ライフサイエンスコーパス: noxa

1 pathways due to loss of Bim-/-, Puma-/-, or Noxa-/-.

2 e in expression of the pro-apoptotic protein Noxa.

3 o selective induction of p53 targets such as NOXA.

4 homology 3 (BH3)-only pro-apoptotic protein NOXA.

5 LF9 to the promoter of the proapoptotic gene NOXA.

6 tion of p63/p73 target genes such as Bax and Noxa.

7 including miR-34a, PUMA, p21(waf), Bax, and Noxa.

8 ition promote apoptosis by dephosphorylating Noxa.

9 on of p53-regulated genes, including p21 and NOXA.

10 ression of the proapoptotic proteins Bim and Noxa.

11 erexpression, or loss of proapoptotic Bim or Noxa.

12 with induction of the pro-apoptotic protein Noxa.

13 2 homology3 (BH3)-only pro-apoptotic protein NOXA.

14 nducing a shift of balance between Mcl-1 and Noxa.

15 3 transcription targets: p21/WAF1, PUMA, and NOXA.

16 nd up-regulation of the proapoptotic protein Noxa.

17 induced high levels of Bak, Bid, BNip3, and Noxa.

18 AP1-targeted genes, including Bax, Puma, and Noxa.

19 -only protein NBK/BIK, but not BIM, PUMA, or NOXA.

20 GECs, which caused cytoplasmic retention of Noxa.

21 ated the increase in calcium, ER stress, and NOXA.

22 e Bcl-2 homology 3 domain only family member NOXA.

23 s, and up-regulation of the BH3-only protein NOXA.

24 and paradoxical, MYCN-driven upregulation of NOXA.

25 mmune response by inducing MDA-5, RIG-I, and NOXA.

26 described p53-mediated induction of PUMA and NOXA.

27 k treatment caused increased accumulation of NOXA a pro-apoptotic BH3-only member of the BCL2 family.

28 We showed previously that phosphorylation of Noxa, a 54-residue Bcl-2 protein, at serine 13 (Ser13) i

29 rotein translation, and impairs induction of NOXA, a mediator of cell death.

30 tably, short hairpin RNA knockdown of Bim or Noxa abrogated lethality triggered by the flavopiridol/o

31 to the NOXA promoter, which is required for NOXA activation.

32 particular form of ACC in which an external noxa affects the forearm, increasing the intracompartmen

33 ive isoform DeltaNp73, reduced the levels of Noxa after cisplatin exposure in NTERA2 and 2102EP.

34 Increased levels of Noxa also inactivated the remaining levels of Mcl-1 prot

35 proteins expressed in vivo demonstrated that Noxa and Bcl-2 can be pulled down together from a variet

36 servations not only establish the ability of Noxa and Bcl-2 to interact but also identify Bcl-2 overe

37 f cells lacking p53 with PALA induced TAp73, Noxa and Bim and inactivation of these proteins with dom

38 es for the p53 and TAp73 in the induction of Noxa and Bim and regulation of apoptosis.

39 w that Mcl-1 sequesters the BH3-only protein Noxa and Bim and the apoptotic effector Bak.

40 Both NOXA and Bim are avid binders of Mcl-1, but a functional

41 Mcl-1-mediated cross-talk between endogenous NOXA and Bim that occurs upstream of the Bak/Bax-depende

42 the stabilization of BH3-only proteins BIK, NOXA and BIM, appear to be essential for effecting BAX-

43 of DeltaNp73 and inhibiting the induction of Noxa and Bim.

44 s mediated via TAp73-dependent expression of Noxa and Bim.

45 including proteasome substrate accumulation, Noxa and caspase 3/7 induction, and phospho-eIF2alpha su

46 response, characterized by up-regulation of Noxa and cell death, was dependent on ATF4, but not the

47 which activated the proapoptotic BH3 protein Noxa and its downstream targets Usp9X and Mcl-1.

48 chanisms underlying E2-mediated induction of Noxa and its functional significance are unknown.

49 ddiction in basal-like TNBCs was mediated by NOXA and linked to MCL-1 dependence.

