ライフサイエンスコーパス: BIM

1 BIM deficiency did not impair effector T-cell function;

2 BIM exerts its pro-death function via its alpha-helical

3 BIM expression increased in RGCs after axonal injury and

4 BIM is de-phosphorylated and upregulated following MEK1/

5 BIM is induced by lung cancer cell lines that are sensit

6 BIM phosphorylation was dependent on MEK1/2 kinase activ

7 BIM(EL)/BIM(L) phosphorylation was associated with relea

8 ) and BAK 0.02%-preserved bimatoprost 0.01% (BIM) during late-day time points in patients with open-a

9 pression of the genes encoding BCL2-like 11 (BIM), apoptotic peptidase activating factor 1 (APAF-1),

10 M stimulation increased phosphorylation of 2 BIM isoforms, BIM(EL) and BIM(L), in a subset of CLL sam

11 age, 58.3 +/- 11.4 years; TRAV/BIM, n = 41; BIM/TRAV, n = 40).

12 extent of mitochondrial depolarization by a BIM BH3 peptide in vitro was correlated with percentage

13 f phosphorylation at Ser(69), confirmed by a BIM-EL phosphorylation-defective mutant (S69G) that incr

14 We identified a BIM BH3 analogue that showed increased penetration of th

15 alysis revealed a novel GR binding site in a BIM intronic region (IGR) that was engaged only in dexam

16 Furthermore, this highlights the role of a BIM-mediated tumor suppressor pathway that acts in paral

17 no effect on the direct BAX/BAK "activators" BIM or BID (tBID).

18 ore, using RNA interference directed against BIM, we demonstrated that BIM knockdown attenuated the e

19 with a highly-selective novel MC4R agonist (BIM-22493 or RM-493) resulted in transient decreases in

20 BIM from BCL2's BH3-binding pocket, allowing BIM to activate BAX, induce mitochondrial permeabilizati

21 mide (BIM) I, but not by its inactive analog BIM V.

22 The objective of this study was to analyze BIM-23A760 effects on functional parameters (Ca(2+) sign

23 ly increase the expression of both MCL-1 and BIM.

24 nd was associated with MEK1/2 activation and BIM(EL) phosphorylation.

25 BCL2 as assessed by displacement of BAD and BIM from BCL2.

26 d and apoptotic regulatory proteins, BAX and BIM, down-regulated under normoxic condition; (2) beta1

27 tified novel mechanisms of opposing BCL2 and BIM gene regulation that control glucocorticoid-induced

28 Therefore, BID and BIM have nonoverlapping roles in the induction of apopto

29 revealed that the presence of BAX, BID, and BIM differentially regulated the ability of BH3 mimetics

30 ncy was observed for terminal C:O(6)-BnG and BIM:G base pairs respectively.

31 emic cascade, upstream of JNK, caspases, and BIM and BAX activation.

32 osphorylation of 2 BIM isoforms, BIM(EL) and BIM(L), in a subset of CLL samples.

33 proapoptotic protein BIM, and both JNK1 and BIM knockdown protected beta-cells against cytokine-indu

34 date gene, PTPN2, and activation of JNK1 and BIM.

35 and survival through its effect on JunB and BIM, respectively.

36 factor-related apoptosis-inducing ligand and BIM, thereby providing novel insights into the molecular

37 ilization of BH3-only proteins BIK, NOXA and BIM, appear to be essential for effecting BAX- and BAK-d

38 or substrates, including p21, p27, NOXA, and BIM.

39 ted growth suppression via targeting p21 and BIM, we demonstrate for the first time that this same cl

40 -regulated genes such as MnSOD, p27Kip1, and BIM-1.

41 e show a link between the ERK1/2 pathway and BIM expression through miR-494.

42 link between the uPA-uPAR-ERK1/2 pathway and BIM has not been previously demonstrated in GBM, and inv

43 n transcriptional activation of the PUMA and BIM genes.

44 encoding the proapoptotic proteins PUMA and BIM were induced by growth hormone through STAT5, which

45 istic and induced the expression of PUMA and BIM, led to apoptosis and growth inhibition in vitro, an

46 ucleoside-5'-O-triphosphates ( BENZI: TP and BIM: TP) by an engineered KlenTaq DNA polymerase.

