloma, which include

77 PR, resulting in increased production of the antiapoptotic chaperone BiP/GRP78, preparing cancer cell

78 -cell production of various inflammatory and antiapoptotic cytokines.

79 (iii) The mechanism of LAT antiapoptotic effect is distinct from that of the baculo

80 The antiapoptotic effect of AAC-11 may be clinically relevan

81 T phosphorylation and a 20% reduction in the antiapoptotic effect of exogenous MIF.

82 f MCL1, which proved to be essential for the antiapoptotic effect of IFNgamma in an IM-treated CML li

83 onstrated that in an IM-treated CML line the antiapoptotic effect of IFNgamma was independent of BCL6

84 The antiapoptotic effect of MIF was absent in Cxcr7(-/-) mur

85 In vitro studies showed the antiapoptotic effect of MN-siCas-3 on islets in culture,

86 The antiapoptotic effect of rhIL-7 was associated with incre

87 tory diseases and autoimmunity including its antiapoptotic effect on epithelial cells.

88 hannels and adhesion molecules or antagonize antiapoptotic effects on B-cell lymphoma 2 family member

89 MitoNEET-challenged alpha-cells exert potent antiapoptotic effects on beta-cells and prevent cellular

90 potent anti-inflammatory, antinecrotic, and antiapoptotic effects that protect against ischemic AKI.

91 istic studies indicated that CTSH exerts its antiapoptotic effects through decreased JNK and p38 sign

92 tions, tapentadol elicited proneurogenic and antiapoptotic effects via activation of beta2 and alpha2

93 The renal antiapoptotic effects were at least mediated by cGMP/PKG

94 ree iron, which exerts anti-inflammatory and antiapoptotic effects.

95 is factor (TNF)-alpha, the proangiogenic and antiapoptotic enzyme cyclooxygenase-2, the IL-8 receptor

96 and Bcl-XL that support NF-kappaB-dependent antiapoptotic events.

97 mily of proteins, and vaccinia virus harbors antiapoptotic F1L that potently inhibits the mitochondri

98 resulted in the increased expression of the antiapoptotic factor Bcl-2 and decreased expression of t

99 ctivated nuclear factor-kappaB to upregulate antiapoptotic factor Bcl-2 and induced etoposide resista

100 cells (hiPSCs) or hiPSCs overexpressing the antiapoptotic factor BCL2, transferred to synchronized g

101 interaction between the NF-kappaB-regulated antiapoptotic factor GADD45beta and the JNK kinase MKK7

102 STAT3 is considered as a critical antiapoptotic factor in various malignancies.

103 that P38 activation led to a decrease in the antiapoptotic factor MCL1, which is often upregulated in

104 nt activation of STAT3 without affecting the antiapoptotic factor STAT1 and cause increased formation

105 tumor-initiating population and serves as an antiapoptotic factor, facilitating anchorage independenc

106 The long variant (Mcl-1L) acts as an antiapoptotic factor, whereas the short isoform (Mcl-1S)

107 ease significant levels of proangiogenic and antiapoptotic factors in the ischemic microenvironment.

108 induced the expression of Bcl-2 and Bcl-xL, antiapoptotic factors that negatively regulate autophagy

109 optosis and consist of both proapoptotic and antiapoptotic factors.

110 in bioenergetic efficiency and stably uphold antiapoptotic features is unknown.

111 ly, our study reveals that GNL1 executes its antiapoptotic function by a novel mechanism and suggests

112 Surprisingly, we found that the antiapoptotic function of D-cyclins also operates in qui

113 l and appears to be crucial in mediating the antiapoptotic function of Lyn in this disease.

114 ls and primary rat beta-cells, suggesting an antiapoptotic function of SKAP2.

115 ull-length Mcl-1 protein with regards to its antiapoptotic function, and induces cell death in a Bok-

116 ormational change in Bcl2 that abrogates its antiapoptotic function, converting it from a survival mo

117 The BH4 domain of Bcl2 is required for its antiapoptotic function, thus constituting a promising an

118 , Op-IAP3 stabilizes SfIAP and preserves its antiapoptotic function.

119 cholesterol efflux and anti-inflammatory and antiapoptotic functions seemed to be more severely suppr

120 (APC) anticoagulant, anti-inflammatory, and antiapoptotic functions.

