PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 34007045-1 2021 Herein, we screened a novel inhibitor of the Hsp70-Bim protein-protein interaction (PPI), S1g-2, from a Bcl-2 inhibitor library; this compound specifically disrupted the Hsp70-Bim PPI by direct binding to an unknown site adjacent to that of an allosteric Hsp70 inhibitor MKT-077, showing binding affinity in sub-muM concentration range. MKT 077 271-278 BCL2 like 11 Homo sapiens 51-54 33831397-6 2021 Mechanistically, HHT and quizartinib cooperatively inhibit FLT3-AKT and its downstream targets GSK3beta, c-Myc, and cyclin D1, cooperatively up-regulate the pro-apoptosis proteins Bim and Bax, and down-regulate the anti-apoptosis protein Mcl1. quizartinib 25-36 BCL2 like 11 Homo sapiens 180-183 34007050-2 2021 Here, we show that activating IL7R pathway mutations and physiological IL7R signaling activate MAPK-ERK signaling, which provokes steroid resistance by phosphorylation of BIM. Steroids 130-137 BCL2 like 11 Homo sapiens 171-174 33311449-0 2020 Anti-PD1 therapy induces lymphocyte-derived exosomal miRNA-4315 release inhibiting Bim-mediated apoptosis of tumor cells. mirna-4315 53-63 BCL2 like 11 Homo sapiens 83-86 33934994-0 2021 Quantification of BIM mRNA in circulating tumor cells of osimertinib-treated patients with EGFR mutation-positive lung cancer. osimertinib 57-68 BCL2 like 11 Homo sapiens 18-21 33929994-5 2021 High degrees of apoptosis were observed among cell lines in which vandetanib suppressed ERK1/2 phosphorylation and upregulated the proapoptotic protein Bim, but this did not appear essential for vandetanib-induced cell death in all cell lines. vandetanib 66-76 BCL2 like 11 Homo sapiens 152-155 33118830-9 2021 Furthermore, Bim and p21 were upregulated in OS cells following apcin treatment. apcin 64-69 BCL2 like 11 Homo sapiens 13-16 33485989-7 2021 After olanzapine treatment, the FASLG mRNA expression level was restored and exhibited a pairwise correlation with the FOXO3A and BCL2L11 mRNA expression levels but not with the FOXO1 mRNA expression level, and FASLG mRNA expression was also correlated with the duration of the disease. Olanzapine 6-16 BCL2 like 11 Homo sapiens 130-137 33387147-8 2021 We found that the BH3-only proteins NOXA, BIM and PUMA participate in fluorizoline-induced apoptosis and that the induction of NOXA and PUMA is dependent on PHB expression. Fluorizoline 70-82 BCL2 like 11 Homo sapiens 42-45 33524514-14 2021 Furthermore, in an assay of gene and protein expression, we found that DP could downregulate the gene and protein expression levels of Bcl-2, upregulate the gene and protein expression levels of Bax and Bim, and downregulate the protein expression levels of PI3k, p-Akt, and p-FoxO3a. 12-deoxyphorbol 13-palmitate 71-73 BCL2 like 11 Homo sapiens 203-206 33108571-5 2021 The inhibitory effect induced by Curcusone C was greatly impaired by the overexpression of survivin or Bax-/- MEFs or the knockdown of Bim expression. Curcusone C 33-44 BCL2 like 11 Homo sapiens 135-138 33296806-0 2021 Clinical implications of germline BCL2L11 deletion polymorphism in pretreated advanced NSCLC patients with osimertinib therapy. osimertinib 107-118 BCL2 like 11 Homo sapiens 34-41 33296806-2 2021 Nevertheless, the impact of BIM-del in advanced NSCLC patients treated with the third-generation EGFR-TKI osimertinib remains undetermined. osimertinib 106-117 BCL2 like 11 Homo sapiens 28-31 33296806-3 2021 This study aims to evaluate the relationship between BIM-del and therapeutic efficacy of osimertinib in pretreated NSCLC patients. osimertinib 89-100 BCL2 like 11 Homo sapiens 53-56 33296806-14 2021 CONCLUSIONS: BIM-del is associated with poor clinical responses and outcomes, and might be a negative predictive and prognostic biomarker in EGFR T790 M NSCLC patients with osimertinib treatment. osimertinib 173-184 BCL2 like 11 Homo sapiens 13-16 33352965-8 2020 Similarly, melatonin reduced bile acid-induced proapoptotic caspase 3 and Bim levels. Melatonin 11-20 BCL2 like 11 Homo sapiens 74-77 33352965-8 2020 Similarly, melatonin reduced bile acid-induced proapoptotic caspase 3 and Bim levels. Bile Acids and Salts 29-38 BCL2 like 11 Homo sapiens 74-77 34025070-15 2021 Furthermore, SB203580 significantly reversed changes in the bronchoalveolar lavage fluid protein concentration, Evans blue accumulation, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cell numbers, apoptosis-related proteins (cle-caspase3, Bim and Bax) and endothelial microstructure. SB 203580 13-21 BCL2 like 11 Homo sapiens 272-275 33939252-11 2021 Foretinib led to a decrease in Bcl-2, and an increase in p27, Bax, Bim, cleaved PARP-1 and cleaved caspase-3. GSK 1363089 0-9 BCL2 like 11 Homo sapiens 67-70 33953834-10 2021 Western blotting analysis showed that acetylshikonin treatment induced increase of cleaved PARP, gammaH2AX, FOXO3, Bax, Bim, Bad, p21, p27, and active forms of caspase-3, caspase-7, caspase-9, caspase-6, and caspase-8 protein levels, while those of inactive forms were decreased. acetylshikonin 38-52 BCL2 like 11 Homo sapiens 120-123 32844279-6 2021 The experimental data suggest a new mechanistic role for the BIM-BH3 domain, and demonstrate, for the first time, that an apoptotic peptide forms toxic amyloid fibrils. BH 3 65-68 BCL2 like 11 Homo sapiens 61-64 33576217-10 2021 RESULTS: VPA downregulated class I histone deacetylase (HDAC) 1, 2, and 3, Bcl-2, Bcl-xL, and Mcl-1 and upregulated p21, p53, Bax, Bak, and Bim resulting in apoptosis induction. Valproic Acid 9-12 BCL2 like 11 Homo sapiens 140-143 33328303-8 2020 In addition to its effect of KSHV reactivation, this study revealed that SBHA induces apoptosis in PEL cells in a dose-dependent manner, inducing acetylation and phosphorylation of p53, cleavage of caspases, and expression of pro-apoptotic factors such as Bim and Bax. suberoyl bis-hydroxamic acid 73-77 BCL2 like 11 Homo sapiens 256-259 33437374-0 2020 In vitro investigation of protective mechanisms of triptolide against coronary heart disease by regulating miR-24-3p-BCL2L11 axis and PPARs-PGC1alpha pathway. triptolide 51-61 BCL2 like 11 Homo sapiens 117-124 33311449-9 2020 At molecular level, we discern that the apopto-resistance phenomenon was associated with the miRNA-4315-mediated downregulation of Bim, a proapoptotic protein. mirna-4315 93-103 BCL2 like 11 Homo sapiens 131-134 33292156-6 2021 The molecular docking of bilirubin on CDKs (Cyclin-dependent kinases 2, 4, and 6) and pro-apoptotic factors Bad, Bak, Bax, Bid, Bik, and Bim were done by Autodock software version 2. Bilirubin 25-34 BCL2 like 11 Homo sapiens 137-140 33125118-12 2020 In view of these corrections, in the "Matrine induces cell apoptosis by increasing Bim and Bax and decreasing Bcl-2 protein levels in prostate cancer cell lines" subsection of the Results section towards the bottom of p. 2822, in the penultimate sentence, the text "...LY294002 resulted in 25.88% cell apoptosis in the PC-3 cells and 18.88% in the RWPE1 cells, compared to 3.11 and 6.89%, respectively, with LY294002 treatment only (Fig. matrine 38-45 BCL2 like 11 Homo sapiens 83-86 33216827-7 2020 Moreover, TAK-580 enhanced bortezomib-induced cytotoxicity and apoptosis in MM cells via the FOXO3-Bim axis and the terminal unfolded protein response. tak-580 10-17 BCL2 like 11 Homo sapiens 99-102 33312341-7 2020 Western blot analysis showed that 6,8-diprenylorobol treatment increased the expression of cleaved PARP1, cleaved caspase-3, FOXO3, Bax, Bim, p21, and p27 but decreased the expression of Bcl2 and BclXL. 6,8-Diprenylorobol 34-52 BCL2 like 11 Homo sapiens 137-140 33216827-7 2020 Moreover, TAK-580 enhanced bortezomib-induced cytotoxicity and apoptosis in MM cells via the FOXO3-Bim axis and the terminal unfolded protein response. Bortezomib 27-37 BCL2 like 11 Homo sapiens 99-102 32798467-0 2020 The BCL-2 family members NOXA and BIM mediate fluorizoline-induced apoptosis in multiple myeloma cells. Fluorizoline 46-58 BCL2 like 11 Homo sapiens 34-37 33109551-0 2020 Heat Shock Protein 90 Inhibitors AUY922, BIIB021 and SNX5422 Induce Bim-mediated Death of Thyroid Carcinoma Cells. 5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide 33-39 BCL2 like 11 Homo sapiens 68-71 33109551-0 2020 Heat Shock Protein 90 Inhibitors AUY922, BIIB021 and SNX5422 Induce Bim-mediated Death of Thyroid Carcinoma Cells. 6-chloro-9-(4-methoxy-3,5-dimethylpyridin-2-ylmethyl)-9H-purin-2-ylamine 41-48 BCL2 like 11 Homo sapiens 68-71 33109551-0 2020 Heat Shock Protein 90 Inhibitors AUY922, BIIB021 and SNX5422 Induce Bim-mediated Death of Thyroid Carcinoma Cells. SNX-5422 53-60 BCL2 like 11 Homo sapiens 68-71 33109551-9 2020 CONCLUSION: AUY922, BIIB021 and SNX5422 induce cytotoxicity by modulating Bim and ERK1/2, AKT and AMPK signaling in thyroid carcinoma cells. 5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide 12-18 BCL2 like 11 Homo sapiens 74-77 33193095-10 2020 E2 treatment also upregulated the expression levels of TGF-beta and PGC-1alpha mRNAs and downregulated PUMA and Bim mRNAs. Estradiol 0-2 BCL2 like 11 Homo sapiens 112-115 33109551-9 2020 CONCLUSION: AUY922, BIIB021 and SNX5422 induce cytotoxicity by modulating Bim and ERK1/2, AKT and AMPK signaling in thyroid carcinoma cells. 6-chloro-9-(4-methoxy-3,5-dimethylpyridin-2-ylmethyl)-9H-purin-2-ylamine 20-27 BCL2 like 11 Homo sapiens 74-77 33109551-9 2020 CONCLUSION: AUY922, BIIB021 and SNX5422 induce cytotoxicity by modulating Bim and ERK1/2, AKT and AMPK signaling in thyroid carcinoma cells. SNX-5422 32-39 BCL2 like 11 Homo sapiens 74-77 33163272-6 2020 The HQP8361 and AZD9291 combination synergistically decreased the survival of these HCC827/AR cell lines with enhanced induction of apoptosis that involved alteration of Bim and Mcl-1 levels via modulating their degradation. hqp8361 4-11 BCL2 like 11 Homo sapiens 170-173 33163272-6 2020 The HQP8361 and AZD9291 combination synergistically decreased the survival of these HCC827/AR cell lines with enhanced induction of apoptosis that involved alteration of Bim and Mcl-1 levels via modulating their degradation. osimertinib 16-23 BCL2 like 11 Homo sapiens 170-173 32982289-8 2020 The molecular data showed that TB up-regulated the gene expressions of NOXA, PUMA, P21, Bax, and Bim and up-regulated the protein expressions of ASK-1, Bax, phosphorylated JNK, and phosphorylated c-Jun with down-regulation of Bcl-2. theabrownin 31-33 BCL2 like 11 Homo sapiens 97-100 33042417-4 2020 Here, we showed that ATO reduced cell viability and promoted apoptosis of cervical cancer cells by inducing caspase-3 and PARP activation and upregulating Bim. Atorvastatin 21-24 BCL2 like 11 Homo sapiens 155-158 32633363-10 2020 Meanwhile, simvastatin treatment caused cell cycle arrest in G0/G1 phase, remarkably downregulated expression of cyclin D1, and upregulated expressions of p21 and Bim. Simvastatin 11-22 BCL2 like 11 Homo sapiens 163-166 31601689-6 2020 Treatment with ABT-199 displaced BAX and BIM from BCL-2, leading subsequently to BAK activation and apoptosis. 