47 ences of mild ocular hyperemia with TRAV and BIM were 31% and 39%, respectively; moderate hyperemia w

48 st that MCL-1 may be necessary to antagonize BIM during macrophage effector responses.

49 f MCL-1 but importantly induce pro-apoptotic BIM expression.

50 -LIMK1, Tyr-NEDD9, Arg-BID, Asp-BCL(XL), Arg-BIM(EL), Asp-EPHA4, and Tyr-MET bear destabilizing N-ter

51 eric somatostatin/dopamine compounds such as BIM-23A760, an sst2/sst5/D2 receptors-agonist, have emer

52 on of NOXA protein, whereas BCL-2, BAX, BAK, BIM, BAD, BID, and PUMA remained unchanged.

53 cellular stress induces proteins (e.g., BID, BIM, and cytosolic p53) capable of directly activating B

54 ating an essential role of the proteins BID, BIM, and PUMA in activating BAX and BAK.

55 at the mitochondria by a member of the BID, BIM, or PUMA family of proteins.

56 Bisindolylmaleimide (BIM; a protein kinase C blocker), a protein kinase C inh

57 yr(1068) was blocked by bisindolylmaleimide (BIM), a PKC inhibitor, and rottlerin, a PKCdelta-specifi

58 The PKC inhibitor bisindolylmaleimide (BIM) abolished PDBu-mediated potentiation of TRPV1-depen

59 ed by the PKC inhibitor bisindolylmaleimide (BIM) I, but not by its inactive analog BIM V.

60 f PIM-1 in complex with bisindolylmaleimide (BIM-1) and established the structure-activity relationsh

61 ession of prosurvival BCL-XL, known to block BIM and BMF, is not only sufficient to increase the viab

62 T3-mediated overexpression of miR-17 blocked BIM expression and caused resistance to AZD6244.

63 that increased protein stability and blocked BIM induction.

64 in decreased expression of proapototic (BMF, BIM), adrenergic (TH), and cell-cycle genes (e.g., CDC25

65 Using a BMF/BIM-double-knockout epithelial transplant model, we furt

66 horylation of Src, which was blocked by both BIM and rottlerin.

67 PK) signaling attenuation and accompanied by BIM(EL) expression.

68 g h(-1), n=8, P<0.01) and totally blocked by BIM (HA secretion: 3.2+/-0.6 microg h(-1), n=9, P<0.001)

69 in isolated myocytes; an effect inhibited by BIM.

70 restimulation-induced cell death mediated by BIM and FAS as an additional cause of bsAb-mediated TIL

71 oblastoma cell proliferation were reduced by BIM, rottlerin, the MEK inhibitor U0126, and PKCdelta an

72 iminished by BAK knockdown and unaffected by BIM or PUMA down-regulation.

73 and resistant cells, but in resistant cells, BIM was sequestered by the additional BFL-1 and/or MCL-1

74 The chimeric sst2/sst5/D2 compound BIM-23A760 affects multiple, clinically relevant paramet

75 In contrast, BIM did not significantly alter the increase in the extr

76 ethane (BIM) complex [Pt(kappa(2) -N,B-(Cy2) BIM)(CNAr(Dipp2) )] can effect the oxidative insertion o

77 ns BCL-2-interacting mediator of cell death (BIM) and p53 upregulated modulator of apoptosis (PUMA) a

78 nt BCL-2 interacting mediator of cell death (BIM) expression in hepatocytes.

79 th Bcl-2 interacting mediator of cell death (BIM) induction and microphthalmia-associated transcripti

80 ene Bcl2-interacting mediator of cell death (BIM) predicts sensitivity to ABT-263.

81 of BCL-2-interacting mediator of cell death (BIM), which contains one of the most potent BH3 death do

82 es Bcl-2 interacting mediator of cell death (BIM; BCL2L11) and caspase-4 (CASP4), among others, were

83 s (e.g. BCL-2 interacting mediator of death, BIM; BCL-2 interacting-domain death agonist, BID) to ind

84 g a critical mediator of thymocyte deletion, BIM, in the NOD mouse model of autoimmune diabetes.

