ライフサイエンスコーパス: pro-apoptotic protein

1 ily anti-apoptosis proteins is a 'BH3 alone' pro-apoptotic protein.

2 ng and enzymatic activity of procaspase-3, a pro-apoptotic protein.

3 gy to Bax and Bak, has been proposed to be a pro-apoptotic protein.

4 death, is a member of the BH3-only family of pro-apoptotic proteins.

5 e required to induce apoptosis by activating pro-apoptotic proteins.

6 complementary set of anti-proliferative and pro-apoptotic proteins.

7 as reduced expression and/or inactivation of pro-apoptotic proteins.

8 ents in the hydrophobic groove that binds to pro-apoptotic proteins.

9 proteins interact with certain BCL-2 family pro-apoptotic proteins.

10 dependent kinase inhibitors and upregulating pro-apoptotic proteins.

11 ulation of gamma secretase, tau kinases, and pro-apoptotic proteins.

12 ling results in the release of mitochondrial pro-apoptotic proteins.

13 guously into the Bax-like Bcl-2 subfamily of pro-apoptotic proteins.

14 activation of BNIP3 and BNIP3L, which encode pro-apoptotic proteins.

15 s the founding member of the BH3-only family pro-apoptotic proteins.

16 Pro-apoptotic protein 24p3, a member of lipocalin family

17 l-2 and Bcl-xL), while reduced expression of pro-apoptotic proteins (AIF and Bax).

18 from auranofin-mediated upregulation of NOXA pro-apoptotic protein and potent induction of apoptotic

19 e include the BH3 sequence shared with other pro-apoptotic proteins and an unexpected sequence locate

20 was associated with increased expression of pro-apoptotic proteins and decreased expression of antia

21 member of the BH3-contaning BCL-2 family of pro-apoptotic proteins and functions in mitochondria.

22 for death" by elevated BCL-2, which binds to pro-apoptotic proteins and holds them in check.

23 rst report to demonstrate that inhibition of pro-apoptotic proteins and induction of autophagy sensit

24 (IAPs) physically interact with a variety of pro-apoptotic proteins and inhibit apoptosis induced by

25 IAPs physically interact with a variety of pro-apoptotic proteins and inhibit apoptosis induced by

26 he activated Akt then phosphorylates several pro-apoptotic proteins and prevents apoptosis mediated b

27 the active Bcl-2 homology 3 (BH3) domains of pro-apoptotic proteins and the threshold for cytochrome

28 his complex induced the upregulation of BAX (pro-apoptotic protein) and downregulation of BCL-2 (anti

29 The Bcl-2 family member Bad is a pro-apoptotic protein, and phosphorylation of Bad by cyt

30 ell apoptosis through induction of CHOP, the pro-apoptotic protein, and sensitizes cells to lipopolys

31 diated cell death using purified recombinant pro-apoptotic proteins, and cell-free extracts from the

32 ved through upregulating death receptors and pro-apoptotic proteins, and downregulating major anti-ap

33 s, the pore opens, increasing the release of pro-apoptotic proteins, and ultimately resulting in cell

34 llele occurrence and increased levels of the pro-apoptotic protein appoptosin in PSP patients.

35 The BH3 domains of pro-apoptotic proteins are sufficient to trigger cytochr

36 The BH3-only pro-apoptotic proteins are upstream sensors of cellular

37 n of p90RSK and decreased phosphorylation of pro-apoptotic protein BAD (BCL2-antagonist of cell death

38 , p90(RSK), which in turn phosphorylates the pro-apoptotic protein BAD and C/EBPbeta.

39 ated phosphorylation and inactivation of the pro-apoptotic protein Bad as well as transcription of su

40 e Rsks, catalyzed the phosphorylation of the pro-apoptotic protein BAD at serine 112 both in vitro an

41 s also led to reduced phosphorylation of the pro-apoptotic protein BAD at the protein phosphatase 2A

42 trated that Rsk1 directly phosphorylated the pro-apoptotic protein Bad at the serine residues that, w

43 The finding that the pro-apoptotic protein BAD is a substrate of Akt/PKB has

44 In particular, the formula explains how the pro-apoptotic protein BAD lowers the threshold at which

45 However, the kinase can phosphorylate the pro-apoptotic protein BAD on serine 112, which accounts

46 modules revealed that phosphorylation of the pro-apoptotic protein Bad was elevated in mitochondria.

