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 deletion rescued the developmental block.

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

4 BIM expression increased in RGCs after axonal injury and

5 BIM is de-phosphorylated and upregulated following MEK1/

6 BIM phosphorylation was dependent on MEK1/2 kinase activ

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

8 BIM-EL was rapidly degraded in cells lacking wild-type V

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

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

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

12 ion to IL-15 was tightly linked to the BCL-2/BIM ratio, which rapidly dropped during IL-15 withdrawal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 ferential expressions of IGF-1R, FOXO3A, and BIM in the benign versus malignant prostate tissues supp

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

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

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

38 h a single target is essential for life, and BIM regulation by miRNAs serves as a rheostat controllin

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

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

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

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

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

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

45 n transcriptional activation of the PUMA and BIM genes.

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

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

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

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

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

51 te increasing the abundance of pro-apoptotic BIM and BMF, ERK1/2 pathway inhibition is predominantly

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

53 arily by reducing the level of pro-apoptotic BIM.

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

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

56 pendence and the 'primed' state via the ATF4-BIM/NOXA axis.

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

58 und tumour cell death that requires BAK/BAX, BIM and BMF, and inhibiting tumour growth in vivo.

59 of the pro-apoptotic BH3-only gene, BCL2L11 (BIM), by directly binding to BCL2L11 intronic regions an

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

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

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

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

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

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

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

67 that increased protein stability and blocked BIM induction.

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

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

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

71 in isolated myocytes; an effect inhibited by BIM.

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

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

74 This causes BIM-EL to escape from proteasomal degradation, allowing

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

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

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

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

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

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

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

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

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

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

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

86 l molecule (FX1) BCL6 inhibitors derepressed BIM and synergized with the BH3-mimetic ABT-199 in eradi

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

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

89 ates the proapoptotic BCL2L11 locus encoding BIM.

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

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

92 llular apoptosis through control of MAPK/ERK-BIM signaling.

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

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

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

96 enuated induction of the proapoptotic factor BIM.

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

98 ings suggest that targeting the IGF-1/FOXO3A/BIM signaling axis could be an attractive strategy for p

99 ed a negative association between the FOXO3A/BIM axis and IGF-1R expression in human prostate adenoca

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

101 cause upregulation of the pro-apoptotic gene BIM.

102 -inflammatory cytokines, pro-apoptotic genes BIM and TRAIL and expression of a suppressor of hepatocy

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

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

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

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

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

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

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

110 VHL mutants fail to bind hydroxylated BIM-EL, regardless of whether they have the ability to b

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

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

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

114 ity was blocked with bisindolylmaleimide II (BIM).

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

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

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

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

119 of proteins that induce apoptosis, including BIM, cleaved PARP, and cleaved caspase 3.

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

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

122 te PD-L1 expression that was shown to induce BIM and BIK to enhance chemotherapy-induced apoptosis.

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

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

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

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

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

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

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

130 VHL binding inhibits BIM-EL phosphorylation by extracellular signal-related k

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

132 99 observed in hypodiploid leukemias lacking BIM expression (the major reported mediator of ABT-199-i

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

134 Mechanistically, BIM deficiency improved mitochondrial function and decre

135 Mechanistically, BIM expression appears to be epigenetically silenced by

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

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

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

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

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

141 vation of the proapoptotic BH3-only molecule BIM, while BCL6 was required to curb MLL-induced express

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

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

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

145 anism of action of ABT-199 in the absence of BIM.

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

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

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

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

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

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

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

153 apoptotic response due to downregulation of BIM and PUMA.

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

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

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

157 s required to curb MLL-induced expression of BIM.

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

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

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

161 erved a proliferation-dependent induction of BIM short, a highly proapoptotic splice variant of BIM i

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

163 3A and EBNA3C together inhibit initiation of BIM transcripts.

164 y re-expression of PD-L1; re-introduction of BIM enhanced apoptosis.

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

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

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

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

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

170 BRD4 was associated with decreased levels of BIM.

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

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

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

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

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

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

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

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

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

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

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

182 nd PRC1 subunits disrupted EBV repression of BIM.

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

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

185 he BIM promoter to activate transcription of BIM mRNA.

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

187 TKI sensitivity and promoted upregulation of BIM levels.

188 ort, a highly proapoptotic splice variant of BIM in IL-15-activated NK cells.

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

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

191 Deletion of PD-L1 suppressed BH3-only BIM and BIK proteins that could be restored by re-expres

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

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

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

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

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

197 s of reaction products with carbazole and Ph-BIM.

198 ores carbazole and 2-phenylbenzimidazole (Ph-BIM) with two representative isolable singlet carbenes.

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 tor and increased expression of proapoptotic BIM.

206 way by pharmacologic mimicry of proapoptotic BIM.

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

208 evels of nuclear FOXO3A and the proapoptotic BIM protein.

209 on of PI3Ki and BH3 mimetics had a profound, BIM-dependent cytotoxic effect in PIK3CA-mutant cancer c

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

211 inhibitor U0126 attenuate the SOX7 promoted BIM degradation.

212 urable ERK pathway suppression that promotes BIM-dependent apoptosis.

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

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

215 iR-17~92 miRNAs is the pro-apoptotic protein BIM, central to life-death decisions in mammalian cells.

216 ediated degradation of pro-apoptotic protein BIM.

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

218 ation of the proapoptotic BH3 domain protein BIM.

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

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

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

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

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

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

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

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

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

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

229 ent upregulation of the proapoptotic protein BIM and proteasomal degradation of the antiapoptotic pro

230 l death by upregulating proapoptotic protein BIM via a PTEN-dependent mechanism.

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

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

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

234 ls of expression of the proapoptotic protein BIM.

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

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

237 While the BH3-only proteins BIM, PUMA, and tBID have been confirmed to directly acti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 oncomitant ERK attenuation, which stabilizes BIM.

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

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

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

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

260 repressed expression of the tumor suppressor BIM.

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

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

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

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

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

266 We found that BIM-EL, a proapoptotic BH3-only protein, is hydroxylated

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

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

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

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

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

272 The BIM incorporated direct costs only, associated with the

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

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

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

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

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

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

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

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

281 oarene stapled alpha-helical peptides of the BIM BH3 peptide to the BCL(XL) receptor.

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

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

284 f these stapled peptides with respect to the BIM BH3 peptide.

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

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

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

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

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

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

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

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

293 Thus, noninferiority of TRAV versus BIM was demonstrated.

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

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

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

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

298 ant for certain developmental functions with BIM.

299 moderate ocular hyperemia was observed with BIM.

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

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