85 Despite BIM and BIK induction, the isogenic KRAS mutant versus w

86 ABT-737 displaced BIM from BCL2's BH3-binding pocket, allowing BIM to acti

87 BIM(EL)/BIM(L) phosphorylation was associated with release of th

88 ates the proapoptotic BCL2L11 locus encoding BIM.

89 s with PLX4720 and a PI3K inhibitor enhanced BIM expression at both the mRNA and protein level and in

90 ERK silencing enhanced BIM up-regulation by GDC-0623 that was due to its loss o

91 d MCL-1 protein levels, thereby facilitating BIM-mediated apoptosis.

92 romoted apoptosis of the proapoptotic factor BIM (Bcl-2 interacting mediator of cell death), whose ex

93 al involving Lyn and the proapoptotic factor BIM that promotes deletion of the B cell and failure of

94 reas EBV-induced BATF/IRF4 were critical for BIM suppression and MYC induction in LCLs.

95 Forced BIM(EL) expression removed the block to cytochrome c rel

96 deletion of HIF-1alpha combined with forced BIM(EL) expression completely reversed the ability of lo

97 The ability of the free BIM to effect bond activation reactions is contrasted wi

98 n represses the pro-apoptotic BH3-only genes BIM and BMF.

99 articular, SCLC cell lines possessed greater BIM transcript levels than most other solid tumors and a

100 Hence, BIM phosphorylation appears to play a key role in apopto

101 To determine the consequences of hepatic BIM deficiency in diet-induced obesity, we generated liv

102 Low MCL1 expression and high BIM:MCL1 or BIM:BCL2 ratios in leukemic cells correlated

103 However, BIM-23A760 elicited stimulatory effects in a subset of G

104 The specificity of the human BIM-SAHB-BAX interaction is highlighted by point mutagen

105 of PKC activity with bisindolylmaleimide I (BIM I) produced the same enhancing effect on carbachol-e

106 Bisindolylmaleimide I (BIM), a protein kinase C signaling pathway inhibitor, si

107 of the PKC inhibitors bisindolylmaleimide I (BIM; 30 microM) or chelerythrine chloride (100 microM) t

108 on MEK1/2 kinase activity, and we identified BIM(EL) serine 69, previously linked to pro-survival res

109 screen of BCL-2 family members, we identify BIM, PUMA, and BCL-XL as key regulators of the apoptotic

110 ity was blocked with bisindolylmaleimide II (BIM).

111 The unligated (boryl)iminomethane BIM is also synthetically accessible and functions as a

112 in is that the platinum (boryl)iminomethane (BIM) complex [Pt(kappa(2) -N,B-(Cy2) BIM)(CNAr(Dipp2) )]

113 turing a bidentate "LZ" (boryl)iminomethane (BIM) ligand is reported.

114 erlotinib resistance is present, a block in BIM up-regulation downstream of EGFR inhibition.

115 h RNA interference resulted in a decrease in BIM(EL) protein and a corresponding decrease in the sens

116 ling proteins of the BCL-2 family, including BIM, were found to be up-regulated after erlotinib treat

117 PLX4720 treatment significantly increased BIM expression in the PTEN+ (>14-fold) compared with the

118 ermore, death signals initiated at ER induce BIM and PUMA to activate mitochondrial apoptosis.

119 IL-21-induced BIM up-regulation is critical for apoptosis because inhi

120 In CLL, anti-IgM-induced BIM phosphorylation correlated with unmutated IGHV gene

121 tized resistant cells to AZD6244 by inducing BIM and PARP cleavage.

122 as activation of the STAT3 pathway inhibited BIM expression and elicited resistance to MEK inhibitors

123 xpression, and overexpressing pVHL inhibited BIM(EL) polyubiquitination.

124 Directly inhibiting BIM(EL) expression in pVHL-expressing RCC cells caused a

125 blocked by pretreatment of the PKC inhibitor BIM and NADPH oxidase inhibitor DPI.