121 tance to apoptosis by directly targeting the antiapoptotic gene BCL2 Finally, mir-200 was able to ant

122 e a chromosomal translocation that links the antiapoptotic gene BCL2 to the regulatory elements of im

123 se 7 and de-repressing the expression of the antiapoptotic gene cFlar.

124 d the proliferation capacity and upregulated antiapoptotic gene expression in AMs but not IMs.

125 hift in the balance between proapoptotic and antiapoptotic gene expression programs.

126 oncomitant upregulation of NF-kappaB-induced antiapoptotic gene expression, thereby suppressing IFN-g

127 eopolyhedrovirus (AcMNPV) mutant lacking the antiapoptotic gene p35 (vAc(P35)) and a cosmid represent

128 cells by selectively enhancing mRNA decay of antiapoptotic gene transcripts, including Bcl2L1, Bcl2A1

129 Ki67, minichromosome maintenance genes 2-5, antiapoptotic gene X-linked inhibitor of apoptosis, and

130 We detected upregulation of antiapoptotic genes (e.g., XIAP and GADD45B) and downreg

131 families then targeted and downregulated the antiapoptotic genes Bcl-2 and Bcl-xL, respectively, to i

132 romoter of target genes c-Myc and Mcl-1, and antiapoptotic genes Bcl2 and Bcl-xL.

133 associated with the marked expression of the antiapoptotic genes BIRC5 and IFI6 When the expression o

134 AA-induced apoptosis and down-regulation of antiapoptotic genes can be inhibited by overexpressing G

135 Tuberculosis cases had reduced levels of antiapoptotic genes compared to HHCs with a significant

136 al cells leads to up-regulation of NF-kappaB antiapoptotic genes upon TNF stimulation and renders cel

137 e 21, leading to the sustained expression of antiapoptotic genes, including IGF1, B cell CLL/lymphoma

138 defective expression of NF-kappaB-dependent antiapoptotic genes.

139 , partially inhibiting expression of several antiapoptotic genes.

140 e of known IGF2BP3 binding mRNA, such as the antiapoptotic HMGA2 mRNA, as well as the oncogenic c-MYC

141 gly reduces the expression of the inducible, antiapoptotic HSP70 family members HSPA1L and HSPA2, the

142 decreased expression of transcripts encoding antiapoptotic HuR target RNAs.

143 oxide, suggesting that MrBI-1 contributes to antiapoptotic-like cell death via the endoplasmic reticu

144 splicing variant (MCL1-S) and diminishes the antiapoptotic, long variant (MCL1-L).

145 poptotic programmed cell death protein 5 and antiapoptotic macrophage migration inhibitory factor acc

146 tory reactions; and induce the expression of antiapoptotic markers in the retina, preventing the dege

147 rophage-specific overexpression of the human antiapoptotic Mcl-1 protein, a factor upregulated in AMs

148 Here, we describe a novel antiapoptotic mechanism in vascular SMCs that involves i

149 However, the antiapoptotic mechanism of viral IAPs in host insects ha

150 y affected by O-GlcNAcylation as a potential antiapoptotic mechanism.

151 YAP as a key regulator of proliferation and antiapoptotic mechanisms in CC and provide first evidenc

152 l blood malignant cell samples suggested the antiapoptotic mediator B-cell lymphoma 2 (BCL2) as a pot

153 lation of STAT5 and Akt and transcription of antiapoptotic mediator bcl-xL Several small-molecule inh

154 ctor (HGF), is known to function as a potent antiapoptotic mediator in normal and neoplastic cells.

155 Myeloid cell leukemia-1 (Mcl-1) is an antiapoptotic member of the Bcl-2 family of proteins tha

156 It is an antiapoptotic member of the Bcl-2 family of proteins, wh

157 Myeloid cell leukemia 1 (Mcl-1), an antiapoptotic member of the Bcl-2 family of proteins, wh

158 MCL-1 is an antiapoptotic member of the BCL-2 protein family, whose

159 t promote plasma cell survival by regulating antiapoptotic members of the Bcl-2 family including Mcl-

160 ften associated with the upregulation of the antiapoptotic members of the Bcl-2 family of proteins.