2-(4'-diethylaminophenyl)benzothiazole 15-18 BCL2 like 11 Homo sapiens 41-44 31601689-8 2020 Finally, the MCL-1 inhibitor S63845 induced mainly BAX-dependent apoptosis mediated by a displacement of BAK, BIM and NOXA from MCL-1. Sulfur 29-35 BCL2 like 11 Homo sapiens 110-113 32344260-8 2020 Furthermore, endosulfan significantly increased the expression of Bim, and inhibited the expressions of PI3K/Akt/FoxO3a signaling pathways in cardiomyocytes (p < 0.05). Endosulfan 13-23 BCL2 like 11 Homo sapiens 66-69 32353423-9 2020 Crocin induced ROS production, FOXO3a expression and nuclear translocation, and then, elevation of the expression of FOXO3a target genes (Bim and PTEN) and caspase-3 activation. crocin 0-6 BCL2 like 11 Homo sapiens 138-141 32353423-10 2020 Application of N-acetylcysteine blocked AKT/FOXO3a/Bim signaling. Acetylcysteine 15-31 BCL2 like 11 Homo sapiens 51-54 32591507-3 2020 Targeted disruption of SMS in CRC cells results in spermidine accumulation, which inhibits FOXO3a acetylation and allows subsequent translocation to the nucleus to transcriptionally induce expression of the proapoptotic protein Bim. Spermidine 51-61 BCL2 like 11 Homo sapiens 228-231 32242100-9 2020 GCS-3 in combination with dexamethasone downregulated C-MYC and significantly upregulated BIM expression in a glucocorticoid-resistant ALL xenograft. Dexamethasone 26-39 BCL2 like 11 Homo sapiens 90-93 32242100-10 2020 The GCS-3/dexamethasone combination significantly increased binding of the glucocorticoid receptor to a novel BIM enhancer, which is associated with glucocorticoid sensitivity. Dexamethasone 10-23 BCL2 like 11 Homo sapiens 110-113 31504249-11 2020 Furthermore, activation of AKT by EFs led to phosphorylation of forkhead box O3a (FOXO3a), and reduction in nuclear translocation of FOXO3a induced by osimertinib, resulting in decreased expression of Bim and attenuated cytotoxicity of osimertinib. osimertinib 151-162 BCL2 like 11 Homo sapiens 201-204 31504249-11 2020 Furthermore, activation of AKT by EFs led to phosphorylation of forkhead box O3a (FOXO3a), and reduction in nuclear translocation of FOXO3a induced by osimertinib, resulting in decreased expression of Bim and attenuated cytotoxicity of osimertinib. osimertinib 236-247 BCL2 like 11 Homo sapiens 201-204 31504249-12 2020 Taken together, we demonstrated that EFs suppressed the anti-tumor activity of osimertinib through AKT/FOXO3a/Bim pathway, and combination of PI3K/AKT inhibitor with osimertinib counteracted the effects of EFs. osimertinib 79-90 BCL2 like 11 Homo sapiens 110-113 31504249-12 2020 Taken together, we demonstrated that EFs suppressed the anti-tumor activity of osimertinib through AKT/FOXO3a/Bim pathway, and combination of PI3K/AKT inhibitor with osimertinib counteracted the effects of EFs. osimertinib 166-177 BCL2 like 11 Homo sapiens 110-113 32459381-6 2020 CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bcl-xL, Bim and c-Myc. CUDC-907 0-8 BCL2 like 11 Homo sapiens 69-72 32256723-9 2020 In addition, it was found that downregulation of miR-24-3p suppressed VSMC proliferation and promoted VSMC apoptosis, while the effects of the miR-24-3p inhibitor on cell viability and apoptosis were reversed by Bcl-2L11-small interfering (si)RNA. mir-24-3p 49-58 BCL2 like 11 Homo sapiens 212-220 32239624-6 2020 The combination of osimertinib and aspirin induced strong anti-proliferative and proapoptotic effects in osimertinib-resistant NSCLC cells through inhibition of Akt/FoxO3a signaling component phosphorylation and increased Bim expression. osimertinib 19-30 BCL2 like 11 Homo sapiens 222-225 32239624-6 2020 The combination of osimertinib and aspirin induced strong anti-proliferative and proapoptotic effects in osimertinib-resistant NSCLC cells through inhibition of Akt/FoxO3a signaling component phosphorylation and increased Bim expression. Aspirin 35-42 BCL2 like 11 Homo sapiens 222-225 32239624-6 2020 The combination of osimertinib and aspirin induced strong anti-proliferative and proapoptotic effects in osimertinib-resistant NSCLC cells through inhibition of Akt/FoxO3a signaling component phosphorylation and increased Bim expression. osimertinib 105-116 BCL2 like 11 Homo sapiens 222-225 32239624-7 2020 Furthermore, Bim knockdown by siRNA significantly attenuated osimertinib resensitization by aspirin. osimertinib 61-72 BCL2 like 11 Homo sapiens 13-16 32239624-7 2020 Furthermore, Bim knockdown by siRNA significantly attenuated osimertinib resensitization by aspirin. Aspirin 92-99 BCL2 like 11 Homo sapiens 13-16 32239624-11 2020 In summary, aspirin synergistically enhances the antitumor activity of osimertinib in osimertinib-resistant lung cancer cells through promoting Bim-dependent apoptosis. Aspirin 12-19 BCL2 like 11 Homo sapiens 144-147 32547023-9 2020 AgNP treatment also increased the Bax, Bik, and Bim protein levels as well as NOX4-dependent ROS generation. agnp 0-4 BCL2 like 11 Homo sapiens 48-51 32424251-0 2020 Bim, Puma and Noxa upregulation by Naftopidil sensitizes ovarian cancer to the BH3-mimetic ABT-737 and the MEK inhibitor Trametinib. naftopidil 35-45 BCL2 like 11 Homo sapiens 0-3 32424251-0 2020 Bim, Puma and Noxa upregulation by Naftopidil sensitizes ovarian cancer to the BH3-mimetic ABT-737 and the MEK inhibitor Trametinib. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 91-94 BCL2 like 11 Homo sapiens 0-3 32424251-0 2020 Bim, Puma and Noxa upregulation by Naftopidil sensitizes ovarian cancer to the BH3-mimetic ABT-737 and the MEK inhibitor Trametinib. trametinib 121-131 BCL2 like 11 Homo sapiens 0-3 32424251-6 2020 Based on these arguments, we evaluated the effects of Naftopidil on ovarian carcinoma and showed that Naftopidil reduced cell growth and increased the expression of the BH3-only proteins Bim, Puma and Noxa. naftopidil 102-112 BCL2 like 11 Homo sapiens 187-190 32239624-0 2020 Aspirin sensitizes osimertinib-resistant NSCLC cells in vitro and in vivo via Bim-dependent apoptosis induction. Aspirin 0-7 BCL2 like 11 Homo sapiens 78-81 32239624-0 2020 Aspirin sensitizes osimertinib-resistant NSCLC cells in vitro and in vivo via Bim-dependent apoptosis induction. osimertinib 19-30 BCL2 like 11 Homo sapiens 78-81 31972357-12 2020 Furthermore, oleandrin treatment increased expression of Bax and Bim but decreased that of Bcl-2. oleandrin 13-22 BCL2 like 11 Homo sapiens 65-68 31812766-5 2020 Moreover, formaldehyde significantly potentiated the induction of death receptor-5, caspase 8/10, cleaved caspase 3/7/9, pro-apoptotic proteins (Bim, Bad and Bax), depolarization of MMP (mitochondrial membrane potential) and AIF (apoptosis-inducing factor) induced by acrolein, and synergistically decreased expressions of pro-survival proteins (Bcl-2 and Bcl-XL) and poly ADP-ribose polymerase. Formaldehyde 10-22 BCL2 like 11 Homo sapiens 145-148 32256723-10 2020 Additionally, downregulation of miR-24-3p increased the levels of Bcl-2L11, caspase-3 and Bax, and decreased Bcl-2 expression in VSMCs; these changes were abolished by Bcl-2L11-siRNA. mir-24-3p 32-41 BCL2 like 11 Homo sapiens 66-74 32256723-10 2020 Additionally, downregulation of miR-24-3p increased the levels of Bcl-2L11, caspase-3 and Bax, and decreased Bcl-2 expression in VSMCs; these changes were abolished by Bcl-2L11-siRNA. mir-24-3p 32-41 BCL2 like 11 Homo sapiens 168-176 32256723-11 2020 In conclusion, the aforementioned results indicated that miR-24-3p was an important regulator in VSMC proliferation and apoptosis by targeting Bcl-2L11, which suggested that miR-24-3p might be a potential therapeutic target for the treatment of CHD. mir-24-3p 57-66 BCL2 like 11 Homo sapiens 143-151 32256723-11 2020 In conclusion, the aforementioned results indicated that miR-24-3p was an important regulator in VSMC proliferation and apoptosis by targeting Bcl-2L11, which suggested that miR-24-3p might be a potential therapeutic target for the treatment of CHD. mir-24-3p 174-183 BCL2 like 11 Homo sapiens 143-151 32075913-5 2020 Here we demonstrate that DOX exposure induces CDK2-dependent phosphorylation of the transcription factor forkhead box O1 (FOXO1) at Ser-249, leading to transcription of its proapoptotic target gene, Bcl-2-interacting mediator of cell death (Bim). Doxorubicin 25-28 BCL2 like 11 Homo sapiens 199-239 32075913-5 2020 Here we demonstrate that DOX exposure induces CDK2-dependent phosphorylation of the transcription factor forkhead box O1 (FOXO1) at Ser-249, leading to transcription of its proapoptotic target gene, Bcl-2-interacting mediator of cell death (Bim). Doxorubicin 25-28 BCL2 like 11 Homo sapiens 241-244 32075913-5 2020 Here we demonstrate that DOX exposure induces CDK2-dependent phosphorylation of the transcription factor forkhead box O1 (FOXO1) at Ser-249, leading to transcription of its proapoptotic target gene, Bcl-2-interacting mediator of cell death (Bim). Serine 132-135 BCL2 like 11 Homo sapiens 199-239 32075913-5 2020 Here we demonstrate that DOX exposure induces CDK2-dependent phosphorylation of the transcription factor forkhead box O1 (FOXO1) at Ser-249, leading to transcription of its proapoptotic target gene, Bcl-2-interacting mediator of cell death (Bim). Serine 132-135 BCL2 like 11 Homo sapiens 241-244 31976859-0 2020 The carboxyl-terminal sequence of bim enables bax activation and killing of unprimed cells. carboxyl radical 4-12 BCL2 like 11 Homo sapiens 34-37 32210727-5 2020 Results: In ER-/PR-/HER2- breast cancer, CHK1 inhibition enhanced adriamycin (ADR) chemosensitivity which was mediated by the mitotic checkpoint complex (MCC)-anaphase-promoting complex/cyclosome (APC/C)-cyclin B1 axis, Msh homeobox 2 (MSX2) and Bcl-2-like protein 11 (BIM). Doxorubicin 66-76 BCL2 like 11 Homo sapiens 246-267 31976859-2 2020 Bim binds to these proteins via its BH3 domain and to the mitochondrial membrane by a carboxyl-terminal sequence (CTS). carboxyl radical 86-94 BCL2 like 11 Homo sapiens 0-3 31408950-3 2019 This study has incorporated the potent BH3 alpha-helical death domain of BIM into peptide amphiphile (PA) nanostructures designed to facilitate cellular uptake and induce cell death. BH 3 39-42 BCL2 like 11 Homo sapiens 73-76 30819918-5 2019 CUDC-907-induced apoptosis was partially dependent on Mcl-1, Bim, and c-Myc. CUDC-907 0-8 BCL2 like 11 Homo sapiens 61-64 33148913-3 2020 Here, we investigated whether resminostat, a histone deacetylase inhibitor, circumvents BIM-del-associated apoptosis resistance. circumvents 76-87 BCL2 like 11 Homo sapiens 88-91 31608224-1 2019 Patients" clinical factors and genetics factors such as anaplastic lymphoma kinase (ALK) fusion variants and BIM (Bcl-2-like 11) polymorphism were reported to be associated with clinical outcome in crizotinib-treated advanced non-small cell lung cancer (NSCLC). Crizotinib 198-208 BCL2 like 11 Homo sapiens 114-127 31001849-0 2019 Overexpression miR-24-3p repressed Bim expression to confer tamoxifen resistance in breast cancer. Tamoxifen 60-69 BCL2 like 11 Homo sapiens 35-38 30793308-0 2019 Resistance to bortezomib in breast cancer cells that downregulate Bim through FOXA1 O-GlcNAcylation. Bortezomib 14-24 BCL2 like 11 Homo sapiens 66-69 30793308-9 2019 Our results have revealed a new regulatory mechanism that involves O-GlcNAc elevation mediated Bim deficiency, which plays a key role in the apoptotic dysregulation and BTZ resistance in breast cancer cells. Bortezomib 169-172 BCL2 like 11 Homo sapiens 95-98 31001849-8 2019 Silencing of Bim expression blocked miR-24-3p inhibitor-induced elevation of tamoxifen sensitivity of MCF7/TAM cells. Tamoxifen 77-86 BCL2 like 11 Homo sapiens 13-16 31001849-6 2019 In our established tamoxifen resistant MCF7 cell line (MCF7/TAM), there was a significant elevation of miR-24-3p and decrease of BIM expression compared with parental MCF7 cells. Tamoxifen 19-28 BCL2 like 11 Homo sapiens 129-132 31001849-8 2019 Silencing of Bim expression blocked miR-24-3p inhibitor-induced elevation of tamoxifen sensitivity of MCF7/TAM cells. mir-24-3p 36-45 BCL2 like 11 Homo sapiens 13-16 31001849-8 2019 Silencing of Bim expression blocked miR-24-3p inhibitor-induced elevation of tamoxifen sensitivity of MCF7/TAM cells. Tamoxifen 107-110 BCL2 like 11 Homo sapiens 13-16 31332289-6 2019 Treatment of either a proteasome inhibitor MG132 or bortezomib, or with a p-ERK/MEK inhibitor U0126 attenuate the SOX7 promoted BIM degradation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 43-48 BCL2 like 11 Homo sapiens 128-131 31332289-6 2019 Treatment of either a proteasome inhibitor MG132 or bortezomib, or with a p-ERK/MEK inhibitor U0126 attenuate the SOX7 promoted BIM degradation. Bortezomib 52-62 BCL2 like 11 Homo sapiens 128-131 31332289-6 2019 Treatment of either a proteasome inhibitor MG132 or bortezomib, or with a p-ERK/MEK inhibitor U0126 attenuate the SOX7 promoted BIM degradation. U 0126 94-99 BCL2 like 11 Homo sapiens 128-131 31463128-2 2019 Bcl-2-like 11 (BIM) is involved in the generation of ROS via forkhead box O3 (FOXO3), and a BIM deletion polymorphism related to apoptosis has been reported to be specific to Asians. Reactive Oxygen Species 53-56 BCL2 like 11 Homo sapiens 0-13 30787174-0 2019 Genipin Enhances the Therapeutic Effects of Oxaliplatin by Upregulating BIM in Colorectal Cancer. genipin 0-7 BCL2 like 11 Homo sapiens 72-75 31056264-5 2019 We further showed that Irinotecan increased the amount of p53 only in the presence of MDM2 and inhibited the physical interaction of Bcl-xL with Bim, a core pro-apoptotic protein. Irinotecan 23-33 BCL2 like 11 Homo sapiens 145-148 30841958-9 2019 Since Bim and Noxa act as key proapoptotic proteins in mitochondrial apoptosis, miR-374a inhibitor was able to enhance the etoposide-induced apoptosis pathway in glioma. Etoposide 123-132 BCL2 like 11 Homo sapiens 6-9 30954776-5 2019 Interestingly, simultaneous BIM knockdown in RCC cells partially rescues growth suppression triggered by depletion of SAG, but not ROC1, suggesting a differential role of BIM. sagopilone 118-121 BCL2 like 11 Homo sapiens 28-31 30784282-0 2019 Ambra1 inhibits paclitaxel-induced apoptosis in breast cancer cells by modulating the Bim/mitochondrial pathway. Paclitaxel 16-26 BCL2 