126 increased phosphorylation of 2 BIM isoforms, BIM(EL) and BIM(L), in a subset of CLL samples.

127 earance does not require BAX, BAK, BCL-X(L), BIM, or PUMA, indicating that NIX does not function thro

128 BCL-XL, and the proapoptotic BH3-only ligand BIM were found to be coexpressed at relatively high leve

129 MAPK/ERK kinase (MEK) (bisindolyl maleimide (BIM) or U0126, respectively) blocked both PMA-induced El

130 Mechanistically, BIM deficiency improved mitochondrial function and decre

131 Mechanistically, BIM expression appears to be epigenetically silenced by

132 r PTEN in the regulation of PLX4720-mediated BIM expression was confirmed by siRNA knockdown of PTEN

133 The pro-apoptotic Bcl-2 family member BIM is known to induce BAX activation.

134 The proapoptotic BCL-2 family member BIM is up-regulated after CDK inhibition and contributes

135 A budget impact model (BIM) was developed from UK NHS hospital perspective to e

136 A Building Information Modeling (BIM) of a reference 43,000 ft(2) office building was dev

137 e to down-regulate the proapoptotic molecule BIM in Taci(-/-) plasma cells.

138 reduced expression of proapoptotic molecules BIM and PUMA during the various phases of response, and

139 A nonphosphorylatable BIM molecule (S55A, S65A, and S100A) demonstrates enhanc

140 fter IL-3 withdrawal, only nonphosphorylated BIM interacts with the multidomain proapoptotic effector

141 oapoptotic BH3-only protein NBK/BIK, but not BIM, PUMA, or NOXA.

142 Ablation of BIM could rescue ASC formation in Taci(-/-) mice, sugges

143 s characterized by the rapid accumulation of BIM on the outer mitochondrial membrane, which could be

144 e was stabilization of FoxO3a, activation of BIM and PUMA, and a significant decrease in c-Myc transc

145 AX interaction and the pro-death activity of BIM.

146 articular, enhance expression and binding of BIM to BCL-2, consequently sensitizing these cells to th

147 Importantly, blockade of BIM using siRNA significantly abrogates NPI-0052 plus le

148 ty in RCC cells, and that destabilization of BIM(EL) in the absence of pVHL contributes to the increa

149 ed increase in apoptosis and dissociation of BIM from BCL-2.

150 al, prevents apoptosis via downregulation of BIM and achieves immunosuppression by MAPK/NF-kB-depende

151 apoptotic response due to downregulation of BIM and PUMA.

152 r, information on direct in vitro effects of BIM-23A760 in normal and tumoral pituitaries remains inc

153 inhibitor with AZD6244 induced expression of BIM and PARP cleavage, whereas activation of the STAT3 p

154 by MEKi/PI3Ki, with decreased expression of BIM and PUMA relative to BCL-XL in cell lines with intri

155 not modified in cells lacking expression of BIM or of BAX/BAK.

156 dephosphorylated and deubiquitinated form of BIM as well as triggered the accumulation of the transcr

157 sion of the shorter, more cytotoxic forms of BIM.

158 for continued survival despite induction of BIM could be due to binding and sequestration of BIM to

159 e in the striatum, intracortical infusion of BIM enhanced MDMA-induced release of DA in the mPFC.

160 critical for apoptosis because inhibition of BIM expression using small interfering RNA prevented IL-

161 3A and EBNA3C together inhibit initiation of BIM transcripts.

162 Moreover, siRNA knockdown of BIM abrogated AZD6244-related apoptosis, while shRNA kno

163 A small interfering RNA knockdown of BIM confirms this BH3-only member is important for the c

164 all CRC cell lines studied and knockdown of BIM reduces cell death, indicating that repression of BI

165 Importantly, short-term knockdown of BIM rescued obese mice from insulin resistance, evidence

166 rther studies showed that siRNA knockdown of BIM significantly blunted the apoptotic response in PTEN

167 In addition to BIK, enhanced level of BIM was observed in Ad-infected cells.

168 rm ERK1(-/-) mice expressed higher levels of BIM under growth factor-deprived conditions and reduced

169 BRD4 was associated with decreased levels of BIM.

170 to VHL-null cells increased the half-life of BIM(EL) protein without affecting its mRNA expression, a

171 ancer (NSCLC) through the down-modulation of BIM.