161 found that IFNgamma also upregulated several antiapoptotic members of the BCL2 and BIRC gene families

162 Bcl-2 protein family comprises both pro- and antiapoptotic members that control the permeabilization

163 Here we report that alphaB-crystallin, an antiapoptotic molecular chaperone implicated in the path

164 l number was marked by low expression of the antiapoptotic molecule B cell lymphoma 2 (Bcl2) and incr

165 te the expression of the gene coding for the antiapoptotic molecule Bcl-2, the proapoptotic molecule

166 et, interferon gamma, interleukin 2, and the antiapoptotic molecule Bcl-2, whereas it dampened the di

167 ted the expression of the cytoprotective and antiapoptotic molecule heme oxygenase-1 (HO-1) at the tr

168 -pathway reaction, has been identified as an antiapoptotic molecule in mammals.

169 els of cytokines, expressed higher levels of antiapoptotic molecules and proliferated more slowly tha

170 und that GLI1 binds to the promoter of these antiapoptotic molecules and regulates their expression a

171 Bax, and Fas in CD28(null) T cells, whereas antiapoptotic molecules Bcl-2 and Bcl-xL were similar in

172 nregulation and an inverted ratio of pro- to antiapoptotic molecules, both of which were reversed by

173 ling cascade that results in upregulation of antiapoptotic molecules, cytokine secretion, and enhance

174 or growth, cell viability, and expression of antiapoptotic molecules.

175 lines has concomitant high expression of the antiapoptotic myeloid cell leukemia 1 (MCL-1).

176 Here, antiapoptotic myeloid cell leukemia 1 (MCL1) was found t

177 ily members including harakiri (HRK) and its antiapoptotic partner BCL extra large (BCL-xL), BCL2 rel

178 ly promotes the understanding of the role of antiapoptotic pathways in bacterial infection, but has a

179 The cytokine induces proliferative and antiapoptotic pathways in epithelial cells allowing enha

180 eceptor) genes involved in proliferation and antiapoptotic pathways in mouse B cells.

181 Antiapoptotic pathways of the host cell play integral ro

182 MV-dependent shift from Mcl-1 as the primary antiapoptotic player to the related protein, Bcl-2, late

183 d IAPs explains their relative stability and antiapoptotic potency.

184 Interestingly, IAPs with the strongest antiapoptotic potential contain two BIR and two RING dom

185 rotein (BAX) and B-cell lymphoma 2 toward an antiapoptotic profile.

186 is proactive effect through activation of an antiapoptotic program in cardiomyocytes.

187 tosis in the presence of agents blocking the antiapoptotic program.

188 The antiapoptotic, prometastatic JAK-STAT3 pathway was activ

189 Functions of the CLN3 protein include antiapoptotic properties and facilitating anterograde tr

190 1 activity, can confer anti-inflammatory and antiapoptotic properties in cellular models of toxicity

191 Current strategies for halting the antiapoptotic properties of MCL1 revolve around inhibiti

192 iPSC-EVs enhanced angiogenic, migratory, and antiapoptotic properties of murine cardiac endothelial c

193 oepoxy derivative of DHEA, was shown to have antiapoptotic properties via mechanisms involving the ne

194 tion and noticeable in vitro antioxidant and antiapoptotic properties.

195 eraction module, and that can prevent AAC-11 antiapoptotic properties.

196 e treatment of multiple sclerosis and exerts antiapoptotic properties.

197 pathway, is a powerful antioxidant, and has antiapoptotic properties.

198 s protection was mediated by upregulation of antiapoptotic protein (c-IAP-2) through calmodulin-depen

199 ted chemoresistance in AML.Significance: The antiapoptotic protein ARC promotes AML aggressiveness by

200 which results in constitutive activation of antiapoptotic protein B cell lymphoma 2 (BCL2) in a subs

201 Similarly, inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) has been

202 appaB phosphorylation, and the expression of antiapoptotic protein B-cell lymphoma 2, which were reve

203 Pim kinases control the translation of antiapoptotic protein Bcl-2 at an internal ribosome entr

204 Overexpression of the antiapoptotic protein Bcl-2 is observed in the majority

205 senger RNA and protein concentrations of the antiapoptotic protein Bcl-2 were increased after Ucp2 kn

206 ay but not the AKT pathway to upregulate the antiapoptotic protein Bcl-2, which protects cells from d

207 41 also binds with nanomolar affinity to the antiapoptotic protein Bcl-2, which sequesters Casp8p41 a

208 nts), and the concomitant down-regulation of antiapoptotic protein Bcl-2.

209 and identified 1 of the substrates to be the antiapoptotic protein Bcl-xL.

210 damage, and rupture by sequestration of the antiapoptotic protein Bcl-xL.