like 11 Homo sapiens 86-89 30753811-0 2019 Piperlongumine-induced nuclear translocation of the FOXO3A transcription factor triggers BIM-mediated apoptosis in cancer cells. piperlonguminine 0-14 BCL2 like 11 Homo sapiens 89-92 30753811-4 2019 We report here that an association of FOXO3A with the pro-apoptotic protein BIM (also known as BCL2-like 11, BCL2L11) has a direct and specific function in PL-induced cancer cell death. piperlonguminine 156-158 BCL2 like 11 Homo sapiens 76-79 30753811-4 2019 We report here that an association of FOXO3A with the pro-apoptotic protein BIM (also known as BCL2-like 11, BCL2L11) has a direct and specific function in PL-induced cancer cell death. piperlonguminine 156-158 BCL2 like 11 Homo sapiens 95-107 30753811-4 2019 We report here that an association of FOXO3A with the pro-apoptotic protein BIM (also known as BCL2-like 11, BCL2L11) has a direct and specific function in PL-induced cancer cell death. piperlonguminine 156-158 BCL2 like 11 Homo sapiens 109-116 30753811-5 2019 Using HeLa cells stably expressing a FOXO3A-GFP fusion protein and several other cancer cell lines, we found that PL treatment induces FOXO3A dephosphorylation and nuclear translocation and promotes its binding to the BIM gene promoter, resulting in the up-regulation of BIM in the cancer cell lines. piperlonguminine 114-116 BCL2 like 11 Homo sapiens 218-221 30753811-5 2019 Using HeLa cells stably expressing a FOXO3A-GFP fusion protein and several other cancer cell lines, we found that PL treatment induces FOXO3A dephosphorylation and nuclear translocation and promotes its binding to the BIM gene promoter, resulting in the up-regulation of BIM in the cancer cell lines. piperlonguminine 114-116 BCL2 like 11 Homo sapiens 271-274 30753811-8 2019 In vivo, the PL treatment markedly inhibited xenograft tumor growth, and this inhibition was accompanied by the activation of the FOXO3A-BIM axis. piperlonguminine 13-15 BCL2 like 11 Homo sapiens 137-140 30753811-10 2019 In summary, our findings indicate that PL activates the FOXO3A-BIM apoptotic axis by promoting dephosphorylation and nuclear translocation of FOXO3A via Akt signaling inhibition. piperlonguminine 39-41 BCL2 like 11 Homo sapiens 63-66 31182924-0 2019 miR-30e-5p Mitigates Hypoxia-Induced Apoptosis in Human Stem Cell-Derived Cardiomyocytes by Suppressing Bim. mir-30e-5p 0-10 BCL2 like 11 Homo sapiens 104-107 31182924-9 2019 The luciferase reporter assay showed that miR-30e-5p can directly target the 3"-UTR of Bim, which is an apoptosis activator and autophagy suppressor. mir-30e-5p 42-52 BCL2 like 11 Homo sapiens 87-90 30896891-2 2019 In this study, the anti-infective drug nitroxoline (NXQ) was screened out to effectively inhibit cell survival of small-cell lung cancer (SCLC) cells, and induce SCLC cell apoptosis by suppressing antiapoptotic proteins (such as Bcl-2 and MCL1) and upregulating proapoptotic protein Bim. nitroxoline 39-50 BCL2 like 11 Homo sapiens 283-286 30896891-2 2019 In this study, the anti-infective drug nitroxoline (NXQ) was screened out to effectively inhibit cell survival of small-cell lung cancer (SCLC) cells, and induce SCLC cell apoptosis by suppressing antiapoptotic proteins (such as Bcl-2 and MCL1) and upregulating proapoptotic protein Bim. 2-[5-fluoranyl-2-[[3-[methyl(oxidanyl)-$l^{3}-sulfanyl]phenyl]methylcarbamoyl]phenoxy]ethanoic acid 52-55 BCL2 like 11 Homo sapiens 283-286 30787174-0 2019 Genipin Enhances the Therapeutic Effects of Oxaliplatin by Upregulating BIM in Colorectal Cancer. Oxaliplatin 44-55 BCL2 like 11 Homo sapiens 72-75 30787174-5 2019 Our study showed that a combination of genipin and oxaliplatin exerts synergistic antitumor effects in vitro and in vivo in colorectal cancer cell lines through the reactive oxygen species (ROS)/endoplasmic reticulum (ER) stress/BIM pathway. genipin 39-46 BCL2 like 11 Homo sapiens 229-232 30787174-5 2019 Our study showed that a combination of genipin and oxaliplatin exerts synergistic antitumor effects in vitro and in vivo in colorectal cancer cell lines through the reactive oxygen species (ROS)/endoplasmic reticulum (ER) stress/BIM pathway. Oxaliplatin 51-62 BCL2 like 11 Homo sapiens 229-232 30679390-5 2019 Proteomic analyses of adaptive responses to GDC-0973 revealed that GDC-0973 upregulated the proapoptotic protein BIM, thus priming the cells for apoptosis regulated by BCL2-family proteins. cobimetinib 44-52 BCL2 like 11 Homo sapiens 113-116 30929387-10 2019 When combination of the two drugs on MV4-11 after 24 hours, the levels of pro-apoptotic protein Bim and the cleaved activation of Caspase-3 and autophagy-related protein LC3B were up-regulated and the anti-apoptotic protein Bcl-2 expressions was down-regulated. mv4-11 37-43 BCL2 like 11 Homo sapiens 96-99 30860026-0 2019 Bim escapes displacement by BH3-mimetic anti-cancer drugs by double-bolt locking both Bcl-XL and Bcl-2. BH 3 28-31 BCL2 like 11 Homo sapiens 0-3 30860026-4 2019 Using automated Fluorescence Lifetime Imaging Microscopy - Fluorescence Resonance Energy Transfer (FLIM-FRET) we show that the two binding interfaces enable Bim to double-bolt lock Bcl-XL and Bcl-2 in complexes resistant to displacement by BH3-mimetic drugs currently in use or being evaluated for cancer therapy. BH 3 240-243 BCL2 like 11 Homo sapiens 157-160 30860026-5 2019 Quantifying in live cells the contributions of individual amino acids revealed that residue L185 previously thought involved in binding Bim to membranes, instead contributes to binding to anti-apoptotic proteins. 2-Amino-5-methoxybenzoic acid 92-96 BCL2 like 11 Homo sapiens 136-139 30845397-11 2019 The expression of pro-apoptotic protein BIM in H1975-OR was significantly higher in 2-deoxyglucose+ osimertinib combination therapy group (177.8+-28.1)% and the expression of anti-apoptotic protein Bcl-2 in H1975-OR was significantly lower in 2-deoxyglucose+ osimertinib combination therapy group (24.6+-5.2)%, compared to control group (100+-0)%, all P<0.05. Deoxyglucose 84-98 BCL2 like 11 Homo sapiens 40-43 30845397-11 2019 The expression of pro-apoptotic protein BIM in H1975-OR was significantly higher in 2-deoxyglucose+ osimertinib combination therapy group (177.8+-28.1)% and the expression of anti-apoptotic protein Bcl-2 in H1975-OR was significantly lower in 2-deoxyglucose+ osimertinib combination therapy group (24.6+-5.2)%, compared to control group (100+-0)%, all P<0.05. osimertinib 100-111 BCL2 like 11 Homo sapiens 40-43 30845397-11 2019 The expression of pro-apoptotic protein BIM in H1975-OR was significantly higher in 2-deoxyglucose+ osimertinib combination therapy group (177.8+-28.1)% and the expression of anti-apoptotic protein Bcl-2 in H1975-OR was significantly lower in 2-deoxyglucose+ osimertinib combination therapy group (24.6+-5.2)%, compared to control group (100+-0)%, all P<0.05. Deoxyglucose 243-257 BCL2 like 11 Homo sapiens 40-43 30845397-11 2019 The expression of pro-apoptotic protein BIM in H1975-OR was significantly higher in 2-deoxyglucose+ osimertinib combination therapy group (177.8+-28.1)% and the expression of anti-apoptotic protein Bcl-2 in H1975-OR was significantly lower in 2-deoxyglucose+ osimertinib combination therapy group (24.6+-5.2)%, compared to control group (100+-0)%, all P<0.05. osimertinib 259-270 BCL2 like 11 Homo sapiens 40-43 30850026-13 2019 The expression of Bim increased at protein level after DMAMCL treatment both in vitro and in vivo. dimethylaminomicheliolide 55-61 BCL2 like 11 Homo sapiens 18-21 30850026-15 2019 Transfection of Bim siRNA into RMS cells blocked the DMAMCL-induced increase of Bim and partially attenuated the DMAMCL-induced cell death. dimethylaminomicheliolide 53-59 BCL2 like 11 Homo sapiens 16-19 30850026-15 2019 Transfection of Bim siRNA into RMS cells blocked the DMAMCL-induced increase of Bim and partially attenuated the DMAMCL-induced cell death. dimethylaminomicheliolide 53-59 BCL2 like 11 Homo sapiens 80-83 30850026-15 2019 Transfection of Bim siRNA into RMS cells blocked the DMAMCL-induced increase of Bim and partially attenuated the DMAMCL-induced cell death. dimethylaminomicheliolide 113-119 BCL2 like 11 Homo sapiens 16-19 30850026-16 2019 CONCLUSION: DMAMCL had an anti-tumor growth effect in vitro and in vivo that potentially mediated by Bim, NF-kappaB pathway and ROS. dimethylaminomicheliolide 12-18 BCL2 like 11 Homo sapiens 101-104 30679390-5 2019 Proteomic analyses of adaptive responses to GDC-0973 revealed that GDC-0973 upregulated the proapoptotic protein BIM, thus priming the cells for apoptosis regulated by BCL2-family proteins. cobimetinib 67-75 BCL2 like 11 Homo sapiens 113-116 30501963-0 2019 BH3 mimetics derived from Bim-BH3 domain core region show PTP1B inhibitory activity. BH 3 30-33 BCL2 like 11 Homo sapiens 26-29 31031856-7 2019 In both RCC cell lines, everolimus-ABT-737 combination not only induced apoptosis, caspase and PARP-1 cleavage but also a decrease in Bcl-2 protein levels in parallel with a concomitant increase in Bim and Noxa levels. Everolimus 24-34 BCL2 like 11 Homo sapiens 198-201 31031856-7 2019 In both RCC cell lines, everolimus-ABT-737 combination not only induced apoptosis, caspase and PARP-1 cleavage but also a decrease in Bcl-2 protein levels in parallel with a concomitant increase in Bim and Noxa levels. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 35-38 BCL2 like 11 Homo sapiens 198-201 30389710-11 2019 In contrast, TRIM59 overexpression could increase cell proliferation, up-regulate Survivin, beta-catenin and c-myc, down-regulate Bax and Bim, and these effects could be blocked by XAV939, which is an inhibitor of Wnt/beta-catenin signaling pathway. XAV939 181-187 BCL2 like 11 Homo sapiens 138-141 30501963-0 2019 BH3 mimetics derived from Bim-BH3 domain core region show PTP1B inhibitory activity. BH 3 0-3 BCL2 like 11 Homo sapiens 26-29 30501963-1 2019 A series of our previously described BH3 peptide mimetics derived from Bim-BH3 domain core region were found to exhibit weak to potent PTP1B binding affinity and inhibitory activities via target-based drug screening. BH 3 37-40 BCL2 like 11 Homo sapiens 71-74 30501963-2 2019 Among these compounds, a 12-aa Bim-BH3 core sequence peptide conjugated to palmitic acid (SM-6) displayed good PTP1B binding affinity (KD = 8.38 nmol/L), inhibitory activity (IC50 = 1.20 mumol/L) and selectivity against other PTPs (TCPTP, LAR, SHP-1 and SHP-2). Palmitic Acid 75-88 BCL2 like 11 Homo sapiens 31-34 30501963-2 2019 Among these compounds, a 12-aa Bim-BH3 core sequence peptide conjugated to palmitic acid (SM-6) displayed good PTP1B binding affinity (KD = 8.38 nmol/L), inhibitory activity (IC50 = 1.20 mumol/L) and selectivity against other PTPs (TCPTP, LAR, SHP-1 and SHP-2). sm-6 90-94 BCL2 like 11 Homo sapiens 31-34 30614795-0 2019 The ratio of Bcl-2/Bim as a predictor of cisplatin response provides a rational combination of ABT-263 with cisplatin or radiation in small cell lung cancer. Cisplatin 41-50 BCL2 like 11 Homo sapiens 19-22 30614795-0 2019 The ratio of Bcl-2/Bim as a predictor of cisplatin response provides a rational combination of ABT-263 with cisplatin or radiation in small cell lung cancer. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 95-98 BCL2 like 11 Homo sapiens 19-22 30614795-0 2019 The ratio of Bcl-2/Bim as a predictor of cisplatin response provides a rational combination of ABT-263 with cisplatin or radiation in small cell lung cancer. Cisplatin 108-117 BCL2 like 11 Homo sapiens 19-22 30614795-5 2019 RESULTS: The IC50 value of cisplatin was significantly correlated with the ratio of Bcl-2/Bim mRNA expression in 33 SCLC cell lines (P= 0.041) as well as the ratio of Bcl-2/Bim protein expression in 7 SCLC cell lines (P= 0.0252). Cisplatin 27-36 BCL2 like 11 Homo sapiens 90-93 30614795-5 2019 RESULTS: The IC50 value of cisplatin was significantly correlated with the ratio of Bcl-2/Bim mRNA expression in 33 SCLC cell lines (P= 0.041) as well as the ratio of Bcl-2/Bim protein expression in 7 SCLC cell lines (P= 0.0252). Cisplatin 27-36 BCL2 like 11 Homo sapiens 173-176 30614795-7 2019 The synergistic and additive antitumor activity of ABT-263 combined with cisplatin or radiation was associated with the enhanced apoptosis, which may be caused by the disruption of Bcl-2 binding to Bim by ABT-263. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 51-54 BCL2 like 11 Homo sapiens 198-201 30614795-7 2019 The synergistic and additive antitumor activity of ABT-263 combined with cisplatin or radiation was associated with the enhanced apoptosis, which may be caused by the disruption of Bcl-2 binding to Bim by ABT-263. Cisplatin 73-82 BCL2 like 11 Homo sapiens 198-201 30614795-7 2019 The synergistic and additive antitumor activity of ABT-263 combined with cisplatin or radiation was associated with the enhanced apoptosis, which may be caused by the disruption of Bcl-2 binding to Bim by ABT-263. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 205-208 BCL2 like 11 Homo sapiens 198-201 30614795-8 2019 CONCLUSIONS: Our study indicates that the ratio of Bcl-2/Bim could be a SCLC response predictor to cisplatin, and ABT-263 addition could be an effective strategy to improve the activity of chemo- or radio-therapy in SCLC. Cisplatin 99-108 BCL2 like 11 Homo sapiens 57-60 29916288-0 2019 BIM deletion polymorphism profiling complements prognostic values of risk scores in imatinib-treated Asian chronic myeloid leukemia patients. Imatinib Mesylate 84-92 BCL2 like 11 Homo sapiens 0-3 30598523-4 2019 Use of aforementioned pathway inhibitors blocked FoxO3a-phosphorylation and partially improved DEX-mediated killing of GC-resistant T-ALL cells, further revealing the essential role of the FoxO3a/Bim pathway in the development of GC resistance. Dexamethasone 95-98 BCL2 like 11 Homo sapiens 196-199 30426809-6 2019 PCN triggered the activation of Bim, Bid, Bik, Bak, and phospho-Bad in NK92 cells in a concentration-dependent manner, but these pro-apoptotic Bcl-2 family proteins were not inhibited by EGTA. Pyocyanine 0-3 BCL2 like 11 Homo sapiens 32-35 30353128-6 2019 The combination of ERK1/2, Akt, and NF-kappaB inhibitors with melphalan reversed melphalan resistance via suppression of Survivin expression and enhanced Bim expression in melphalan-resistant cells. Melphalan 62-71 BCL2 like 11 Homo sapiens 154-157 30598523-2 2019 Here, we found T-acute lymphoblastic leukemia (T-ALL) cells acquire resistance to dexamethasone (DEX)-mediated killing through abnormal activation of Akt, resulting in inhibition of the FoxO3a/Bim pathway. Dexamethasone 82-95 BCL2 like 11 Homo sapiens 193-196 30598523-2 2019 Here, we found T-acute lymphoblastic leukemia (T-ALL) cells acquire resistance to dexamethasone (DEX)-mediated killing through abnormal activation of Akt, resulting in inhibition of the FoxO3a/Bim pathway. Dexamethasone 97-100 BCL2 like 11 Homo sapiens 193-196 30226552-6 2018 In vitro assays also revealed that knockdown of HuR resulted in primary EGFR-TKI resistance and reduced gefitinib-induced apoptosis in HCC827 cells by decreasing Bim expression. Gefitinib 104-113 BCL2 like 11 Homo sapiens 162-165 30596398-7 2018 However, binding of Bim to Mcl-1 induced by ABT-199 was abrogated by KPT-330 at the same time as apoptosis initiation. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 44-47 BCL2 like 11 Homo sapiens 20-23 30596398-7 2018 However, binding of Bim to Mcl-1 induced by ABT-199 was abrogated by KPT-330 at the same time as apoptosis initiation. selinexor 69-76 BCL2 like 11 Homo sapiens 20-23 30596398-8 2018 KPT-330 treatment increased binding of Bcl-2 to Bim but was overcome by ABT-199 treatment, demonstrating that KPT-330 and ABT-199 reciprocally overcome apoptosis resistance. coptisine 0-3 BCL2 like 11 Homo sapiens 48-51 30195041-7 2018 Alpha-mangostin significantly sensitized anoikis in HepG2 through the inhibition of cell survival by induced caspase-9, caspase-8 and caspase-3 activities, increased pro-apoptotic protein (Bax, Bim, t-Bid) levels, and decreased anti-apoptotic protein (c-FLIP, Mcl-1) levels. mangostin 0-15 BCL2 like 11 Homo sapiens 194-197 30257366-10 2018 The real time PCR assay demonstrated that parthenolide down-regulated the expression of Bcl-2 and up-regulated the expression of E2F1, P53, GADD45, BAX, BIM, and CASP 3,7,8,9, which indicates an activation of P53- dependent apoptosis pathway in response to parthenolide. parthenolide 42-54 BCL2 like 11 Homo sapiens 153-156 30226552-7 2018 Furthermore, elevated HuR expression restored gefitinib sensitivity and enhanced gefitinib-induced apoptosis in H1650 cells by increasing Bim expression. Gefitinib 81-90 BCL2 like 11 Homo sapiens 138-141 30249504-12 2018 Overexpression of miR-23 decreased the levels of BCL2L11 and caspase-3, and downregulate of miR-23 increased the levels of BCL2L11and caspase-3 in VSMCs. mir-23 18-24 BCL2 like 11 Homo sapiens 49-56 30249504-12 2018 Overexpression of miR-23 decreased the levels of BCL2L11 and caspase-3, and downregulate of miR-23 increased the levels of BCL2L11and caspase-3 in VSMCs. mir-23 92-98 BCL2 like 11 Homo sapiens 123-130 30249504-13 2018 CONCLUSION: Our findings suggest that miR-23 plays a crucial role in controlling VSMCs proliferation and apoptosis by targeting BCL2L11. mir-23 38-44 BCL2 like 11 Homo sapiens 128-135 30249871-4 2018 TSA-induced caspase-dependent or -independent apoptosis according to cell types, TSA enhanced the expression levels of Bim protein by dephosphorylating ERK1/2 pathway in HSC-3 cells. trichostatin A 0-3 BCL2 like 11 Homo sapiens 119-122 30233720-8 2018 In addition, propofol treatment significantly increased the levels of forkhead box (FOX)O1, FOXO3, Bim, pro-caspase-3, active caspase-3, p53 and p21. Propofol 13-21 BCL2 like 11 Homo sapiens 99-102 30224718-0 2018 Idelalisib promotes Bim-dependent apoptosis through AKT/FoxO3a in hepatocellular carcinoma. idelalisib 0-10 BCL2 like 11 Homo sapiens 20-23 30224718-4 2018 Our results show that idelalisib treatment promotes Bim induction in HCC via the FoxO3a pathway following PI3K/AKT inactivation. idelalisib 22-32 BCL2 like 11 Homo sapiens 52-55 30224718-5 2018 Moreover, our results show that Bim is required for idelalisib-mediated apoptosis in HCC. idelalisib 52-62 BCL2 like 11 Homo sapiens 32-35 30224718-7 2018 Furthermore, a xenograft experiment reveals that the Bim deficiency abolishes apoptosis and antitumor effects of idelalisib in vivo. idelalisib 113-123 BCL2 like 11 Homo sapiens 53-56 30224718-8 2018 In summary, our results indicate a key role of Bim in mediating the antitumor effects of idelalisib in HCC. idelalisib 89-99 BCL2 like 11 Homo sapiens 47-50 30249871-4 2018 TSA-induced caspase-dependent or -independent apoptosis according to cell types, TSA enhanced the expression levels of Bim protein by dephosphorylating ERK1/2 pathway in HSC-3 cells. trichostatin A 81-84 BCL2 like 11 Homo sapiens 119-122 29767411-6 2018 Furthermore, binimetinib significantly increased the sensitivity of CLL cells co-cultured with CD40 ligand (CD40L)-expressing fibroblasts to the BH3-mimetics ABT-737 and Venetoclax (ABT-199) via a mechanism involving down-regulation of Mcl-1 (MCL1) activity and Bim (BCL2L11) and Bcl-xL (BCL2L1) expression. binimetinib 13-24 BCL2 like 11 Homo sapiens 262-265 29767411-6 2018 Furthermore, binimetinib significantly increased the sensitivity of CLL cells co-cultured with CD40 ligand (CD40L)-expressing fibroblasts to the BH3-mimetics ABT-737 and Venetoclax (ABT-199) via a mechanism involving down-regulation of Mcl-1 (MCL1) activity and Bim (BCL2L11) and Bcl-xL (BCL2L1) expression. binimetinib 13-24 BCL2 like 11 Homo sapiens 267-274 29749500-8 2018 Mechanistic analysis revealed that Vacq upregulated the expressions of pro-apoptotic proteins [B-cell lymphoma 2 (bcl-2)-associated X protein (Bax) and Bcl-2-like protein 11] and downregulated the pro-survival protein, Bcl-2, expression in HCC cells. vacquinol-1 35-39 BCL2 like 11 Homo sapiens 152-173 29907952-3 2018 The B-cell lymphoma 2 (BCL-2)-like 11 (BIM) deletion polymorphism, which occurs at a frequency of 21% in East Asians but is absent in African and European populations, has been associated with resistance to first-generation EGFR TKIs, such as gefitinib and erlotinib; and is a poor prognostic factor for NSCLC patients with EGFR mutations. Gefitinib 243-252 BCL2 like 11 Homo sapiens 23-37 29907952-3 2018 The B-cell lymphoma 2 (BCL-2)-like 11 (BIM) deletion polymorphism, which occurs at a frequency of 21% in East Asians but is absent in African and European populations, has been associated with resistance to first-generation EGFR TKIs, such as gefitinib and erlotinib; and is a poor prognostic factor for NSCLC patients with EGFR mutations. Erlotinib Hydrochloride 257-266 BCL2 like 11 Homo sapiens 23-37 29901174-9 2018 Furthermore, Bim and p21 were upregulated in OS cells following apcin treatment. apcin 64-69 BCL2 like 11 Homo sapiens 13-16 29899957-8 2018 Moreover, the use of platelet-permeable stapled Bim BH3 peptides confirms the part of Bim in phosphatidyl-serine (PS) exposure and reveals a role for the Bim protein in platelet activatory processes. Phosphatidylserines 93-112 BCL2 like 11 Homo sapiens 48-51 29795285-5 2018 OX40 promoted the survival of cDNT by regulating the expression of Bcl-2, Bcl-xL, Survivin, and BCL2L11. 4-CHLORO-3,5-DINITROBENZOTRIFLUORIDE 30-34 BCL2 like 11 Homo sapiens 96-103 28826228-3 2018 RESULTS: Culturing islets in CO-saturated medium protected them from hypoxia-induced apoptosis and preserved beta cell function by suppressing expression of proapoptotic (Bim, PARP, Cas-3), proinflammatory (TNF-alpha), and endoplasmic reticulum (ER) stress (glucose-regulated protein 94, grp94, CHOP) proteins. co-saturated medium 29-48 BCL2 like 11 Homo sapiens 171-174 29057477-5 2018 Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP). Melphalan 74-83 BCL2 like 11 Homo sapiens 292-295 29057477-5 2018 Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP). Bortezomib 87-97 BCL2 like 11 Homo sapiens 292-295 29899957-8 2018 Moreover, the use of platelet-permeable stapled Bim BH3 peptides confirms the part of Bim in phosphatidyl-serine (PS) exposure and reveals a role for the Bim protein in platelet activatory processes. Phosphatidylserines 93-112 BCL2 like 11 Homo sapiens 86-89 29899957-8 2018 Moreover, the use of platelet-permeable stapled Bim BH3 peptides confirms the part of Bim in phosphatidyl-serine (PS) exposure and reveals a role for the Bim protein in platelet activatory processes. Phosphatidylserines 93-112 BCL2 like 11 Homo sapiens 86-89 29899957-8 2018 Moreover, the use of platelet-permeable stapled Bim BH3 peptides confirms the part of Bim in phosphatidyl-serine (PS) exposure and reveals a role for the Bim protein in platelet activatory processes. Phosphatidylserines 114-116 BCL2 like 11 Homo sapiens 86-89 29899957-8 2018 Moreover, the use of platelet-permeable stapled Bim BH3 peptides confirms the part of Bim in phosphatidyl-serine (PS) exposure and reveals a role for the Bim protein in platelet activatory processes. Phosphatidylserines 114-116 BCL2 like 11 Homo sapiens 86-89 29391601-1 2018 Phosphorylation of Ser/Thr residues is a well-established modulating mechanism of the pro-apoptotic function of the BH3-only protein Bim. Serine 19-22 BCL2 like 11 Homo sapiens 133-136 29584430-6 2018 One bicyclic peptide was shown to inhibit the interaction between a pro-apoptotic protein (Bim) and either endogenous Bcl2A1 or Mcl-1, to induce apoptosis of SKMel28 human melanoma cells, and to sensitize them for enhanced cell death by the anticancer drug etoposide. Etoposide 257-266 BCL2 like 11 Homo sapiens 91-94 29534961-0 2018 Z-FL-COCHO, a cathepsin S inhibitor, enhances oxaliplatin-induced apoptosis through upregulation of Bim expression. Oxaliplatin 46-57 BCL2 like 11 Homo sapiens 100-103 29534961-2 2018 In present study, we revealed that pharmacological inhibitor [Z-FL-COCHO (ZFL)] of cathepsin S up-regulates pro-apoptotic protein Bim expression at the posttranslational levels. zfl 74-77 BCL2 like 11 Homo sapiens 130-133 29534961-4 2018 Interestingly, pretreatment with the chemical chaperones (TUDCA and PBA) and knockdown of protein phosphatase 2A (PP2A) markedly inhibited ZFL-induced Bim upregulation. zfl 139-142 BCL2 like 11 Homo sapiens 151-154 29534961-5 2018 ZFL enhances oxaliplatin-mediated apoptosis through ER stress-induced Bim upregulation in cancer cells. zfl 0-3 BCL2 like 11 Homo sapiens 70-73 29534961-5 2018 ZFL enhances oxaliplatin-mediated apoptosis through ER stress-induced Bim upregulation in cancer cells. Oxaliplatin 13-24 BCL2 like 11 Homo sapiens 70-73 29391601-5 2018 Mechanistically, we show that Lyn-dependent tyrosine phosphorylation of Bim increases its interaction with anti-apoptotic members such as Bcl-xL, therefore limiting mitochondrial outer membrane permeabilization and subsequent apoptosis. Tyrosine 44-52 BCL2 like 11 Homo sapiens 72-75 29391601-1 2018 Phosphorylation of Ser/Thr residues is a well-established modulating mechanism of the pro-apoptotic function of the BH3-only protein Bim. Threonine 23-26 BCL2 like 11 Homo sapiens 133-136 29391601-4 2018 In