172 protein kinase-dependent phosphorylation of BIM in response to survival factor regulates BIM/BAX int

173 Phosphorylation of BIM on exposure of cells to IL-3 dramatically reduces th

174 d protein kinase-mediated phosphorylation of BIM on three serine sites (S55, S65, and S100).

175 i-IgM triggered selective phosphorylation of BIM(EL) only.

176 t on calcium mobilization in the presence of BIM I.

177 Reduction of BIM by siRNA induces resistance to erlotinib.

178 model, and shRNA-mediated down-regulation of BIM in human breast cancer cells.

179 in part by suppressing the up-regulation of BIM(EL).

180 his study, we investigated the regulation of BIM, a proapoptotic BCL2-related protein, which is tight

181 , and MEK inhibition led to up-regulation of BIM.

182 osis by a mechanism that includes release of BIM from its sequestration by BCL-XL.

183 cted to the ERK1/2 pathway for repression of BIM and growth factor-independent survival.

184 es cell death, indicating that repression of BIM is a major part of the ability of BRAF(V600E) to con

185 revealed that this epigenetic repression of BIM was reversible, but took more than 3 weeks from when

186 nd PRC1 subunits disrupted EBV repression of BIM.

187 could be due to binding and sequestration of BIM to alternate pro-survival BCL-2 members.

188 show here that the phosphorylation status of BIM controls its proapoptotic activity.

189 inhibitor resistance via the suppression of BIM-mediated apoptosis.

190 he BIM promoter to activate transcription of BIM mRNA.

191 on of BH-3 protein BIM; (3) translocation of BIM to endoplasmic reticulum; (4) inhibition of migratio

192 Apoptosis was dependent on BIM in some but not all cell lines, indicating that othe

193 Antigen-mediated effects on BIM may be an important determinant of clinical behavior

194 ed by the activator BH3-only proteins BID or BIM, which have been considered to be functionally redun

195 crease reactive oxygen species generation or BIM expression, resulting in reduced necrosis and apopto

196 Low MCL1 expression and high BIM:MCL1 or BIM:BCL2 ratios in leukemic cells correlated with respon

197 splays a differential sensitivity to PMA- or BIM-induced activation or inhibition of DAT function rel

198 randomized 1:1 to receive once-daily TRAV or BIM for 6 weeks followed by an additional 6-week crossov

199 In tumoral pituitaries, BIM-23A760 also inhibited Ca(2+) concentration, hormone

200 teries were exposed to Ang II or Ang II plus BIM (for 2 h), after which these agents were removed and

201 Such resistance can be overcome by potent BIM induction and concurrent BCL-XL antagonism to enable

202 s noninferior to that of BAK 0.02%-preserved BIM; both reduced baseline IOP by 25%.

203 Proapoptotic BIM was displaced from BCL-2 by ABT-737 in both parental

204 Loss of proapoptotic BIM, known to cause autoimmunity, also causes loss of "p

205 way by pharmacologic mimicry of proapoptotic BIM.

206 t that BCL2 tonically sequester proapoptotic BIM in CLL.

207 The proapoptotic BIM protein is an important mediator of glucocorticoid-i

208 evels of nuclear FOXO3A and the proapoptotic BIM protein.

209 esults demonstrate that pVHL acts to promote BIM(EL) protein stability in RCC cells, and that destabi

210 e polymerase; (2) activation of BH-3 protein BIM; (3) translocation of BIM to endoplasmic reticulum;

211 ed with induction of the pro-anoikis protein BIM and decreased ERK and AKT signaling during cell deta

212 ating the level of the pro-apoptotic protein BIM.

213 ation of the proapoptotic BH3 domain protein BIM.

214 els of the proapoptotic Bcl-2 family protein BIM(EL) and are more resistant to etoposide and UV radia

215 ion of the proapoptotic BCL-2 family protein BIM.