47 poptosis through increased activation of the pro-apoptotic protein Bad, a change in the conformation

48 vel of the anti-apoptotic protein Bcl-2, the pro-apoptotic protein Bad, or the inactivated form of Ba

49 of Akt and prolonged phosphorylation of the pro-apoptotic protein Bad, resulting in enhanced cell su

50 uzumab treatment, but rather inactivated the pro-apoptotic protein BAD, the BCl-2-associated death pr

51 gnal, in part through phosphorylation of the pro-apoptotic protein BAD, TPCK reduced BAD phosphorylat

52 rotein Bag-1 and decreased expression of the pro-apoptotic protein Bad.

53 it prevents cell survival by activating the pro-apoptotic protein BAD.

54 ty and selective binder of the BH3 region of pro-apoptotic protein Bad.

55 converge to phosphorylate and inactivate the pro-apoptotic protein BAD.

56 hospho-Erk1/2) proteins, and upregulated the pro-apoptotic proteins (Bad, Bim, Bax and Bid) leading t

57 mitochondria, MCL-1 interacts with the major pro-apoptotic protein BAK and prevents BAK-BAK homo-olig

58 The pro-apoptotic protein Bak is converted from a latent to

59 e crypts and an accompanying increase in the pro-apoptotic protein Bak was expressed in intestinal ep

60 The intensity of immunostaining for the pro-apoptotic protein Bak was reduced compared to that o

61 i-apoptotic proteins Bcl-2 and Mcl-1 and the pro-apoptotic protein Bak, whereas Bax expression is rel

62 tion of this anti-apoptotic protein with the pro-apoptotic protein Bak.

63 Bok is most closely related to the pro-apoptotic proteins Bak and Bax, but in contrast to B

64 ot bind tightly to peptides derived from the pro-apoptotic proteins Bak, Bax, Bik, and Bad.

65 ation of the cell death pathway demonstrated pro-apoptotic protein Bax 'activation' and caspase cleav

66 LPS also augmented expression of the pro-apoptotic protein Bax and the tumor suppressor gene

67 Sequential steps in the activation of the pro-apoptotic protein Bax are described for cells with d

68 The pro-apoptotic protein Bax can homodimerize with itself a

69 he anti-apoptotic protein bcl-2, but not the pro-apoptotic protein bax in these CTCL cells.

70 Here, we show that the pro-apoptotic protein Bax is highly expressed in the SNp

71 ed by the fact that removal of the intrinsic pro-apoptotic protein Bax rescues the germ-cell apoptosi

72 Expression of the pro-apoptotic protein BAX sensitizes ovarian cancer cell

73 he anti-apoptotic protein Bcl-2 binds to the pro-apoptotic protein Bax to prevent Bax homo-oligomeriz

74 ential of a pharmacological activator of the pro-apoptotic protein BAX to suppress acute myeloid leuk

75 membranes are unaffected by addition of the pro-apoptotic protein Bax under a variety of conditions.

76 In contrast, the pro-apoptotic protein Bax was expressed in all prostate

77 ast, the intensity of immunostaining for the pro-apoptotic protein Bax was not significantly altered

78 oth cellular and mitochondrial levels of the pro-apoptotic protein Bax were increased severalfold as

79 oposide resulted in the up-regulation of the pro-apoptotic protein Bax, a result that was prevented b

80 een the tumor suppressor protein p53 and the pro-apoptotic protein Bax, in human melanoma cell lines

81 ough a newly identified BH3 domain, with the pro-apoptotic protein Bax, their co-translocation to the

82 port that ARC co-immunoprecipitated with the pro-apoptotic protein Bax, which causes cytochrome c rel

83 ession of the AvrPto and Pto proteins or the pro-apoptotic protein Bax.

84 however, resulted in marked induction of the pro-apoptotic protein Bax.

85 -independent growth, and accumulation of the pro-apoptotic protein BAX.

86 yeast engineered to ectopically express the pro-apoptotic protein Bax.

87 nformational change in the N terminus of the pro-apoptotic protein Bax.

88 nges in expression of Bcl-2, Bcl-Xl, and the pro-apoptotic protein Bax.

89 ative stress-related protein Romo-1, and the pro-apoptotic protein Bax.

90 , and functions to activate the Bcl-2 family pro-apoptotic protein Bax.

91 merization of Bcl-x(L) with its counterpart, pro-apoptotic protein Bax.

92 rial apoptotic pathway acts through two core pro-apoptotic proteins Bax (Bcl2-associated X protein) a

93 The multidomain pro-apoptotic proteins BAX and BAK constitute an essenti

94 d from cells deficient in one or both of the pro-apoptotic proteins Bax and Bak show that at least on

95 spectively, whereas immunopositivity for the pro-apoptotic proteins Bax and Bak was found in 44 (92%)

96 BH3 domains from the pro-apoptotic proteins Bax and Bak, but not the BH3 doma

97 f these events represses the function of the pro-apoptotic proteins Bax and Bak, which are required f

98 ns Bcl-2 or Bcl-X(L) and genetic ablation of pro-apoptotic proteins Bax and Bak.