the present study, we show that Bim is phosphorylated onto tyrosine residues 92 and 161 by Lyn, which results in an inhibition of its pro-apoptotic function. Tyrosine 62-70 BCL2 like 11 Homo sapiens 35-38 29518944-7 2018 Tannic acid treatment affirmed upregulation of apoptosis-associated markers (Bak, Bim, cleaved caspase 3, and cleaved PARP), while downregulation of pro-survival proteins (Bcl-2 and Bcl-xL). Tannins 0-11 BCL2 like 11 Homo sapiens 82-85 29409480-9 2018 Verticillin A treatment decreased FLIP, Mcl-1, Bcl-x and increased Bak, Bax and Bim protein level in the tumor cells, resulting in activation of caspases, elevated cytochrome C release and increased apoptosis as determined by upregulated PARP cleavage in tumor cells. verticillins 0-13 BCL2 like 11 Homo sapiens 80-83 29196192-7 2018 Moreover, macrovipecetin alone or combined with cisplatin induced the expression of TRADD, p53, Bax, Bim and Bad and down-regulated the Bcl-2 expression and ROS levels in SK-MEL-28 cells. Cisplatin 48-57 BCL2 like 11 Homo sapiens 101-104 29456710-7 2018 In addition, goniothalamin decreased the level of anti-apoptotic proteins myeloid cell leukemia 1, B cell lymphoma (Bcl)-2 and Bcl-extra large, whereas it increased the level of pro-apoptotic proteins, Bcl-2 Associated X, apoptosis regulator, t-BID and Bim in A375 treated cells. goniothalamin 13-26 BCL2 like 11 Homo sapiens 253-256 29409480-11 2018 Verticillin A downregulated H3K4me3 levels at the BCL2L1, CFLAR and MCL-1 promoter to decrease Bcl-x, FLIP and Mcl-1 expression level, and inhibited H3K9me3 levels at the BAK1, BAX and BCL2L11 promoter to upregulate Bak, Bax and Bim expression level. verticillins 0-13 BCL2 like 11 Homo sapiens 185-192 29409480-11 2018 Verticillin A downregulated H3K4me3 levels at the BCL2L1, CFLAR and MCL-1 promoter to decrease Bcl-x, FLIP and Mcl-1 expression level, and inhibited H3K9me3 levels at the BAK1, BAX and BCL2L11 promoter to upregulate Bak, Bax and Bim expression level. verticillins 0-13 BCL2 like 11 Homo sapiens 229-232 29060932-0 2017 miR-34a increases cisplatin sensitivity of osteosarcoma cells in vitro through up-regulation of c-Myc and Bim signal. Cisplatin 18-27 BCL2 like 11 Homo sapiens 106-109 29054700-7 2018 In addition, rebamipide increased the levels of phosphorylated Akt and mTOR, enhanced the Bcl-2 and Bcl-xL expressions, and suppressed the expression of Bax and Bim. rebamipide 13-23 BCL2 like 11 Homo sapiens 161-164 29054700-8 2018 This is in contrast to 5-FU-induced suppression of Akt and mTOR activation, Bcl-2 and Bcl-xL expressions, and the enhanced expression of Bax and Bim. Fluorouracil 23-27 BCL2 like 11 Homo sapiens 145-148 29060932-7 2017 RESULTS: Treatment of U2OS cells with cisplatin induced cell apoptosis by upregulation of c-Myc -dependent Bim expression; Osteosarcoma U2OS cells transfected with miR-34a mimics (miR-34a/U2OS) induced cell apoptosis and inhibited cell survival, and increased the sensitivity of U2OS cells to cisplatin. Cisplatin 38-47 BCL2 like 11 Homo sapiens 107-110 28948407-3 2018 Moreover, 10-chlorocanthin-6-one induced apoptosis through the activation of poly(ADP-ribose) polymerase and caspase-3 cleavage, upregulation of Bcl-2, and downregulation of Bim, x-linked inhibitor of apoptosis protein (XIAP), and survivin in HO8910PM cells. 10-chlorocanthin-6-one 10-32 BCL2 like 11 Homo sapiens 174-177 28948407-4 2018 Furthermore, Bim RNA, upregulated in a concentration-dependent manner, and knockdown of Bim via short-hairpin RNAs attenuated the inhibitory effects of 10-chlorocanthin-6-one on HO8910PM cell growth. 10-chlorocanthin-6-one 152-174 BCL2 like 11 Homo sapiens 13-16 28948407-4 2018 Furthermore, Bim RNA, upregulated in a concentration-dependent manner, and knockdown of Bim via short-hairpin RNAs attenuated the inhibitory effects of 10-chlorocanthin-6-one on HO8910PM cell growth. 10-chlorocanthin-6-one 152-174 BCL2 like 11 Homo sapiens 88-91 28948407-6 2018 The underlying molecular mechanisms of 10-chlorocanthin-6-one include activation of the Bim-mediated mitochondrial apoptotic pathway via upregulation of Bim and downregulation of Bcl-2, XIAP, and survivin. 10-chlorocanthin-6-one 39-61 BCL2 like 11 Homo sapiens 88-91 28948407-6 2018 The underlying molecular mechanisms of 10-chlorocanthin-6-one include activation of the Bim-mediated mitochondrial apoptotic pathway via upregulation of Bim and downregulation of Bcl-2, XIAP, and survivin. 10-chlorocanthin-6-one 39-61 BCL2 like 11 Homo sapiens 153-156 28948407-7 2018 These data suggest that Bim is a potential target of 10-chlorocanthin-6-one, further demonstrating its potential use in the prevention and treatment of ovarian cancer. 10-chlorocanthin-6-one 53-75 BCL2 like 11 Homo sapiens 24-27 30198376-1 2018 We previously demonstrated that Bim is the main BH3-only protein replacing Bak/Bax from Bcl-xl to activate apoptosis in a p53-independent manner in response to doxorubicin in prostate cancer. Doxorubicin 160-171 BCL2 like 11 Homo sapiens 32-35 30071508-11 2018 Since Bim and Noxa act as key pro-apoptotic proteins in mitochondrial apoptosis, anti-miR-135b was able to enhance the oxaliplatin-induced apoptosis dependent on the anti-miR-135b/FOXO1 axis. Oxaliplatin 119-130 BCL2 like 11 Homo sapiens 6-9 28767174-8 2018 We found that UA inhibited collagen synthesis and induced cell apoptosis in HSFBs, evidenced by the deregulated expression of Bim, Bcl-2 and Cyto C. Furthermore, we demonstrated that UA induced autophagy and inactivation of autophagy promoted UA-induced apoptosis and collagen synthesis inhibition in HSFBs. ursolic acid 14-16 BCL2 like 11 Homo sapiens 126-129 28767174-8 2018 We found that UA inhibited collagen synthesis and induced cell apoptosis in HSFBs, evidenced by the deregulated expression of Bim, Bcl-2 and Cyto C. Furthermore, we demonstrated that UA induced autophagy and inactivation of autophagy promoted UA-induced apoptosis and collagen synthesis inhibition in HSFBs. ursolic acid 183-185 BCL2 like 11 Homo sapiens 126-129 28767174-8 2018 We found that UA inhibited collagen synthesis and induced cell apoptosis in HSFBs, evidenced by the deregulated expression of Bim, Bcl-2 and Cyto C. Furthermore, we demonstrated that UA induced autophagy and inactivation of autophagy promoted UA-induced apoptosis and collagen synthesis inhibition in HSFBs. ursolic acid 183-185 BCL2 like 11 Homo sapiens 126-129 29060932-10 2017 In addition, Targeting Bim reversed the chemeresistance of miR-34a/U2OS cells to cisplatin. Cisplatin 81-90 BCL2 like 11 Homo sapiens 23-26 29060932-11 2017 CONCLUSIONS: Our data indicated that miR-34a enhanced the sensitivity to cisplatin by upregulation of c-Myc and Bim pathway. Cisplatin 73-82 BCL2 like 11 Homo sapiens 112-115 29163689-5 2017 In addition, TCS7010 resulted in the production of reactive oxygen species (ROS) and stimulation of the unfolded protein response (UPR), leading to the upregulation of CCAAT/enhancer-binding protein-homologous protein (CHOP), and its downstream target BCL2 like 11 (BIM). Aurora A Inhibitor I 13-20 BCL2 like 11 Homo sapiens 252-264 29340082-2 2017 BH3 mimetics (e.g. ABT-199 (venetoclax)) kill cancer cells by targeting Bcl-2"s hydrophobic cleft and disrupting Bcl-2/Bim complexes. BH 3 0-3 BCL2 like 11 Homo sapiens 119-122 29340082-2 2017 BH3 mimetics (e.g. ABT-199 (venetoclax)) kill cancer cells by targeting Bcl-2"s hydrophobic cleft and disrupting Bcl-2/Bim complexes. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 19-22 BCL2 like 11 Homo sapiens 119-122 29163689-5 2017 In addition, TCS7010 resulted in the production of reactive oxygen species (ROS) and stimulation of the unfolded protein response (UPR), leading to the upregulation of CCAAT/enhancer-binding protein-homologous protein (CHOP), and its downstream target BCL2 like 11 (BIM). Aurora A Inhibitor I 13-20 BCL2 like 11 Homo sapiens 266-269 29163689-6 2017 Pretreatment with N-acetylcystein, a ROS scavenger, significantly abrogated TCS7010-induced accumulation of CHOP, BIM, cleaved caspase-7 and cleaved PARP. N-Acetyl-L-cysteine 18-33 BCL2 like 11 Homo sapiens 114-117 29254208-0 2017 VS-5584 mediates potent anti-myeloma activity via the upregulation of a class II tumor suppressor gene, RARRES3 and the activation of Bim. VS-5584 0-7 BCL2 like 11 Homo sapiens 134-137 29163689-6 2017 Pretreatment with N-acetylcystein, a ROS scavenger, significantly abrogated TCS7010-induced accumulation of CHOP, BIM, cleaved caspase-7 and cleaved PARP. Aurora A Inhibitor I 76-83 BCL2 like 11 Homo sapiens 114-117 29138498-6 2017 Increasing Grx1 reduces the pro-apoptotic protein Bim expression through regulating Akt-FoxO1 signaling and also attenuates H2O2-induced Bim activation via inhibiting JNK phosphorylation, subsequently preventing the apoptosis of endothelial cells. Hydrogen Peroxide 124-128 BCL2 like 11 Homo sapiens 137-140 28902352-7 2017 Knockdown Bim in TAM-sensitive MCF-7 cells or overexpression of Bim in TAM-resistant MCF-7 cells significantly changed its sensibility to TAM through altering the levels of cleaved PARP and caspase-3. Tamoxifen 71-74 BCL2 like 11 Homo sapiens 64-67 29053589-7 2017 CNP058 adopts the conserved Bcl-2 like fold observed in cellular pro-survival Bcl-2 proteins, and utilizes the canonical ligand binding groove to bind Bim BH3. BH 3 155-158 BCL2 like 11 Homo sapiens 151-154 29262554-6 2017 SCH772984 potentiates the cytotoxic effect of CuB on pancreatic cancer cells through complementary inhibition of EGFR, PI3K/Akt/mTOR, STAT3 and ERK signaling, followed by an increase in the pro-apoptotic protein Bim and a decrease in the anti-apoptotic proteins Mcl-1, Bcl-2, Bcl-xl and survivin. SCH772984 0-9 BCL2 like 11 Homo sapiens 212-215 28902352-0 2017 GPER promotes tamoxifen-resistance in ER+ breast cancer cells by reduced Bim proteins through MAPK/Erk-TRIM2 signaling axis. Tamoxifen 14-23 BCL2 like 11 Homo sapiens 73-76 28863346-0 2017 The Imipridone ONC201 Induces Apoptosis and Overcomes Chemotherapy Resistance by Up-Regulation of Bim in Multiple Myeloma. imipridone 4-14 BCL2 like 11 Homo sapiens 98-101 28931802-12 2017 Palmitate-mediated upregulation of BH3-only protein Bim, which acts downstream of JNK, was also enhanced in OR6 cells compared to cured cells. Palmitates 0-9 BCL2 like 11 Homo sapiens 52-55 28990465-6 2017 Moreover, combined treatment of U0126, a mitogen-activated protein kinase kinase 1/2 inhibitor, and rapamycin, a mammalian target of rapamycin inhibitor, induced Bim and p27 expressions. U 0126 32-37 BCL2 like 11 Homo sapiens 162-165 28759561-0 2017 Regenerating Family Member 4 (Reg4) Enhances 5-Fluorouracil Resistance of Gastric Cancer Through Activating MAPK/Erk/Bim Signaling Pathway. Fluorouracil 45-59 BCL2 like 11 Homo sapiens 117-120 28641145-6 2017 Hypermethylation of the BIM gene promoter was associated with lower BIM gene expression and poorer sensitivity to vincristine. Vincristine 114-125 BCL2 like 11 Homo sapiens 24-27 29156797-8 2017 ABT-263 and JQ1 co-treatment in MYCN-amplified SCLC cells markedly disrupted Bim/Bcl-2 interaction, and prevented Bim"s interaction with Mcl-1. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 0-3 BCL2 like 11 Homo sapiens 77-80 29156797-8 2017 ABT-263 and JQ1 co-treatment in MYCN-amplified SCLC cells markedly disrupted Bim/Bcl-2 interaction, and prevented Bim"s interaction with Mcl-1. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 0-3 BCL2 like 11 Homo sapiens 114-117 28900483-0 2017 Sulforaphane Induced Apoptosis via Promotion of Mitochondrial Fusion and ERK1/2-Mediated 26S Proteasome Degradation of Novel Pro-survival Bim and Upregulation of Bax in Human Non-Small Cell Lung Cancer Cells. sulforaphane 0-12 BCL2 like 11 Homo sapiens 138-141 28900483-6 2017 Pro-survival Bim downregulation was shown to induce apoptosis in response to SFN. sulforaphane 77-80 BCL2 like 11 Homo sapiens 13-16 28900483-7 2017 Further, Using the ERK1/2 inhibitor, PD98059, we found that SFN upregulated Bax and downregulated Bim through the ERK1/2-dependent signaling pathway. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 37-44 BCL2 like 11 Homo sapiens 98-101 28642847-7 2017 Moreover, pretreatment with the ROS inhibitor NAC down-regulated GRP78, CHOP, Bim, and cleaved caspase-3 expression, resulting in a reduction in the apoptosis rate from 36.2 to 20.3% in LT-treated HCT-8 cells. Reactive Oxygen Species 32-35 BCL2 like 11 Homo sapiens 78-81 27857021-13 2017 Furthermore, we found that metformin treatment increased the rate of apoptosis, down-regulation of PKM2, and up-regulation of Bim in tumor tissues. Metformin 27-36 BCL2 like 11 Homo sapiens 126-129 28693160-12 2017 MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression. MK-8776 0-7 BCL2 like 11 Homo sapiens 223-226 28693160-12 2017 MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression. MK-8776 136-143 BCL2 like 11 Homo sapiens 223-226 28476040-8 2017 Ganetespib increased Bim expression, activated caspase-3 and induced apoptosis. STA 9090 0-10 BCL2 like 11 Homo sapiens 21-24 29296778-0 2017 ASXL1 and BIM germ line variants predict response and identify CML patients with the greatest risk of imatinib failure. Imatinib Mesylate 102-110 BCL2 like 11 Homo sapiens 10-13 29296778-8 2017 The Sokal risk score was combined with the ASXL1 and BIM variants in a classification tree model to predict imatinib response. Imatinib Mesylate 108-116 BCL2 like 11 Homo sapiens 53-56 28401485-6 2017 RESULTS: We found that silymarin and silibinin dramatically increased the expression of the pro-apoptotic protein Bim in a concentration- and time-dependent manner and, concomitantly, induced apoptosis in MC3 and HN22 cells. Silymarin 23-32 BCL2 like 11 Homo sapiens 114-117 28401485-6 2017 RESULTS: We found that silymarin and silibinin dramatically increased the expression of the pro-apoptotic protein Bim in a concentration- and time-dependent manner and, concomitantly, induced apoptosis in MC3 and HN22 cells. Silybin 37-46 BCL2 like 11 Homo sapiens 114-117 28401485-0 2017 Silymarin and its active component silibinin act as novel therapeutic alternatives for salivary gland cancer by targeting the ERK1/2-Bim signaling cascade. Silymarin 0-9 BCL2 like 11 Homo sapiens 133-136 28401485-0 2017 Silymarin and its active component silibinin act as novel therapeutic alternatives for salivary gland cancer by targeting the ERK1/2-Bim signaling cascade. Silybin 35-44 BCL2 like 11 Homo sapiens 133-136 28401485-7 2017 We also found that ERK1/2 signaling inhibition successfully sensitized these cells to the apoptotic effects of silymarin and silibinin, which indicates that the ERK1/2 signaling pathway may act as an upstream regulator that modulates the silymarin/silibinin-induced Bim signaling pathway. Silymarin 111-120 BCL2 like 11 Homo sapiens 266-269 28401485-7 2017 We also found that ERK1/2 signaling inhibition successfully sensitized these cells to the apoptotic effects of silymarin and silibinin, which indicates that the ERK1/2 signaling pathway may act as an upstream regulator that modulates the silymarin/silibinin-induced Bim signaling pathway. Silybin 125-134 BCL2 like 11 Homo sapiens 266-269 28401485-7 2017 We also found that ERK1/2 signaling inhibition successfully sensitized these cells to the apoptotic effects of silymarin and silibinin, which indicates that the ERK1/2 signaling pathway may act as an upstream regulator that modulates the silymarin/silibinin-induced Bim signaling pathway. Silymarin 238-247 BCL2 like 11 Homo sapiens 266-269 28401485-8 2017 CONCLUSIONS: Taken together, we conclude that ERK1/2 signaling pathway inhibition by silymarin and silibinin increases the expression of the pro-apoptotic Bcl-2 family member Bim which, subsequently, induces mitochondria-mediated apoptosis in salivary gland cancer-derived cells. Silymarin 85-94 BCL2 like 11 Homo sapiens 175-178 28401485-8 2017 CONCLUSIONS: Taken together, we conclude that ERK1/2 signaling pathway inhibition by silymarin and silibinin increases the expression of the pro-apoptotic Bcl-2 family member Bim which, subsequently, induces mitochondria-mediated apoptosis in salivary gland cancer-derived cells. Silybin 99-108 BCL2 like 11 Homo sapiens 175-178 28427129-0 2017 [The role of FOXO3a-Bim signaling in triptolide induced bladder cancer T24 cells apoptosis]. triptolide 37-47 BCL2 like 11 Homo sapiens 20-23 28529032-2 2017 Cereblon is probably targeted by both lenalidomide and dexamethasone, which leads to synergistic cytotoxicity in MCL by inhibiting the interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3), phosphatidylinositol 3-kinase (PI3K)/AKT and AKT2/Forkhead box O3 (FOXO3A)/BCL2-like 11 (BIM) pathways. Lenalidomide 38-50 BCL2 like 11 Homo sapiens 289-301 28529032-2 2017 Cereblon is probably targeted by both lenalidomide and dexamethasone, which leads to synergistic cytotoxicity in MCL by inhibiting the interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3), phosphatidylinositol 3-kinase (PI3K)/AKT and AKT2/Forkhead box O3 (FOXO3A)/BCL2-like 11 (BIM) pathways. Dexamethasone 55-68 BCL2 like 11 Homo sapiens 289-301 28427129-5 2017 Western blot showed that triptolide reduced the expression of p-Akt, p-FOXO3a and increased the expression of Bim, Bax, cleaved-caspase 3.The cell inhibition rate in Triptolide group (30%+-8%) was significantly higher than that in the control group (P<0.05) and the rates in MK2206 group (54% +-6%), FOXO3a-siRNA group (18%+-7%) and Bim-siRNA group (11%+-6%) were also higher than the control group.Compared with the triptolide group, the inhibition rate in MK2206 group was significantly increased, but decreased in FOXO3a-siRNA group and Bim-siRNA group(P<0.05). triptolide 25-35 BCL2 like 11 Homo sapiens 110-113 28294596-0 2017 The Macrolide Toxin Mycolactone Promotes Bim-Dependent Apoptosis in Buruli Ulcer through Inhibition of mTOR. mycolactone 20-31 BCL2 like 11 Homo sapiens 41-44 28518140-7 2017 The apoptosis induced by miR-101-3p-mediated Bim expression is mediated by both caspase-3 and -1, which are activated by two distinct intrinsic mechanisms, cytochrome c release and ROS-induced inflammasome activation, respectively. Reactive Oxygen Species 181-184 BCL2 like 11 Homo sapiens 45-48 28427129-1 2017 Objective: To investigate the role of FOXO3a-Bim signaling in triptolide induced bladder cancer T24 cells apoptosis. triptolide 62-72 BCL2 like 11 Homo sapiens 45-48 28427129-5 2017 Western blot showed that triptolide reduced the expression of p-Akt, p-FOXO3a and increased the expression of Bim, Bax, cleaved-caspase 3.The cell inhibition rate in Triptolide group (30%+-8%) was significantly higher than that in the control group (P<0.05) and the rates in MK2206 group (54% +-6%), FOXO3a-siRNA group (18%+-7%) and Bim-siRNA group (11%+-6%) were also higher than the control group.Compared with the triptolide group, the inhibition rate in MK2206 group was significantly increased, but decreased in FOXO3a-siRNA group and Bim-siRNA group(P<0.05). triptolide 25-35 BCL2 like 11 Homo sapiens 336-339 28427129-5 2017 Western blot showed that triptolide reduced the expression of p-Akt, p-FOXO3a and increased the expression of Bim, Bax, cleaved-caspase 3.The cell inhibition rate in Triptolide group (30%+-8%) was significantly higher than that in the control group (P<0.05) and the rates in MK2206 group (54% +-6%), FOXO3a-siRNA group (18%+-7%) and Bim-siRNA group (11%+-6%) were also higher than the control group.Compared with the triptolide group, the inhibition rate in MK2206 group was significantly increased, but decreased in FOXO3a-siRNA group and Bim-siRNA group(P<0.05). triptolide 25-35 BCL2 like 11 Homo sapiens 336-339 28427129-6 2017 Conclusion: Triptolide induces T24 cells apoptosis through FOXO3a-Bim signaling pathway. triptolide 12-22 BCL2 like 11 Homo sapiens 66-69 29263915-8 2017 Previous studies in AML show that ABT-199 alone decreases the association of proapoptotic protein Bim with Bcl-2, but this is compensated by increased association of Bim with prosurvival protein Mcl-1, stabilizing Mcl-1, resulting in resistance to ABT-199. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 34-37 BCL2 like 11 Homo sapiens 98-101 28445931-0 2017 High glucose induces apoptosis via upregulation of Bim expression in proximal tubule epithelial cells. Glucose 5-12 BCL2 like 11 Homo sapiens 51-54 28445931-8 2017 The autophagy inhibitor 3-MA increased the injury in Bim knockdown HK2 cells by retriggering apoptosis. 3-methyladenine 24-28 BCL2 like 11 Homo sapiens 53-56 29263915-12 2017 While A-1210477 treatment alone also increased Mcl-1 protein levels, combination with ABT-199 reduced binding of Bim to Mcl-1. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 86-89 BCL2 like 11 Homo sapiens 113-116 29263915-13 2017 Our results demonstrate that sequestration of Bim by Mcl-1, a mechanism of ABT-199 resistance, can be abrogated by combined treatment with the Mcl-1 inhibitor A-1201477. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 75-78 BCL2 like 11 Homo sapiens 46-49 29263915-13 2017 Our results demonstrate that sequestration of Bim by Mcl-1, a mechanism of ABT-199 resistance, can be abrogated by combined treatment with the Mcl-1 inhibitor A-1201477. a-1201477 159-168 BCL2 like 11 Homo sapiens 46-49 28350129-10 2017 ABT-263 alone and in combination with BMN 673 induced expression levels of Bim, a pro-apoptotic protein. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 0-3 BCL2 like 11 Homo sapiens 75-78 28151018-0 2017 Calcium Dobesilate Prevents Diabetic Kidney Disease by Decreasing Bim and Inhibiting Apoptosis of Renal Proximal Tubular Epithelial Cells. Calcium Dobesilate 0-18 BCL2 like 11 Homo sapiens 66-69 28151018-4 2017 It is indicated that high glucose promoted abnormal apoptosis of HK2 cells, which was inhibited by treatment of calcium dobesilate, while Bim expression decreased in response to calcium dobesilate in high-glucose-treated HK2 cells. Calcium Dobesilate 178-196 BCL2 like 11 Homo sapiens 138-141 28151018-4 2017 It is indicated that high glucose promoted abnormal apoptosis of HK2 cells, which was inhibited by treatment of calcium dobesilate, while Bim expression decreased in response to calcium dobesilate in high-glucose-treated HK2 cells. Glucose 205-212 BCL2 like 11 Homo sapiens 138-141 28350129-10 2017 ABT-263 alone and in combination with BMN 673 induced expression levels of Bim, a pro-apoptotic protein. bmn 38-41 BCL2 like 11 Homo sapiens 75-78 28454330-7 2017 In a subgroup of patients receiving docetaxel-based second-line chemotherapy, those with high or intermediate levels of BIM exhibited a median OS of 18.2 months [95% confidence interval (CI), 12.8-23.6], compared with 9.6 months (95% CI, 8.9-10.3) in patients with low BIM levels (P=0.008). Docetaxel 36-45 BCL2 like 11 Homo sapiens 120-123 28285685-0 2017 Combination treatment with erlotinib and ampelopsin overcomes erlotinib resistance in NSCLC cells via the Nox2-ROS-Bim pathway. Erlotinib Hydrochloride 27-36 BCL2 like 11 Homo sapiens 115-118 28285685-0 2017 Combination treatment with erlotinib and ampelopsin overcomes erlotinib resistance in NSCLC cells via the Nox2-ROS-Bim pathway. Reactive Oxygen Species 111-114 BCL2 like 11 Homo sapiens 115-118 28285685-7 2017 To determine the effect of Nox2 and Bim on the combined treatment with erlotinib and ampelopsin-induced cell death, we transfected with Nox2 or Bim specific siRNA and performed with western blot assay for evaluation of its expression. Erlotinib Hydrochloride 71-80 BCL2 like 11 Homo sapiens 36-39 28285685-7 2017 To determine the effect of Nox2 and Bim on the combined treatment with erlotinib and ampelopsin-induced cell death, we transfected with Nox2 or Bim specific siRNA and performed with western blot assay for evaluation of its expression. ampelopsin 85-95 BCL2 like 11 Homo sapiens 36-39 28285685-7 2017 To determine the effect of Nox2 and Bim on the combined treatment with erlotinib and ampelopsin-induced cell death, we transfected with Nox2 or Bim specific siRNA and performed with western blot assay for evaluation of its expression. ampelopsin 85-95 BCL2 like 11 Homo sapiens 144-147 28285685-11 2017 CONCLUSION: Here in this study, we demonstrate that the combination of erlotinib and ampelopsin induces cell death via the Nox2-ROS-Bim pathway, and ampelopsin could be used as a novel anti-cancer agent combined with EGFR-TKI to overcome resistance to erlotinib in EGFR-mutant NSCLC. Erlotinib Hydrochloride 71-80 BCL2 like 11 Homo sapiens 132-135 28285685-11 2017 CONCLUSION: Here in this study, we demonstrate that the combination of erlotinib and ampelopsin induces cell death via the Nox2-ROS-Bim pathway, and ampelopsin could be used as a novel anti-cancer agent combined with EGFR-TKI to overcome resistance to erlotinib in EGFR-mutant NSCLC. Reactive Oxygen Species 128-131 BCL2 like 11 Homo sapiens 132-135 28553347-6 2017 Mitomycin C upregulated the expression levels of Fas, DR4, DR5, cleaved caspase-8/9, Bax, Bim and cleaved caspase-3 proteins, and it downregulated Bcl-2 and Bcl-xL expression. Mitomycin 0-11 BCL2 like 11 Homo sapiens 90-93 28335434-5 2017 In addition, FKA induces apoptosis in SKBR3 cells by increasing the protein expression of Bim and BAX and decreasing expression of Bcl2, BclX/L, XIAP, and survivin. flavokawain A 13-16 BCL2 like 11 Homo sapiens 90-93 28119491-6 2017 Fenretinide + romidepsin caused a reactive oxygen species (ROS)-dependent increase in proapoptotic proteins (Bim, tBid, Bax, and Bak), apoptosis, and inhibition of HDAC enzymatic activity, which achieved a synergistic increase in histone acetylation. Fenretinide 0-11 BCL2 like 11 Homo sapiens 109-112 28119491-6 2017 Fenretinide + romidepsin caused a reactive oxygen species (ROS)-dependent increase in proapoptotic proteins (Bim, tBid, Bax, and Bak), apoptosis, and inhibition of HDAC enzymatic activity, which achieved a synergistic increase in histone acetylation. Reactive Oxygen Species 34-57 BCL2 like 11 Homo sapiens 109-112 28119491-6 2017 Fenretinide + romidepsin caused a reactive oxygen species (ROS)-dependent increase in proapoptotic proteins (Bim, tBid, Bax, and Bak), apoptosis, and inhibition of HDAC enzymatic activity, which achieved a synergistic increase in histone acetylation. Reactive Oxygen Species 59-62 BCL2 like 11 Homo sapiens 109-112 28300825-4 2017 Using structure/function studies, we report that dimerization of BST-2 through cysteine residues located in the BST-2 extracellular domain (ECD), leads to anoikis resistance and cell survival through proteasome-mediated degradation of BIM-a key proapoptotic factor. Cysteine 79-87 BCL2 like 11 Homo sapiens 235-238 28300825-6 2017 Furthermore, we demonstrate that restoration of the ECD cysteine residues is sufficient to rescue cell survival and tumor growth via a previously unreported pathway-BST-2/GRB2/ERK/BIM/Cas3. Cysteine 56-64 BCL2 like 11 Homo sapiens 180-183 27873035-0 2017 DMFC (3,5-dimethyl-7H-furo[3,2-g]chromen-7-one) regulates Bim to trigger Bax and Bak activation to suppress drug-resistant human hepatoma. 