50 Together, our findings indicate that NOXA and Mcl-1 are critical determinants for gossypol-me

51 ator p35 attenuated both of these effects on NOXA and miR-23a expression.

52 b-induced apoptosis in pG1 in the absence of Noxa and more profoundly in pG1-S in cooperation with No

53 s (p15 and p21) and proapoptotic regulators (NOXA and PERP), attenuated proliferation, corrected the

54 Coimmunoprecipitation demonstrated that Noxa and Puma bind Mcl-1 to release Bak and Bim within 6

55 elevated expression of proapoptotic targets Noxa and Puma seen in Hdac8-deleted LT-HSCs.

56 ed survival coincident with the induction of Noxa and Puma, independently of immunoglobulin heavy cha

57 sed ATF4 stability and activated its targets NOXA and PUMA.

58 activation of its target proapoptotic genes NOXA and PUMA.

59 creased expression of the proapoptotic genes NOXA and PUMA.

60 NK cells constitutively expressing Noxa and SOCS1 exhibit profound defects in expansion dur

61 of c-MYC enabled normal cells to accumulate NOXA and subsequently activate cell death programs in re

62 gs define the first physiologic function for Noxa and suggest that by repressing Noxa, induction of G

63 onstrate that miR-155 differentially targets Noxa and suppressor of cytokine signaling 1 (SOCS1) in N

64 ription of pro-apoptotic genes Bax, Fas, and Noxa, and apoptosis.

65 interfering RNA-mediated knockdown of BNip3, Noxa, and Bak each protected cells from PQ, but Bax knoc

66 ed binding to the proapoptotic proteins Bim, Noxa, and Bak.

67 cs significantly reduced activation of Puma, Noxa, and Bax as well as attenuated markers of caspase-d

68 le BH3-only proteins, including BimEL, BimL, Noxa, and Bik/NBK.

69 Silencing of Bmf, Noxa, and Bim significantly protected cells from ATO-ind

70 n the extrinsic apoptotic pathway, and PUMA, Noxa, and Bim, which are part of the intrinsic apoptotic

71 r suppressor substrates, including p21, p27, NOXA, and BIM.

72 unexpectedly promiscuous, except for Bad and Noxa, and did not explain the differential antiapoptotic

73 protein, stabilization of the Bak activator Noxa, and down-regulation of antiapoptotic Bcl-XL.

74 ly higher levels of Bcl-2, Bcl-X(L), Bim and Noxa, and lower levels of Mcl-1 characterized naive SCLC

75 d antiapoptotic molecules (e.g., Fas ligand, Noxa, and Mcl-1).

76 of Bcl-2 family members, Bcl-2, Bcl-XL, Bim, Noxa, and Mcl-1; however, effects on Bid have not been s

77 its downstream transcription targets, PUMA, NOXA, and p21/WAF1.

78 elevated p53 levels, and enhanced CD95, BAX, NOXA, and PUMA expression; knockdown of BAX/NOXA/PUMA re

79 he overexpression of BH3-only proteins (Bad, Noxa, and Puma), which in turn facilitates Bax-dependent

80 s classical p53 target genes, including p21, Noxa, and Puma, but it retains the ability to activate a

81 y growth arrest and apoptotic genes p21WAF1, NOXA, and PUMA.

82 ession and aggresome formation, induction of Noxa, and sensitivity to BZ + SAHA-induced apoptosis.

83 and expression of its transcriptional target Noxa, and sensitizes the epidermis to UVB-induced apopto

84 provide strong evidence that Puma, like Bim, Noxa, and tBid, is able to act as a direct Bak activator

85 neuroblastoma as a model, we identify PUMA, NOXA, and TRB3 as executors of Gln-starved cells.

86 on regimen causes autophagy that facilitates NOXA- and Bim-induced and Bak/Bax-mediated mitochondrial

87 uced expression of the pro-apoptotic protein Noxa- and caspase-dependent degradation of the anti-apop

88 these findings were absent or attenuated in Noxa(-/-) animals.

89 one that inhibits BCL2 and one that induces NOXA, apoptosis is induced within 6 h in a BAX/BAK-depen

90 nts that control this specific regulation of NOXA are unknown.