216 the proapoptotic BCL2-family member protein BIM (BCL2L11).

217 ous studies indicate that a BH3-only protein BIM (BCL-2 Interacting Mediator of cell death) plays a r

218 ls and thereby prevents the BH3-only protein BIM (BCL2-interacting mediator of cell death)-dependent

219 We found that loss of the BH3-only protein BIM accelerated lymphoma development in p53-deficient mi

220 vates ERK1/2, represses the BH3-only protein BIM and protects cells from growth factor withdrawal.

221 ession of the pro-apoptotic BH3-only protein BIM, cleaved caspase 3 and cleaved poly (ADP-ribose) pol

222 n of the BCL-2 homology-3 (BH3)-only protein BIM.

223 markedly decreases the proapoptotic protein BIM and attenuates intrinsic, nonreceptor-mediated mitoc

224 A treatment induces the proapoptotic protein BIM and exerts dose-dependent lethality against cultured

225 he up-regulation of the proapoptotic protein BIM via both transcriptional and post-translational mech

226 phosphorylation of the proapoptotic protein BIM, and both JNK1 and BIM knockdown protected beta-cell

227 eased levels of the BH3 proapoptotic protein BIM, which appeared to be regulated by the BRD2 BET prot

228 ls of expression of the proapoptotic protein BIM.

229 t up-regulation of the proapoptotic protein, BIM, followed by induction of apoptosis.

230 ly by the proapoptotic BCL-2 family proteins BIM and BMF, and their proapoptotic function is conserve

231 te the function of the proapoptotic proteins BIM and BAX, JNK signaling, and endoplasmic reticulum st

232 ciated with activation by BH3 only proteins (BIM and BID).

233 ncluding IKAROS (also known as IKZF1), PTEN, BIM, PHF6, NF1 and FBXW7.

234 mia was observed in 2% of patients receiving BIM.

235 Paca2 cells, BEZ and DOX cotreatment reduced BIM expression in H9C2 cardiomyocytes.

236 facilitates GC-induced apoptosis, we reduced BIM mRNA levels and Bim protein levels by RNA interferen

237 GDC-0623 was shown to potently up-regulate BIM expression to a greater extent versus other MEK inhi

238 block MEK/ERK signaling, did not up-regulate BIM, and failed to induce apoptosis.

239 BIM in response to survival factor regulates BIM/BAX interaction and the pro-death activity of BIM.

240 The signaling pathways regulating BIM and BCL2 expression in glucocorticoid-treated lympho

241 ) regulator MIG6 and the apoptosis regulator BIM, which rescue experiments showed were essential to m

242 Whereas ABT-263 released BIM from complexes with BCL-2 and BCL-XL, high expressio

243 tion of MEK or a BH3 mimetic drug to replace BIM function.

244 BRAF(V600E) allele is sufficient to repress BIM and prevent death arising from growth factor withdra

245 ors that are predictive of drug sensitivity (BIM, caspase-3, BCL-XL) and resistance (MCL-1, XIAP).

246 BCL-XL, high expression of MCL-1 sequestered BIM released from BCL-2 and BCL-XL, thereby abrogating a

247 suggest that UPEC can epigenetically silence BIM expression, a molecular switch that prevents apoptos

248 -free extension was observed for the smaller BIM:O(6)-BnG base pair.

249 induced obesity, we generated liver-specific BIM-knockout (BLKO) mice.

250 oncomitant ERK attenuation, which stabilizes BIM.

251 The therapeutic potential of stapled BIM BH3 was highlighted by the selective activation of c

252 UPEC can suppress BIM expression induced by LY249002, which results in att

253 genetic GBM models, uPA is shown to suppress BIM levels through ERK1/2 phosphorylation, which can be

254 ve erythropoiesis, whereby GATA-1 suppresses BIM-mediated apoptosis via LRF.

255 repressed expression of the tumor suppressor BIM.