211 g p73 allele, exhibit elevated levels of the antiapoptotic protein Bcl2 and thus dampen apoptosis.

212 partially restored by overexpression of the antiapoptotic protein BCL2, whereas heterozygous deficie

213 results with venetoclax, an inhibitor of the antiapoptotic protein BCL2.

214 tion that FLT3 TKI treatment upregulates the antiapoptotic protein Bcl6, limiting the drug's apoptoti

215 ession: DAD1 and DAD2, homologs of the human antiapoptotic protein DEFENDER AGAINST CELL DEATH.

216 The antiapoptotic protein HAX-1 (HS-associated protein X-1)

217 We hypothesized that the endogenous antiapoptotic protein humanin (HN) may prevent these eff

218 thesis of myeloid cell leukemia 1 (MCL1), an antiapoptotic protein known to play a role in cancer cel

219 gainst the protein interaction site of human antiapoptotic protein Mcl-1 and found that four of the t

220 sunitinib by enhancing the stability of the antiapoptotic protein MCL-1 and inducing mTORC1 signalin

221 ance, which correlates with induction of the antiapoptotic protein Mcl-1 and less consistently with d

222 ot very effective against melanoma, with the antiapoptotic protein MCL-1 as the main contributor to r

223 USP9x protects the antiapoptotic protein Mcl-1 from degradation, and cells

224 Overexpression of the antiapoptotic protein Mcl-1 provides a survival advantag

225 owever, the transmembrane interactome of the antiapoptotic protein Mcl-1 remains largely unexplored.

226 downregulated constitutive expression of the antiapoptotic protein Mcl-1, in both EMC cell lines and

227 TNBC cells by promoting the synthesis of the antiapoptotic protein Mcl-1.

228 otein BIM and proteasomal degradation of the antiapoptotic protein MCL-1.

229 The antiapoptotic protein MCL1, a member of the BCL2 family,

230 We investigated the functions of the antiapoptotic protein MCL1, another member of the BCL2 f

231 biquitination and enhancing stability of the antiapoptotic protein MCL1; therefore, IRAK inhibition r

232 Helicobacter pylori induces the antiapoptotic protein myeloid cell leukemia 1 (Mcl1) in

233 le of glutathione transferase (GST) P1-1, an antiapoptotic protein often overexpressed in drug-resist

234 Although the antiapoptotic protein on which a cell depends is typical

235 We previously identified the antiapoptotic protein survivin in the autoreactive B cel

236 cytosol of cells increased the levels of the antiapoptotic protein survivin.

237 AAC-11 is an antiapoptotic protein that is upregulated in most cancer

238 hat inhibits the production of clusterin, an antiapoptotic protein that is upregulated in response to

239 Human Bax inhibitor-1 (hBI-1) is an antiapoptotic protein that mediates a calcium leak and i

240 In this study, we identified the antiapoptotic protein YAP, a core component of the Hippo

241 An antiapoptotic protein, AfBIR1, opposes this process by i

242 Upregulation of the antiapoptotic protein, Mcl-1, ROS generation, and NF-kap

243 Bcl-2, an antiapoptotic protein, was upregulated ~3-fold in the mi

244 ess by stabilizing the mRNA for Bcl-x(L), an antiapoptotic protein.

245 urther confirming the role of GST P1-1 as an antiapoptotic protein.

246 idant enzymes (catalase, SOD1, and SOD2) and antiapoptotic proteins (Bcl-2/Bcl-xL).

247 on of specific members of the BCL2 family of antiapoptotic proteins (BCL-W, BCL-XL, and MCL1) selecti

248 rocess stimulates the upregulation of select antiapoptotic proteins allowing for the differentiation

249 e to cadmium in the BEAS-2B cells as well as antiapoptotic proteins and antioxidant enzymes.

250 through NF-kappaB-dependent upregulation of antiapoptotic proteins and NF-kappaB-independent inactiv

251 sensitivity involves increased expression of antiapoptotic proteins and sustained activation of the P

252 and attenuated an Mn-induced decrease in the antiapoptotic proteins Bcl-2 and Bcl-xL.

253 lase and superoxide dismutase as well as the antiapoptotic proteins Bcl-2 and Bcl-xL.

254 ntioxidant proteins catalase and SOD and the antiapoptotic proteins Bcl-2 and Bcl-xL.

255 apoptotic pathway and enhances expression of antiapoptotic proteins Bcl-2 and Bcl-XL.