91 blished the BH3-only proteins Bim, tBid, and Noxa as "direct activators" that are able to directly in

92 to cisplatin-based chemotherapy, and propose Noxa as a predictive factor of therapeutic response.

93 These results establish Noxa as an important regulator of the number of memory c

94 We identified Atg5, Atg7, Bax, Bid, Bik, and Noxa as potential therapeutic targets for adRP treatment

95 We identified Noxa as the only Bcl-2 family protein to be highly corre

96 xpression of Bcl-2 family proteins Bfl-1 and Noxa as well as an increase in cellular glutathione (GSH

97 duction of the proapoptotic BH3-only protein Noxa as well as endoplasmic reticular stress, a disrupti

98 y grafts in which the expression of XAF1 and Noxa as well as the pro-apoptotic effects induced by IFN

99 and Bcl2 and attenuated the proapoptotic p53/Noxa axis.

100 Further analysis showed that the Noxa/Bcl-2 interaction reflected binding between the Nox

101 tion of Mcl-1 in conjunction with an induced Noxa/Bcl-xL interaction may serve as a trigger for mitoc

102 and Bim, which bound Bcl-xL constitutively, Noxa became "Mcl-1-free" and interacted with Bcl-xL afte

103 -2 interaction reflected binding between the Noxa BH3 domain and the Bcl-2 BH3 binding groove.

104 raction of endogenous Mcl-1 and biotinylated Noxa-BH3 peptide, causes cell death through a Bak/Bax-de

105 f the effector Bax or Bak, including Bmf and Noxa BH3s.

106 Not surprisingly, Noxa, Bim, or Bak knockdown partially rescued H23 cells

107 ggest a plausible mechanism for the observed NOXA-Bim linkage.

108 erially expressed proteins demonstrated that Noxa binds with mean dissociation constants (K(D)) of 3.

109 l regions of the BH3-only proteins Bik, Bim, Noxa, Bmf, and Puma into microsomal membranes.

110 ulation of 3 proapoptotic BH3-only proteins (Noxa, Bmf, and Puma) and down-regulation of 2 antiapopto

111 ath to the accumulation of ASF1B, Myc, ODC1, Noxa, BNIP3, Gadd45alpha, p-SMC1A, SREBF1, and p53.

112 ude that PM(2.5)-induced cell death requires Noxa both in vitro and in vivo and that Noxa-dependent c

113 ably to the BH3-only proteins Bim, PUMA, and Noxa but can also bind to Bak and Bax.

114 th p53-independent induction of proapoptotic Noxa but not Puma protein.

115 e lung and increased levels of mRNA encoding Noxa but not Puma.

116 the ordered component for non-phosphorylated Noxa, but left the pSer13 Noxa profile unchanged.

117 -induced increase in calcium, ER stress, and NOXA, but not the increase in PLA2 activity, indicating

118 tionally increased levels of the BH3 protein Noxa by activating the unfolded protein response (UPR),

119 Here, we show that the induction of NOXA by bortezomib is directly dependent on the oncogene

120 The increased abundance of NOXA by CDK5 inhibition was not a result of changes in N

121 Knockdown of Bim (but not Puma or Noxa) by shRNA or ectopic overexpression of Bcl-2, Bcl-x

122 d significant up-regulation of both Mcl1 and Noxa compared with noninfected samples.

123 s was weakly immobilized in unphosphorylated Noxa, consistent with a solvent-exposed helix/loop, but

124 nalyses of TGCTs revealed that expression of Noxa correlates with good clinical prognosis in patients

125 was also induced by Tax, including Puma and Noxa, culminating in a substantial increase in Bax dimer

126 evere organ pathology and premature death in Noxa-deficient mice.

127 ires Noxa both in vitro and in vivo and that Noxa-dependent cell death might contribute to PM-induced

128 combined with MG-132 synergistically induced Noxa-dependent mitochondrial-mediated apoptosis.

129 ression induced apoptosis that was partially NOXA-dependent.

130 modulator-of-apoptosis (PUMA), Fas/CD95, and Noxa depends on p53 transcriptional activity.