256 A-17 approximately 92 cluster thus targeting BIM, a known proapoptotic regulator of melanocyte surviv

257 BAD displaces tBID, BIM or PUMA from BCL-2-BCL-X(L) to activate BAX-BAK, whe

258 The activator BH3s, tBID/BIM/PUMA, attack and expose the alpha1 helix of BAX, res

259 Here we demonstrate by NMR analysis that BIM SAHB binds BAX at an interaction site that is distin

260 Here, we demonstrate that BIM and PUMA, similar to truncated BID (tBID), directly

261 pting the mammary gland and demonstrate that BIM is a critical regulator of apoptosis in vivo.

262 e directed against BIM, we demonstrated that BIM knockdown attenuated the effects of imatinib, sugges

263 This demonstrates that BIM is critical for the induction of apoptosis caused by

264 We show here that BIM is dispensable in apoptosis with paclitaxel treatmen

265 Our data indicate that BIM is an important regulator of liver dysfunction in ob

266 These data suggest that BIM has multiple roles in glaucoma pathophysiology, pote

267 rabine and rituximab in CLL and suggest that BIM up-regulation might serve as relevant pharmacodynami

268 ted the effects of imatinib, suggesting that BIM functionally contributes to imatinib-induced apoptos

269 The BIM incorporated direct costs only, associated with the

270 ydrocarbon-stapled peptide modeled after the BIM BH3 helix broadly targeted BCL-2 family proteins wit

271 etailed analyses of the chromatin around the BIM promoter has revealed that latent Epstein-Barr virus

272 The absence of GR binding at the BIM IGR was associated with BIM silencing and dexamethas

273 y a decrease in histone 4 acetylation at the BIM promoter site.

274 II) occupancy was not altered by EBV at the BIM TSS, but analysis of phospho-serine 5 on Pol II indi

275 f the reactive Pt --> B bond fostered by the BIM ligand allows for a rich reactivity profile toward s

276 ttress, the small bite angle enforced by the BIM ligand is shown to promote a significant metal-boran

277 otential of a "stapled" BH3 peptide from the BIM protein, which inactivates all its prosurvival relat

278 crocyclic analogues of the BH3 domain of the BIM protein to assess if our approach would be applicabl

279 on of the transcription factor FOXO3a on the BIM promoter to activate transcription of BIM mRNA.

280 re of cells to IL-3 dramatically reduces the BIM/BAX interaction.

281 , alkyl migration processes available to the BIM framework allow for post-insertion reaction sequence

282 in the deletion of autoreactive thymocytes, BIM-deficient NOD (NODBim(-/-)) mice developed less insu

283 e ultimate response of pituitary adenomas to BIM-23A760.

284 Instead, BCL2 complexed to BIM is the critical target for ABT-737 in CLL.

285 TRAV was considered noninferior to BIM if the upper limit of the 95% CI of the between-grou

286 nge from baseline, -6.0 mmHg) was similar to BIM (17.2 +/- 2.6 mmHg; change from baseline, -6.3 mmHg)

287 (mean +/- SD age, 58.3 +/- 11.4 years; TRAV/BIM, n = 41; BIM/TRAV, n = 40).

288 ional changes in BAX induced by a triggering BIM BH3 helix were suppressed by the BCL-2 BH4 helix.

289 efficiently inactivated RAF/ERK, upregulated BIM and down-regulated PD-L1 expression in HCC, and faci

290 Thus, noninferiority of TRAV versus BIM was demonstrated.

291 d apoptosis in DLBCL and that cell death was BIM-dependent.

292 ar sst2/sst5/D2 expression patterns, wherein BIM-23A760 inhibited the expression/secretion of several

293 eins: BID preferentially activates BAK while BIM preferentially activates BAX.

294 R binding at the BIM IGR was associated with BIM silencing and dexamethasone resistance.

295 med by the isolation of BCL-2 complexes with BIM.

296 ant for certain developmental functions with BIM.

297 moderate ocular hyperemia was observed with BIM.

298 creases in blood pressure or heart rate with BIM-22493 treatment.

299 phoid infiltrates of mice reconstituted with BIM-deficient bone marrow and in a human AML xenograft m

300 ompetitive inhibitor, 2-methyl-1H-indol-3-yl-BIM-1, was crystallized with the PKCbetaII catalytic dom