256 The antiapoptotic proteins BCL-2 and myeloid cell leukemia s

257 ion, there was upregulated expression of the antiapoptotic proteins Bcl-2, HSP-70, LIVIN, and PON2 wi

258 ion treatment with inhibitors of MTOR or the antiapoptotic proteins BCL-XL and MCL-1.

259 ing along with JAK-dependent upregulation of antiapoptotic proteins Bcl2 and BclXL.

260 NC201, but instead reduced expression of the antiapoptotic proteins FLIP, Mcl-1, Bcl-2, cIAP1, cIAP2,

261 ed transcriptional regulation of short-lived antiapoptotic proteins is critical for the survival of t

262 cytes by inducing the expression of cellular antiapoptotic proteins Mcl-1 and HSP27.

263 The antiapoptotic proteins of the BCL-2 family are key regul

264 ession of Mcl-1 and HSP27, two Akt-dependent antiapoptotic proteins specifically upregulated during H

265 ects of CDK4/6 inhibitors, the expression of antiapoptotic proteins that associate with response to C

266 n of human airway epithelial cells activates antiapoptotic proteins that suppress apoptosis and promo

267 d and tripled drugs, increased expression of antiapoptotic proteins was observed, requiring a fourth-

268 e mechanism of protection was related to the antiapoptotic proteins X-linked inhibitor of apoptosis (

269 lin-dependent kinase inhibitor p27(Kip1) and antiapoptotic proteins X-linked inhibitor of apoptosis a

270 nificantly reduced expression of a subset of antiapoptotic proteins, including BCL2, BFL1/A1, and 4-1

271 ally, HCMV upregulated two specific cellular antiapoptotic proteins, myeloid leukemia sequence 1 (Mcl

272 stress and quickly downregulates short-lived antiapoptotic proteins, XIAP and c-FLIPL by inhibiting g

273 lations of AML tumor cells were enriched for antiapoptotic proteins.

274 expressions of both antioxidant enzymes and antiapoptotic proteins.

275 proteins up-regulate antioxidant enzymes and antiapoptotic proteins.

276 olomide has been related to the induction of antiapoptotic proteins.

277 receptors, and the Bax inhibitor 1 family of antiapoptotic proteins.

278 hionein genes encoding anti-inflammatory and antiapoptotic proteins.

279 tors, the Mcl-1 protein is compared to other antiapoptotic proteins.

280 inhibitors targeting three major classes of antiapoptotic proteins: antiapoptotic B cell lymphoma 2

281 Contrary to antiapoptotic rat and human v1, overexpression of rat v2

282 NAF-1 binds to both the pro- and antiapoptotic regions (BH3 and BH4) of Bcl-2, as demonst

283 Unlike BCL-2 and BCL-XL, the closest antiapoptotic relative BCL-W is required for spermatogen

284 ur systems biology approach has uncovered an antiapoptotic role for MRP8 in monocytes, which was corr

285 ATR may provide a mechanism for the observed antiapoptotic role of ATR in suppressing carcinogenesis

286 We demonstrated the antiapoptotic role of these five IAPs using heterologous

287 show that the activation of Syk provides an antiapoptotic signal, which is independent of Mcl-1, Bcl

288 The antiapoptotic signaling downstream of anaphylatoxin C3a

289 ively, our study identifies a HOIP-regulated antiapoptotic signaling pathway, and we envisage HOIP as

290 and HSPA5/BIP expression, activated ERK and antiapoptotic signaling, and conferred relative resistan

291 nes, which are involved in cell survival and antiapoptotic signaling, in human breast cancer cells.

292 or prognosis by triggering proangiogenic and antiapoptotic signaling.

293 Here we review host antiapoptotic signalling pathways manipulated by translo

294 poptosis, which tips the balance in favor of antiapoptotic signals and endows these cells with resist

295 Mechanistically, TLR9-mediated antiapoptotic signals in ZAP-70-positive CLL trigger sec

296 cell death is closely regulated by pro- and antiapoptotic signals.

297 splantation, with a global cell survival and antiapoptotic signature.

298 plicing targets, enhancing the production of antiapoptotic splicing isoforms and activating the mTOR

299 nction to increase the Bcl-2/Bax ratio to an antiapoptotic state and activate autophagy through induc

300 Consistent with these findings, Mcl-1, an antiapoptotic target of CREB-mediated transcription, was