131 hypersensitivity to a similar extent as did Noxa depletion.

132 olution crystal structure of the dimerized H-NOXA domain of STHK, which reveals a Per-Arnt-Sim (PAS)

133 ning mutagenesis in sGC indicates that the H-NOXA domains of sGC could adopt a similar dimer organiza

134 RP78 suppresses apoptosis induced by BIK and NOXA, either alone or in combination.

135 The combination increased the NOXA expression and caspase-dependent MCL-1 degradation.

136 cells, which was manifested by an increased NOXA expression at the transcriptional level.

137 Knockdown of NOXA expression by short hairpin RNA significantly reduc

138 nse signaling induces apoptosis by eliciting Noxa expression in reovirus-infected cells.

139 erestingly, down-regulation of Sp1 increased Noxa expression in response to cisplatin.

140 Knock down of XAF1 and Noxa expression inhibited the priming of VSMCs to apopto

141 tion following E2 treatment, indicating that Noxa expression is required for cell cycle progression i

142 to ABT-737 in these cells, and knocking down Noxa expression protected the cells from cytotoxicity in

143 Finally, Noxa expression was enhanced by GSH depletion and inhibi

144 ave shown that 17beta-estradiol (E2) induces Noxa expression, although the mechanisms underlying E2-m

145 ptotic BCL-xL expression, high pro-apoptotic NOXA expression, and paradoxical, MYCN-driven upregulati

146 indicated that SBHA increased Bim, Puma, and Noxa expression, while SBHA concentrations that upregula

147 undergo apoptosis concomitant with increased Noxa expression.

148 ne potential, caspase cleavage, and elevated NOXA expression.

149 Activation of p53 increases Bax, PUMA, and NOXA expression.

150 creased p53 protein levels, and induction of Noxa expression.

151 olved in the transcriptional upregulation of Noxa following E2 treatment.

152 selectivity but not absolute specificity of Noxa for Mcl-1.

153 fold more tightly in vitro, pulled down more Noxa from cells, and protected cells against killing by

154 inhibit the ATF4-dependent activation of the NOXA gene because the site-specific substitution mutatio

155 ble genetic variant on 18q21 near the PMAIP1/Noxa gene that is associated with BLM sensitivity.

156 In addition, ABC294640 increased Noxa gene transcription and protein expression.

157 d the transcription of proapoptotic puma and noxa genes at 2 to 4 h p.i. and their BH3-only protein e

158 f irradiated Parp-2-/- mice, whereas loss of Noxa had no such effect.

159 interface mutations did decrease sGCbeta1 H-NOXA homodimerization, heterodimerization of full-length

160 owever, PRIMA-1(Met) increased expression of NOXA in a p53-independent manner, and NOXA silencing dec

161 amatic induction of the proapoptotic protein NOXA in a tumor cell-restricted manner.

162 decreased cisplatin-induced up-regulation of Noxa in EC cell lines.

163 w the transcriptional network that regulates Noxa in EC cells, which is key for their apoptotic respo

164 We wanted to elucidate the status of Noxa in H. pylori-infected GECs.

165 HNSCC cells and reveal an important role for Noxa in mediating synergism by these agents.

166 roach was taken to investigate the role of H-NOXA in STHK and sGC.

167 Therefore, we investigated the role of Noxa in T cell memory during acute and chronic infection

168 n-induced apoptosis, implicating the role of NOXA in the drug synergy.

169 es like GRP78, GADD153, ATF3, IRE1alpha, and NOXA in these cells.

170 more profoundly in pG1-S in cooperation with Noxa in vitro.

171 apoptosis, mediated by the BH3-only protein Noxa, in controlling diversity of the effector T cell po

172 al SCF substrates, including CDT1, WEE1, and NOXA, in parallel with an enhancement of radiation-induc

173 is significantly diminished in cells lacking Noxa, indicating a key prodeath function for this molecu

174 lix/loop, but strongly constrained in pSer13 Noxa, indicating a more ordered peptide backbone, as pre

175 justing expression levels of Bak, Bcl-XL, or Noxa individually altered the level of apoptosis in AML

176 The BCL-2 family member Noxa induces apoptosis by antagonizing the prosurvival p

177 d proteins, which led to enhanced ER stress, NOXA induction and apoptosis.