99 -apoptotic proteins BCL-2 and BCL-XL and the pro-apoptotic proteins BAX and BCL-XS in T/null-cell ALC

100 ses in the mitochondrial levels of activated pro-apoptotic proteins Bax and Bid, and to a lesser exte

101 cl-2 and Bfl-1 as well as high levels of the pro-apoptotic proteins Bax and Bid.

102 s associated with elevated expression of the pro-apoptotic proteins Bax, Bad, and TRAIL (tumor necros

103 ition as evidenced by an upregulation of the pro-apoptotic proteins Bax, cleaved caspase-3, and downr

104 ntrations at the mitochondria surface of the pro-apoptotic proteins Bax/Bak.

105 pha) significantly reduced the expression of pro-apoptotic proteins (Bax and PUMA) and autophagic pro

106 ins functioned to inhibit the ability of the pro-apoptotic protein, Bax to induce PCD in plants and y

107 f 1, 2 and 10mg/kg could alter the levels of pro-apoptotic protein, Bax, anti-apoptotic protein, Bcl-

108 The mammalian pro-apoptotic protein, Bax, confers a lethal phenotype w

109 In this report we demonstrate that the pro-apoptotic protein, Bax, translocates from the cytoso

110 t shares a conserved domain, BH3, with other pro-apoptotic proteins, Bax, Bak, Bid, and Hrk, and cert

111 late the ability of p53 to interact with the pro-apoptotic proteins BCL-XL and BAK.

112 s correlates with increased abundance of the pro-apoptotic proteins BCL2L11 and BBC3, and with decrea

113 The pro-apoptotic protein BID underwent posttranslational (r

114 nduced cleavage of both procaspase-8 and the pro-apoptotic protein Bid, indicating that Bcl-2 functio

115 ) were increased, and the cellular levels of pro-apoptotic proteins Bid and Bax were reduced.

116 In contrast to Bax, another pro-apoptotic protein (Bid) proteolytically cleaved with

117 The pro-apoptotic proteins, Bid and Bax, as well as factors

118 old level of Ca(m) and DeltaPsi(m) while the pro-apoptotic protein Bik has the opposite effect.

119 On the other hand, ectopic expression of the pro-apoptotic protein Bik led to decreased Ca(m) load an

120 The human Bik gene codes for a strong pro-apoptotic protein BIK.

121 Increased apoptosis and expression of the pro-apoptotic protein Bim accompanied this depletion.

122 NK cells showed increased expression of the pro-apoptotic protein Bim and glucose metabolism was imp

123 Furthermore, our data implicate the pro-apoptotic protein Bim as a miRNA target in nephron p

124 s significantly reduced the induction of the pro-apoptotic protein Bim both in vitro and in mice.

125 rtinib treatment increased expression of the pro-apoptotic protein Bim by as much as 144% in Z119 cel

126 Increasing Grx1 reduces the pro-apoptotic protein Bim expression through regulating

127 ATAD1 directly and specifically extracts the pro-apoptotic protein BIM from mitochondria to inactivat

128 The pro-apoptotic protein BIM has also been shown to double-

129 beta-induced apoptosis and expression of the pro-apoptotic protein Bim in WEHI 231 B lymphocytes.

130 hat was 'rescued' by genetic deletion of the pro-apoptotic protein Bim or transgenic expression of Bc

131 A shared target of miR-17~92 miRNAs is the pro-apoptotic protein BIM, central to life-death decisio

132 tion may arise through the inhibition of the pro-apoptotic protein Bim, which is normally repressed b

133 eins such as Bcl-2 and Bcl-xL, and decreases pro-apoptotic protein Bim.

134 eins such as Bcl-2 and Bcl-xL, and decreases pro-apoptotic protein Bim.

135 dd45alpha, the tumor suppressor PTEN and the pro-apoptotic protein Bim.

136 nting the proteasome mediated degradation of pro-apoptotic protein BIM.

137 ed cell death by regulating the level of the pro-apoptotic protein BIM.

138 mor cell apoptosis, increasing levels of the pro-apoptotic protein Bim/Bod, and cleavage of caspase-7

139 We find that levels of the BH3-only pro-apoptotic proteins Bim and Noxa are proteasomally re

140 GrB: the pro-survival protein Mcl-1L and the pro-apoptotic protein, Bim.

141 that occurred with decreases in the BH3-only pro-apoptotic protein, Bim.