178 study establishes ER stress stimulation and NOXA induction as novel mediators of reovirus-induced ap

179 TF4-dependent, but p53-independent, PUMA and NOXA induction.

180 tion for Noxa and suggest that by repressing Noxa, induction of G arrest by p18 bypasses a homeostati

181 Consistent with a role for Noxa inhibition of Mcl-1, the Bad-mimetic ABT-737 synerg

182 Mechanistically, the newly generated NOXA interacted with Mcl-1 and displaced Bim from the Mc

183 JNK inhibition enhanced Mcl1-Noxa interaction in the mitochondrial fraction of infect

184 1 and Noxa was indicative of an impaired Mcl-Noxa interaction.

185 Noxa is a Bcl-2-homology domain (BH3)-only protein repor

186 NOXA is a BH3-only protein whose expression is induced b

187 In conclusion, our study indicates that Noxa is a central determinant of hypersensitivity to cis

188 NOXA is a pro-apoptotic protein that functions by bindin

189 Noxa is a proapoptotic BH3-domain-only protein of the Bc

190 Noxa is constitutively expressed in proliferating cells

191 ondrial response to an induced expression of NOXA is executed by endogenous Bim and suggest a plausib

192 ated that the BH3 domain of unphosphorylated Noxa is housed within a flexible loop connecting two ant

193 Expression of Noxa is induced during B-cell activation, peaks in iPCs,

194 Noxa is induced in activated B cells, and its ablation p

195 We show that Noxa is phosphorylated on a serine residue (S(13)) in th

196 We found that Noxa is strongly induced at late times (36 to 48 h) foll

197 se to cisplatin, and found that proapoptotic Noxa is transcriptionally up-regulated following cisplat

198 cells as an experimental model, we show that Noxa is upregulated by E2 via p53-independent processes

199 rsely, the pro-apoptotic Bcl2 family member, Noxa, is a critical initiator of mitotic cell death.

200 The BH3-only protein, Noxa, is induced in response to apoptotic stimuli, such

201 We identify Cdk5 as the Noxa kinase and show that Cdk5 knockdown or expression o

202 Down-modulation of Noxa largely eliminates the enhancing effect of GSK-3 in

203 Chronic immune activation in the absence of Noxa leads to excessive accumulation of primed cells, wh

204 NOXA levels were increased substantially by treatment wi

205 ared with differentiated cells, constitutive Noxa levels were significantly higher in Oct-4-positive

206 an upregulation of the pro-apoptotic protein Noxa, loss of mitochondrial transmembrane potential, and

207 ration of the prosurvival binding partner of NOXA, Mcl-1, and effectively blocks apoptosis.

208 ally masks Noxa's BH3 domain, inhibiting the Noxa-Mcl-1 interaction.

209 Mcl1-expressing cells is mainly regulated by Noxa-mediated degradation of Mcl1.

210 nd obatoclax-initiated autophagy depended on NOXA-mediated displacement of the prosurvival BCL-2 fami

211 ), Bax3(-)/(-), Bak(-)/(-), PUMA(-)/(-), and Noxa(-)/(-) mice.

212 After immunization or influenza infection, Noxa(-/-) mice display enlarged GCs, in which B cells wi

213 Upon influenza infection, Noxa(-/-) mice generate a memory compartment of increase

214 As a consequence, Noxa(-/-) mice mount low affinity antibody responses com

215 Chronic infection of Noxa(-/-) mice with mouse CMV resulted in enhanced memor

216 olar epithelial cells from wild-type but not Noxa(-/-) mice.

217 nst lymphocyte apoptosis whereas Puma-/- and Noxa-/- mice had modest or no protection, respectively.

218 Instead, CDK5 inhibition increased NOXA mRNA and protein levels by decreasing the expressio

219 ssical proteasomal targets that can regulate NOXA mRNA under stress).

220 main of the proapoptotic Bcl-2 family member Noxa only interacts with the anti-apoptotic proteins Mcl

221 This domain is termed H-NOXA (or H-NOBA) because it is often associated with the

222 rs of p53- and p63-mediated apoptosis--Puma, Noxa, or both--are normal.

223 xpression of the BH3 proteins Bim, Bid, Bad, Noxa, or Puma.

224 tion against killing by Puma or ABT-737 plus Noxa overexpression.

225 esponse to Nutlin-3 also increased levels of Noxa, p53-upregulated modulator of apoptosis (PUMA), and

226 strong activation of TNFalpha and MEKK4-p38-Noxa pathways that render them susceptible to cystine de

227 crystal structure of a biphenyl-cross-linked Noxa peptide in complex with its target Mcl-1 at 2.0 A r

228 studies demonstrated that both caspase-4 and Noxa play significant roles in Myc-driven sensitivity to

229 We propose that Noxa plays both growth-promoting and proapoptotic roles

230 procal amplification of the Src-p38 (MAPK14)-Noxa (PMAIP1) signaling and TNFalpha-RIP1/3 (RIPK1/RIPK3

231 egulated by the proapoptotic BH3-only member Noxa (Pmaip1), as a critical factor for the selection of

232 non-phosphorylated Noxa, but left the pSer13 Noxa profile unchanged.

233 the recruitment of c-Myc and ERalpha to the NOXA promoter in chromatin immunoprecipitation (ChIP) as

234 evealed that ATF4 occupancy increased at the NOXA promoter in TT cells treated with tyrosine kinase i

235 A detailed analysis of the Noxa promoter revealed that p73 and Sp1-like factors, Sp

236 TF4 form a complex capable of binding to the NOXA promoter, which is required for NOXA activation.

237 Knocking down NOXA protected cells from combination-induced apoptosis,

238 , in an almost complete loss of constitutive Noxa protein and decreased cisplatin hypersensitivity to

239 pression of Akt, but not of TORC1, increases Noxa protein levels and downregulates Bfl-1 protein supp

240 K5 inhibition was not a result of changes in NOXA protein turnover.

241 ed in dramatic up-regulation of proapoptotic Noxa protein, and small interfering RNA (siRNA)-mediated

242 ccurred, accompanied by a rapid induction of NOXA protein, whereas BCL-2, BAX, BAK, BIM, BAD, BID, an

243 ns and upregulates the proapoptotic BH3-only Noxa protein.

244 xpression levels of p21 and the proapoptotic NOXA protein.

245 mics attenuated etoposide-induced changes in Noxa, Puma, and Bax, reduced downstream markers of caspa

246 ion of the proapoptotic Bcl-2 family members Noxa, Puma, and Bax.

247 regulation of Mcl-1 and the up-regulation of Noxa, Puma, and Bim in H196 cells.

248 ted in up-regulation of pro-apoptotic genes, NOXA, PUMA, and FAS receptor in gastric epithelial cells

249 n was found in the apoptotic function (DR-4, NOXA, PUMA, and PIG-3).

250 Indeed, the expression of Bax, Noxa, PUMA, BNIP(3), and cleaved caspase-3 was not affec

251 ls lacking the BH3-only proapoptotic members Noxa, Puma, or Bim were also sensitized by CR mimetics t

252 scription of the proapoptotic Bcl-2 proteins Noxa, Puma, or both.

253 NOXA, and PUMA expression; knockdown of BAX/NOXA/PUMA reduced CDK inhibitor-stimulated cell killing.

254 Blockade of Noxa reduced the apoptotic response of embryonal carcino

255 However, siRNA-mediated knockdown of Noxa resulted in cell cycle arrest in G(0)/G(1)-phase an

256 hereas overexpression of nonphosphorylatable Noxa resulted in enhanced mitochondria-mediated apoptosi

257 uestration of Mcl-1 and Bfl-1 by upregulated Noxa results in the activation of Bid, and the consequen

258 show that Cdk5 knockdown or expression of a Noxa S(13) to A mutant increases sensitivity to glucose

259 phosphoregulatory mechanism that inactivates Noxa's apoptotic function and triggers its capacity to m

260 on caused by phosphorylation partially masks Noxa's BH3 domain, inhibiting the Noxa-Mcl-1 interaction

261 cl-1 expression or shRNA knockdown of Bim or Noxa significantly attenuated MDA-7/IL-24-mediated leuke

262 shRNA knockdown of Bim, Bak, or Bax, but not Noxa, significantly attenuated obatoclax/sorafenib letha

263 ion of NOXA in a p53-independent manner, and NOXA silencing decreased PRIMA1(Met)-induced cell death.