142 We report that unlike other pro-apoptotic proteins, Bim contains two distinct bindin

143 ulation and suppresses the expression of the pro-apoptotic protein BimEL, as has been observed in Her

144 The transmembrane domain of the pro-apoptotic protein BNIP3 self-associates strongly in

145 human BCL-2/EIB-19K interacting BCL-2 family pro-apoptotic protein BNIP3.

146 coding not only antiviral, inflammatory, and pro-apoptotic proteins but also proteins of other functi

147 ry cytokine leptin, and incurred loss of the pro-apoptotic protein C/EBP homologous protein (CHOP).

148 stress with the additional expression of the pro-apoptotic protein C/EBP-homologous protein/growth ar

149 lear membrane protein lamin A, expression of pro-apoptotic proteins c-Jun N-terminal kinase 3, caspas

150 ), an outer mitochondrial membrane-targeting pro-apoptotic protein, can be used for light-mediated in

151 ic genetic model Caenorhabditis elegans, the pro-apoptotic protein CED-4 activates the CED-3 caspase

152 In this manner, treatments that increase pro-apoptotic protein expression increase the efficacy o

153 related with CO-induced up-regulation of the pro-apoptotic protein FADD as well as activation of casp

154 c PYD interaction between NLRP12 PYD and the pro-apoptotic protein Fas-associated factor 1 (FAF-1), w

155 Bax, a pro-apoptotic protein from the Bcl-2 family, is central

156 channels may be one mechanism for releasing pro-apoptotic proteins from mitochondria during the indu

157 s such as Bax and Bak mediate the release of pro-apoptotic proteins from the mitochondria by clusteri

158 -cell survival in part via inhibition of the pro-apoptotic proteins glycogen synthase kinase-3alpha/b

159 In cooperation with the pro-apoptotic protein Grim and dREAM/MMB, DMyb promotes

160 lopmental apoptosis--showing that these core pro-apoptotic proteins have separable roles.

161 from Bcl-xL or a homologous region from the pro-apoptotic protein HID.

162 s been shown to be an important activity for pro-apoptotic proteins in Drosophila (Reaper, HID, and G

163 and our understanding of the roles played by pro-apoptotic proteins in non-death scenarios.

164 olytic degradation of the BH3-only family of pro-apoptotic proteins in the mitochondrial pathway.

165 ks the ability of BCL-XL to bind and inhibit pro-apoptotic proteins, in combination with a MEK inhibi

166 ound to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage.

167 Neuronal pentraxin 1 (NP1) is a pro-apoptotic protein induced by low neuronal activity t

168 Death receptor 5 (DR5) is a pro-apoptotic protein involved in mediating the extrinsi

169 eclin-1 contains a BH3-only motif typical of pro-apoptotic proteins, it is a negligible modulator of

170 tion of B-cell migration, and in RNA for the pro-apoptotic protein kinase C eta gene.

171 , EBER-1, binds to the growth inhibitory and pro-apoptotic protein kinase R (PKR) and blocks activati

172 ment binding protein (phospho-CREB), and the pro-apoptotic protein kinases extracellular signal-regul

173 and is the founding member of a subfamily of pro-apoptotic proteins known as "BH3-alone" proteins.

174 he mitochondrial envelope and the release of pro-apoptotic proteins, leading to cell death.

175 rom 11 of 41 tumor lines that expressed this pro-apoptotic protein migrated in gels as a clear double

176 physiology, thereby promoting the release of pro-apoptotic proteins normally contained within this or

177 Bortezomib induced an upregulation of the pro-apoptotic protein Noxa, loss of mitochondrial transm

178 bination treatment induced expression of the pro-apoptotic protein Noxa- and caspase-dependent degrad

179 in Bfl-1 and a decrease in expression of the pro-apoptotic protein Noxa.

180 induction of the Bcl-2 homology 3 (BH3)-only pro-apoptotic protein NOXA.

181 hese events correlated with induction of the pro-apoptotic protein Noxa.

182 regulation of the Bcl-2 homology3 (BH3)-only pro-apoptotic protein NOXA.