264 quent induction of apoptosis is inhibited by Noxa silencing.

265 Paradoxically, Noxa stimulates glucose consumption and may enhance gluc

266 ion of miR-23a and subsequent suppression of NOXA synthesis.

267 emarkably, neither the loss of both Puma and Noxa, the loss of both Puma and Bim, nor the loss of all

268 ation can regulate the apoptotic function of Noxa, this could be a potential target molecule for futu

269 as well as the pro-apoptotic genes PUMA and NOXA, three transcriptional targets of p53.

270 otected cells against killing by transfected Noxa to a greater extent.

271 perates with other BH3-only proteins such as NOXA to cause rapid release of cytochrome c from mitocho

272 , the HER-2 cleavage products cooperate with Noxa to induce apoptosis in cells expressing both Bcl-x(

273 iated knockdown of Oct-4 resulted in reduced Noxa transcript, in an almost complete loss of constitut

274 of histone H2A to relieve its inhibition on NOXA transcription.

275 certain lymphoma-derived Bcl-2 mutants bound Noxa up to 20-fold more tightly in vitro, pulled down mo

276 Importantly, KLF9 knockdown impaired NOXA up-regulation and apoptosis caused by bortezomib, L

277 n-induced melanoma cell apoptosis depends on Noxa up-regulation as confirmed by siRNA rescue experime

278 terfering RNA (siRNA)-mediated inhibition of Noxa up-regulation partially attenuated cell death by th

279 nduction, Mcl-1 down-regulation, and Bim and Noxa up-regulation.

280 pathway, the resulting FOXO3a activation and Noxa upregulation are critical molecular mechanisms unde

281 Noxa upregulation is associated with nuclear translocati

282 trate that both EerI and bortezomib activate NOXA via an unanticipated mechanism that requires cooper

283 Coexistence of Mcl1 and Noxa was indicative of an impaired Mcl-Noxa interaction.

284 X protein)-dependent neuronal death, whereas Noxa was not apoptogenic.

285 Interestingly, E2-mediated upregulation of Noxa was not associated with apoptosis.

286 We proved that Noxa was phosphorylated at Ser(13) residue by JNK in inf

287 Jurkat T-cell leukemia cells is dependent on Noxa) was examined, apoptosis was enhanced by the Bcl-2/

288 Mcl-1 and Noxa were identified to be the major anti-apoptotic and

289 The pro-apoptotic members Bak, Bad, Bim, and Noxa were required for apoptosis induced by DNA damaging

290 nally, transcripts of the p53 target Pmaip1 (Noxa) were significantly increased in IRF8-deficient GC

291 of apoptosis associated factor-1 (XAF1) and Noxa, were verified by real time quantitative reverse tr

292 Overexpression of TAp73 induced Noxa whereas the dominant negative isoform DeltaNp73, re

293 lum stress response inducing ATF4, ATF3, and NOXA, which can then bind to and inhibit MCL1.

294 This SNP is approximately 64 kb from PMAIP1/Noxa, which is a radiation-inducible gene and exhibits h

295 als targets involved in apoptosis, including NOXA, which is important for inducing cell death during

296 -SV1 binds the proapoptotic BH3-only protein NOXA, which results in their mutual HDM2-dependent degra

297 xamined the interaction of full-length human Noxa with anti-apoptotic human Bcl-2 family members.

298 Complexes of either PUMA or Noxa with Bax or Bak were always detected at mitochondri

299 d a direct interaction between Bim, PUMA, or Noxa with either Bax or Bak during apoptosis induction.

300 EPR of unphosphorylated Noxa, with spin-labeled amino acid TOAC incorporated wit