183 BAX is a pro-apoptotic protein of the BCL-2 family that is statio

184 1 also induced the phosphorylation of Bad (a pro-apoptotic protein of the Bcl-2 family), which was in

185 Furthermore, the expression levels of the pro-apoptotic proteins of CHOP/GADD153 and caspase-12 we

186 eted NSCLC cells show elevated expression of pro-apoptotic proteins of the Bcl-2 family, caspase recr

187 Reaper is a potent pro-apoptotic protein originally identified in a screen

188 onsequent DNA fragmentation, accumulation of pro-apoptotic proteins (p27, p53, p89 PARP fragments), a

189 r of apoptosis protein, and up-regulated the pro-apoptotic proteins p53 and Bax.

190 own on a 3D in vitro testbed by upregulating pro-apoptotic proteins, p53, and caspase-9.

191 n inhibitor of apoptosis proteins (IAPs) and pro-apoptotic proteins (PAPs) tightly and precisely regu

192 We report that Akt physically binds to the pro-apoptotic protein Par-4 via the Par-4 leucine zipper

193 Now, Simon et al. identify the pro-apoptotic protein Puma as a key factor in this cell

194 uggesting that E1B 19K may act to antagonize pro-apoptotic proteins rather than as an effector of sur

195 ng with cytochrome c and other mitochondrial pro-apoptotic proteins represent important regulatory ch

196 we identify a novel protein, named Parcs for pro-apoptotic protein required for cell survival, that i

197 mphoma-x large (BCL-X(L)) and BAX, anti- and pro-apoptotic proteins, respectively, followed by BAX ac

198 imer formation occurs through binding of the pro-apoptotic protein's BH3 domain into the hydrophobic

199 2 family antiapoptotic proteins with various pro-apoptotic proteins, several of which are also member

200 Reduced expression of the pro-apoptotic protein SMAC (second mitochondria-derived

201 ns of key mitophagic/autophagic proteins and pro-apoptotic protein such as ROS, VDAC1, LC-3II and Cas

202 y interacting with and negatively regulating pro-apoptotic proteins such as Bax and Bad, as a target

203 their pro-apoptotic functions through BH1-3 pro-apoptotic proteins such as BAX and BAK, while their

204 hich bind to the BH3 alpha-helical domain of pro-apoptotic proteins such as Bax, Bak, Bad, and Bim, a

205 cytochrome c from mitochondria, effected by pro-apoptotic proteins such as Bax.

206 gnificant alterations in the ability to bind pro-apoptotic proteins such as Bax.

207 In contrast, certain pro-apoptotic proteins such as BIK and BID share a singl

208 These results support a model in which pro-apoptotic proteins, such as Bax and Bak, bind to Bcl

209 with FAKi + MEKi showed increased levels of pro-apoptotic proteins, such as PUMA and BIM, which prom

210 One of the pro-apoptotic proteins, tBid, can induce apoptosis by pr

211 NOXA is a pro-apoptotic protein that functions by binding the BCL2

212 perties of a small molecule mimic of Smac, a pro-apoptotic protein that functions by relieving inhibi

213 Therefore, galectin-7 is a pro-apoptotic protein that functions intracellularly ups

214 One primary pro-apoptotic protein that responds to both PERK and Ire

215 dings identify Par-4 as a novel example of a pro-apoptotic protein that selectively inhibits oncogeni

216 BAX is a pro-apoptotic protein that transforms from a cytosolic m

217 -ATPase (SERCA), and decreases levels of the pro-apoptotic protein thioredoxin-interacting protein (T

218 and in intact human cancer cells, freeing up pro-apoptotic proteins to induce apoptosis.

219 imetics kill cells by displacing sequestered pro-apoptotic proteins to initiate tumor-cell death.

220 BCL-2 inhibition drives sequestered pro-apoptotic proteins to MCL-1 and vice versa, explaini

221 tant cancers also downregulate or inactivate pro-apoptotic proteins to suppress apoptosis.

222 Death receptor 5 (DR5), a cell surface pro-apoptotic protein, triggers apoptosis upon ligation

223 rane (OM), thus promoting recruitment of the pro-apoptotic proteins truncated Bid (tBid) and Bax for

224 the "BCL-2 homology (BH) 3-only" members of pro-apoptotic proteins, truncated BID (tBID) has been im

225 e SW48 cells increased the expression of the pro-apoptotic proteins, whereas the SW480 cells increase

226 Bik is a potent pro-apoptotic protein, which complexes with various anti

227 hondrial calcium overload and the release of pro-apoptotic proteins, which triggers delayed cell deat

228 sive gene 3)) is a human caspase-independent pro-apoptotic protein with some similarity to apoptosis-

229 The Bcl-2 family includes both anti- and pro-apoptotic proteins with opposing biological function

230 -apoptotic proteins to counter expression of pro-apoptotic proteins, WM samples expressed both pro- a