3,5-dimethyl-7H-furo(3,2-g)chromen-7-one 0-4 BCL2 like 11 Homo sapiens 58-61 27873035-0 2017 DMFC (3,5-dimethyl-7H-furo[3,2-g]chromen-7-one) regulates Bim to trigger Bax and Bak activation to suppress drug-resistant human hepatoma. 3,5-dimethyl-7H-furo(3,2-g)chromen-7-one 6-46 BCL2 like 11 Homo sapiens 58-61 27873035-4 2017 In the molecular level, we observed that DMFC treatment decreases Bcl-2 level by a post-transcriptional mechanism and activates Bim transcription to increase Bim mRNA and protein level in hepatoma cells. 3,5-dimethyl-7H-furo(3,2-g)chromen-7-one 41-45 BCL2 like 11 Homo sapiens 128-131 27873035-4 2017 In the molecular level, we observed that DMFC treatment decreases Bcl-2 level by a post-transcriptional mechanism and activates Bim transcription to increase Bim mRNA and protein level in hepatoma cells. 3,5-dimethyl-7H-furo(3,2-g)chromen-7-one 41-45 BCL2 like 11 Homo sapiens 158-161 27873035-5 2017 Furthermore, co-immunoprecipitation studies revealed that DMFC-induced Bim interrupts interactions between Bcl-2 and Bax and between Mcl-1 and Bak, resulting in dissociation of Bax from Bcl-2 and Bak from Mcl-1 and subsequent activation of both Bax and Bak. 3,5-dimethyl-7H-furo(3,2-g)chromen-7-one 58-62 BCL2 like 11 Homo sapiens 71-74 27873035-8 2017 Therefore, we determine that DMFC suppresses hepatoma growth through decreasing Bcl-2 and increasing Bim to induce tumor cell apoptosis and hold great promise for further development as a therapeutic agent to treat chemoresistant hepatoma. 3,5-dimethyl-7H-furo(3,2-g)chromen-7-one 29-33 BCL2 like 11 Homo sapiens 101-104 28454330-7 2017 In a subgroup of patients receiving docetaxel-based second-line chemotherapy, those with high or intermediate levels of BIM exhibited a median OS of 18.2 months [95% confidence interval (CI), 12.8-23.6], compared with 9.6 months (95% CI, 8.9-10.3) in patients with low BIM levels (P=0.008). Docetaxel 36-45 BCL2 like 11 Homo sapiens 269-272 28454330-10 2017 Therefore, BIM may be considered as a biomarker to identify whether patients could benefit from docetaxel-based second-line chemotherapy in GC. Docetaxel 96-105 BCL2 like 11 Homo sapiens 11-14 27892697-7 2017 Furthermore, we found that DAE-induced inactivation of Akt kinase led to the activation of its target FOXO3 transcription factor, enhancing the expression of FOXO3-regulated proapoptotic effectors, Bim and Bax, and cell cycle inhibitor p27. o,p-dinitrophenyl aminoethyldiphosphate-beryllium trifluoride 27-30 BCL2 like 11 Homo sapiens 198-201 28076456-8 2017 Propofol statistically decreased cell viability but increased the percentages of apoptotic cells and protein expressions of FOXO1, FOXO3, Bim, and pro- and activated caspases-3; however, miR-486 inhibitor reversed the effects of propofol on cell viability, apoptosis, and protein expression (P<0.05 or P<0.01). Propofol 0-8 BCL2 like 11 Homo sapiens 138-141 28079897-6 2017 Indeed, Tsc1 promotes DC survival through restraining independent mTORC1 and ROS-Bim pathways. ros 77-80 BCL2 like 11 Homo sapiens 81-84 27452907-5 2016 The NAD+-dependent histone deacetylase sirtuin (SIRT)1 amplified the pro-apoptotic effect by deacetylating FOXO3a, which induced EGR1 binding to the Bim promoter and activated Bim expression. NAD 4-8 BCL2 like 11 Homo sapiens 149-152 27678524-6 2016 Subsequently, ABT-751 triggered apoptosis with marked downregulation of B-cell CLL/lymphoma 2, upregulation of mitochondrial BCL2 antagonist/killer 1 and BCL2 like 11 protein levels, and cleavages of caspase 8 (CASP8), CASP9, CASP3 and DNA fragmentation factor subunit alpha proteins. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 14-17 BCL2 like 11 Homo sapiens 154-166 27779703-6 2016 In addition, resveratrol was observed to arrest cell cycle progression in G1/S phase by increasing the protein expression levels of p53 and p21, and concurrently reducing the protein expression levels of CDK2, cyclin A and cyclin E. Furthermore, resveratrol treatment significantly induced apoptosis in eosinophils, likely through the upregulation of Bim and Bax protein expression levels and the downregulation of Bcl-2 protein expression. Resveratrol 13-24 BCL2 like 11 Homo sapiens 351-354 28105181-0 2016 Activator protein 1 promotes gemcitabine-induced apoptosis in pancreatic cancer by upregulating its downstream target Bim. gemcitabine 29-40 BCL2 like 11 Homo sapiens 118-121 28105181-5 2016 c-Jun overexpression increased gemcitabine-induced apoptosis through Bim activation, while cell apoptosis and Bim expression decreased following c-Jun knockdown. gemcitabine 31-42 BCL2 like 11 Homo sapiens 69-72 28105181-6 2016 Furthermore, gemcitabine-induced apoptosis and Bim levels decreased when c-Jun phosphorylation was blocked by SP600125. gemcitabine 13-24 BCL2 like 11 Homo sapiens 47-50 28105181-6 2016 Furthermore, gemcitabine-induced apoptosis and Bim levels decreased when c-Jun phosphorylation was blocked by SP600125. pyrazolanthrone 110-118 BCL2 like 11 Homo sapiens 47-50 28105181-7 2016 Our findings suggest that c-Jun, which is a member of the AP-1 complex, functions in gemcitabine-induced apoptosis by regulating its downstream target Bim in pancreatic cancer cells. gemcitabine 85-96 BCL2 like 11 Homo sapiens 151-154 27452907-5 2016 The NAD+-dependent histone deacetylase sirtuin (SIRT)1 amplified the pro-apoptotic effect by deacetylating FOXO3a, which induced EGR1 binding to the Bim promoter and activated Bim expression. NAD 4-8 BCL2 like 11 Homo sapiens 176-179 27452907-9 2016 In addition, shikonin-induced FOXO3a nuclear localization was blocked by AKT activation and SIRT1 inhibition, which blocked Bim expression and conferred resistance to the cytotoxic effects of shikonin. shikonin 13-21 BCL2 like 11 Homo sapiens 124-127 27103402-0 2016 Binding of Released Bim to Mcl-1 is a Mechanism of Intrinsic Resistance to ABT-199 which can be Overcome by Combination with Daunorubicin or Cytarabine in AML Cells. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 75-78 BCL2 like 11 Homo sapiens 20-23 27582546-0 2016 Eupafolin enhances TRAIL-mediated apoptosis through cathepsin S-induced down-regulation of Mcl-1 expression and AMPK-mediated Bim up-regulation in renal carcinoma Caki cells. eupafolin 0-9 BCL2 like 11 Homo sapiens 126-129 27582546-6 2016 In addition, eupafolin increased Bim expression at the post-translational levels via AMP-activated protein kinase (AMPK)-mediated inhibition of proteasome activity. eupafolin 13-22 BCL2 like 11 Homo sapiens 33-36 27582546-7 2016 Knock-down of Bim expression by siRNA inhibited eupafolin plus TRAIL-induced apoptosis. eupafolin 48-57 BCL2 like 11 Homo sapiens 14-17 27582546-9 2016 Taken together, these results suggest that eupafolin enhanced TRAIL-mediated apoptosis via down-regulation of Mcl-1 and up-regulation of Bim in renal carcinoma Caki cells. eupafolin 43-52 BCL2 like 11 Homo sapiens 137-140 27512118-10 2016 Accordingly, bcl-2 inhibitors (Obatoclax, ABT-199) markedly synergized with trabectedin paralleled by deregulated expression of the bcl-2 family members bcl-2, bim, bax, Mcl-1, and bcl-xL as a consequence of trabectedin exposure. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 42-45 BCL2 like 11 Homo sapiens 160-163 27512118-10 2016 Accordingly, bcl-2 inhibitors (Obatoclax, ABT-199) markedly synergized with trabectedin paralleled by deregulated expression of the bcl-2 family members bcl-2, bim, bax, Mcl-1, and bcl-xL as a consequence of trabectedin exposure. Trabectedin 76-87 BCL2 like 11 Homo sapiens 160-163 27103402-6 2016 RESULTS: Immunoprecipitation of Bim from ABT-199-treated cell lines and a primary patient sample demonstrated decreased association with Bcl-2, but increased association with Mcl-1 without corresponding change in mitochondrial outer membrane potential. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 41-44 BCL2 like 11 Homo sapiens 32-35 27103402-7 2016 ABT-199 treatment resulted in increased levels of Mcl-1 protein, unchanged or decreased Mcl-1 transcript levels, and increased Mcl-1 protein half-life, suggesting that the association with Bim plays a role in stabilizing Mcl-1 protein. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 0-3 BCL2 like 11 Homo sapiens 189-192 27103402-9 2016 CONCLUSIONS: Our results demonstrate that sequestration of Bim by Mcl-1 is a mechanism of intrinsic ABT-199 resistance and supports the clinical development of ABT-199 in combination with cytarabine or daunorubicin for the treatment of AML. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 100-103 BCL2 like 11 Homo sapiens 59-62 27661108-2 2016 This study investigates activity of the BH3 mimetic venetoclax (ABT-199), which targets BCL-2, and mechanisms of acquired resistance in FL.The sensitivity of FL cells to venetoclax treatment correlated with BCL-2/BIM ratio. BH 3 40-43 BCL2 like 11 Homo sapiens 213-216 27661108-2 2016 This study investigates activity of the BH3 mimetic venetoclax (ABT-199), which targets BCL-2, and mechanisms of acquired resistance in FL.The sensitivity of FL cells to venetoclax treatment correlated with BCL-2/BIM ratio. venetoclax 52-62 BCL2 like 11 Homo sapiens 213-216 27661108-4 2016 Venetoclax induced dissociation of BCL-2/ BIM complex and a decrease in mitochondrial potential. venetoclax 0-10 BCL2 like 11 Homo sapiens 42-45 27661108-5 2016 Interestingly the population of cells that survived venetoclax treatment showed increased p-ERK1/2 and p-BIM (S69), as well as a decrease in total BIM levels. venetoclax 52-62 BCL2 like 11 Homo sapiens 105-108 27661108-5 2016 Interestingly the population of cells that survived venetoclax treatment showed increased p-ERK1/2 and p-BIM (S69), as well as a decrease in total BIM levels. venetoclax 52-62 BCL2 like 11 Homo sapiens 147-150 27103402-9 2016 CONCLUSIONS: Our results demonstrate that sequestration of Bim by Mcl-1 is a mechanism of intrinsic ABT-199 resistance and supports the clinical development of ABT-199 in combination with cytarabine or daunorubicin for the treatment of AML. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 160-163 BCL2 like 11 Homo sapiens 59-62 27103402-9 2016 CONCLUSIONS: Our results demonstrate that sequestration of Bim by Mcl-1 is a mechanism of intrinsic ABT-199 resistance and supports the clinical development of ABT-199 in combination with cytarabine or daunorubicin for the treatment of AML. Cytarabine 188-198 BCL2 like 11 Homo sapiens 59-62 27103402-9 2016 CONCLUSIONS: Our results demonstrate that sequestration of Bim by Mcl-1 is a mechanism of intrinsic ABT-199 resistance and supports the clinical development of ABT-199 in combination with cytarabine or daunorubicin for the treatment of AML. Daunorubicin 202-214 BCL2 like 11 Homo sapiens 59-62 27103402-0 2016 Binding of Released Bim to Mcl-1 is a Mechanism of Intrinsic Resistance to ABT-199 which can be Overcome by Combination with Daunorubicin or Cytarabine in AML Cells. Daunorubicin 125-137 BCL2 like 11 Homo sapiens 20-23 27103402-0 2016 Binding of Released Bim to Mcl-1 is a Mechanism of Intrinsic Resistance to ABT-199 which can be Overcome by Combination with Daunorubicin or Cytarabine in AML Cells. Cytarabine 141-151 BCL2 like 11 Homo sapiens 20-23 26981780-0 2016 Ruxolitinib synergizes with DMF to kill via BIM+BAD-induced mitochondrial dysfunction and via reduced SOD2/TRX expression and ROS. ruxolitinib 0-11 BCL2 like 11 Homo sapiens 44-47 27490929-5 2016 TH/TR signaling promoted chemotherapy resistance through negatively regulating the pro-apoptotic protein, Bim, resulting in doxorubicin-induced metastasis of chemotherapy-resistant HCC cells. Doxorubicin 124-135 BCL2 like 11 Homo sapiens 106-109 27490929-10 2016 Our findings collectively suggest that expression of Bim is mediated by FoxO1 and indirectly downregulated by TH/TR, leading to chemotherapy resistance and doxorubicin-promoted metastasis of hepatoma cells. Doxorubicin 156-167 BCL2 like 11 Homo sapiens 53-56 26640142-0 2016 Targeting glutamine metabolism in multiple myeloma enhances BIM binding to BCL-2 eliciting synthetic lethality to venetoclax. Glutamine 10-19 BCL2 like 11 Homo sapiens 60-63 26640142-6 2016 Cells continuing to survive in the absence of glucose or glutamine were found to maintain expression of MCL-1 but importantly induce pro-apoptotic BIM expression. Glucose 46-53 BCL2 like 11 Homo sapiens 147-150 26640142-6 2016 Cells continuing to survive in the absence of glucose or glutamine were found to maintain expression of MCL-1 but importantly induce pro-apoptotic BIM expression. Glutamine 57-66 BCL2 like 11 Homo sapiens 147-150 26640142-8 2016 Our investigation revealed that cells surviving glutamine withdrawal in particular, enhance expression and binding of BIM to BCL-2, consequently sensitizing these cells to the BH3 mimetic venetoclax. Glutamine 48-57 BCL2 like 11 Homo sapiens 118-121 26640142-8 2016 Our investigation revealed that cells surviving glutamine withdrawal in particular, enhance expression and binding of BIM to BCL-2, consequently sensitizing these cells to the BH3 mimetic venetoclax. BH 3 176-179 BCL2 like 11 Homo sapiens 118-121 27383270-5 2016 Also, overexpression of miR-139-5p decreased PDE4D levels and increased cellular cAMP levels, leading to BIM-mediated cell growth arrest. Cyclic AMP 81-85 BCL2 like 11 Homo sapiens 105-108 27383270-7 2016 Finally, overexpression of miR-139-5p suppressed the growth of xenograft tumors, accompanied by decrease in PDE4D and increase in BIM. mir-139-5p 27-37 BCL2 like 11 Homo sapiens 130-133 26486506-6 2016 RESULTS: BIM (BCL2L11)-BH3 profiling results correlated with docetaxel sensitivity and BAK protein expression, whose knockdown caused docetaxel resistance. BH 3 23-26 BCL2 like 11 Homo sapiens 14-21 26486506-6 2016 RESULTS: BIM (BCL2L11)-BH3 profiling results correlated with docetaxel sensitivity and BAK protein expression, whose knockdown caused docetaxel resistance. Docetaxel 61-70 BCL2 like 11 Homo sapiens 14-21 26486506-6 2016 RESULTS: BIM (BCL2L11)-BH3 profiling results correlated with docetaxel sensitivity and BAK protein expression, whose knockdown caused docetaxel resistance. Docetaxel 134-143 BCL2 like 11 Homo sapiens 14-21 27144333-0 2016 The role of VDR and BIM in potentiation of cytarabine-induced cell death in human AML blasts. Cytarabine 43-53 BCL2 like 11 Homo sapiens 20-23 27203692-9 2016 Expression analysis revealed that pro-apoptotic genes (BCL2L11/BIM and AIFM2) were DHT-induced, whereas pro-survival genes (BCL2L1/BCL-XL and MCL1) were DHT-repressed. Dihydrotestosterone 83-86 BCL2 like 11 Homo sapiens 55-62 27087117-7 2016 The knockdown of the bim gene repressed the anisomycin-boosted apoptosis through the attenuation of the active Bak and Bax. Anisomycin 44-54 BCL2 like 11 Homo sapiens 21-24 27087117-8 2016 The findings indicate for the first time that miR let-7c is essential for the anisomycin-triggered apoptosis by linking JNK1/2 to AP-1/STAT1/STAT3/Bim/Bcl-xL/Bax/Bak signaling. Anisomycin 78-88 BCL2 like 11 Homo sapiens 147-150 26915975-6 2016 Treatment with 2,3-dihydroxy-9,10-anthraquinone was found to trigger intrinsic apoptotic pathway as indicated by down regulation of Bcl-2, Bcl-xl; up regulation of Bim, Bax, Bad; release of cytochrome c and pro-caspases cleaving to caspases. 2,3-dihydroxy-9,10-anthraquinone 15-47 BCL2 like 11 Homo sapiens 164-167 27582059-7 2016 Furthermore, the multikinase inhibitors dasatinib and ponatinib appear to have the added advantage of inducing Lck/Yes novel tyrosine kinase (LYN)-mediated proapoptotic BCL-2-like protein 11 (BIM) expression and inhibiting up-regulation of antiapoptotic myeloid cell leukemia 1 (MCL-1), thereby potentially overcoming the development of venetoclax resistance. Dasatinib 40-49 BCL2 like 11 Homo sapiens 169-190 27582059-7 2016 Furthermore, the multikinase inhibitors dasatinib and ponatinib appear to have the added advantage of inducing Lck/Yes novel tyrosine kinase (LYN)-mediated proapoptotic BCL-2-like protein 11 (BIM) expression and inhibiting up-regulation of antiapoptotic myeloid cell leukemia 1 (MCL-1), thereby potentially overcoming the development of venetoclax resistance. ponatinib 54-63 BCL2 like 11 Homo sapiens 169-190 27363900-7 2016 The simultaneous treatment for 24h with protolichesterinic acid plus doxorubicin caused an increase of Bim protein expression and the appearance of cleaved form of Bid protein. protolichesterinic acid 40-63 BCL2 like 11 Homo sapiens 103-106 27363900-7 2016 The simultaneous treatment for 24h with protolichesterinic acid plus doxorubicin caused an increase of Bim protein expression and the appearance of cleaved form of Bid protein. Doxorubicin 69-80 BCL2 like 11 Homo sapiens 103-106 27195679-0 2016 Myt3 suppression sensitizes islet cells to high glucose-induced cell death via Bim induction. Glucose 48-55 BCL2 like 11 Homo sapiens 79-82 27195679-8 2016 Specifically, we find that Myt3 suppression sensitizes islet cells to high glucose-induced cell death via upregulation of the pro-apoptotic Bcl2 family member Bim. Glucose 75-82 BCL2 like 11 Homo sapiens 159-162 27056887-3 2016 ABT199 caused apoptosis more potently in neuroblastoma cell lines expressing high BCL-2 and BIM/BCL-2 complex levels than low expressing cell lines. venetoclax 0-6 BCL2 like 11 Homo sapiens 92-95 27056887-6 2016 We showed that neuroblastoma cells might survive ABT199 treatment due to its acute upregulation of the anti-apoptotic BCL-2 family protein myeloid cell leukaemia sequence 1 (MCL-1) and BIM sequestration by MCL-1. venetoclax 49-55 BCL2 like 11 Homo sapiens 185-188 27056887-8 2016 Our findings suggest that neuroblastoma patients with high BCL-2 and BIM/BCL-2 complex levels might benefit from combination treatment with ABT199 and compounds that inhibit MCL-1 expression. venetoclax 140-146 BCL2 like 11 Homo sapiens 69-72 26981780-0 2016 Ruxolitinib synergizes with DMF to kill via BIM+BAD-induced mitochondrial dysfunction and via reduced SOD2/TRX expression and ROS. Dimethyl Fumarate 28-31 BCL2 like 11 Homo sapiens 44-47 26981780-4 2016 The combination of [ruxolitinib + MMF] inactivated ERK1/2, AKT, STAT3 and STAT5; reduced expression of MCL-1, BCL-XL, SOD2 and TRX; increased BIM expression; decreased BAD S112 S136 phosphorylation; and enhanced pro-caspase 3 cleavage. ruxolitinib 20-31 BCL2 like 11 Homo sapiens 142-145 26981780-4 2016 The combination of [ruxolitinib + MMF] inactivated ERK1/2, AKT, STAT3 and STAT5; reduced expression of MCL-1, BCL-XL, SOD2 and TRX; increased BIM expression; decreased BAD S112 S136 phosphorylation; and enhanced pro-caspase 3 cleavage. citraconic acid 34-37 BCL2 like 11 Homo sapiens 142-145 26449824-0 2016 Caffeine-induced nuclear translocation of FoxO1 triggers Bim-mediated apoptosis in human glioblastoma cells. Caffeine 0-8 BCL2 like 11 Homo sapiens 57-60 26887050-10 2016 Instead, we identified the induction of autophagy to be regulated downstream of the miR-138/BIM axis and to promote cell survival following TMZ exposure. Temozolomide 140-143 BCL2 like 11 Homo sapiens 92-95 26332363-8 2016 Interestingly, withaferin A (WA), a bioactive component of MEAG, clearly induced apoptosis accompanied by upregulation of Bim, t-Bid, caspase-8, and DR5 similar to the effects of MEAG. withaferin A 15-27 BCL2 like 11 Homo sapiens 122-125 26503209-0 2016 Knockdown of miR-221 promotes the cisplatin-inducing apoptosis by targeting the BIM-Bax/Bak axis in breast cancer. Cisplatin 34-43 BCL2 like 11 Homo sapiens 80-83 26503209-8 2016 Our results suggest the anti-miR-221 could promote the cisplatin-inducing apoptosis by targeting the Bim-Bax/Bak axis in breast cancer. Cisplatin 55-64 BCL2 like 11 Homo sapiens 101-104 26449824-6 2016 Results showed that caffeine inhibited proliferation and survival of human glioma cells, induced apoptosis, and increased the expression of FoxO1 and its proapoptotic target Bim. Caffeine 20-28 BCL2 like 11 Homo sapiens 174-177 26449824-8 2016 In summary, our data indicates that FoxO1-Bim mediates caffeine-induced regression of glioma growth by activating cell apoptosis, thereby providing new mechanistic insight into the possible use of caffeine in treating human cancer. Caffeine 55-63 BCL2 like 11 Homo sapiens 42-45 26449824-8 2016 In summary, our data indicates that FoxO1-Bim mediates caffeine-induced regression of glioma growth by activating cell apoptosis, thereby providing new mechanistic insight into the possible use of caffeine in treating human cancer. Caffeine 197-205 BCL2 like 11 Homo sapiens 42-45 26572075-9 2016 Importantly, we demonstrated that miR-181b inhibitors increased the level of Bim in the T-47D-R cells, resulting in the loss of mitochondrial membrane potential (MMP) and the activation of caspases caused by DOX. mir-181b 34-42 BCL2 like 11 Homo sapiens 77-80 26493374-7 2016 Mechanistically, pBcl-2 inhibited the effects of the ABT compounds on the displacement of Bax and Bim from Bcl-2, thereby suppressing mitochondrial apoptosis. pbcl-2 17-23 BCL2 like 11 Homo sapiens 98-101 26493374-7 2016 Mechanistically, pBcl-2 inhibited the effects of the ABT compounds on the displacement of Bax and Bim from Bcl-2, thereby suppressing mitochondrial apoptosis. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 53-56 BCL2 like 11 Homo sapiens 98-101 26824181-9 2016 Collectively, our data suggest that rs3809783 A > T in pri-miR-10a may be conductive to the genetic predisposition to RSA by disrupting the production of mature miR-10a and reinforcing the expression of Bim. rabbit sperm membrane autoantigen 121-124 BCL2 like 11 Homo sapiens 206-209 26874859-13 2016 Treatment with ABT-199 displaces Bim from Bcl-2 in NB to activate caspase 3, confirming the restoration of mitochondrial apoptosis. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 15-18 BCL2 like 11 Homo sapiens 33-36 26709007-0 2016 Resveratrol induces apoptosis through modulation of the Akt/FoxO3a/Bim pathway in HepG2 cells. Resveratrol 0-11 BCL2 like 11 Homo sapiens 67-70 26709007-4 2016 It was demonstrated that resveratrol treatment induced apoptosis in HepG2 cells, and that this pro-apoptotic effect was accompanied with increases in the expression of apoptotic protein Bim. Resveratrol 25-36 BCL2 like 11 Homo sapiens 186-189 26709007-6 2016 Furthermore, resveratrol enhanced the nuclear levels of FoxO3a and mediated neuronal death via Bim. Resveratrol 13-24 BCL2 like 11 Homo sapiens 95-98 26709007-7 2016 The present study demonstrated that resveratrol induced apoptosis in HepG2 cells through activation of the transcription factor FoxO3a and increasing the expression of Bim protein. Resveratrol 36-47 BCL2 like 11 Homo sapiens 168-171 26572075-9 2016 Importantly, we demonstrated that miR-181b inhibitors increased the level of Bim in the T-47D-R cells, resulting in the loss of mitochondrial membrane potential (MMP) and the activation of caspases caused by DOX. Doxorubicin 208-211 BCL2 like 11 Homo sapiens 77-80 26511491-5 2016 FLLL12 strongly inhibited the expression of p-EGFR, EGFR, p-AKT, AKT, Bcl-2, and Bid and increased the expression of Bim. flll12 0-6 BCL2 like 11 Homo sapiens 117-120 26511491-6 2016 Overexpression of constitutively active AKT or Bcl-2 or ablation of Bim or Bid significantly inhibited FLLL12-induced apoptosis. flll12 103-109 BCL2 like 11 Homo sapiens 68-71 26511491-9 2016 Taken together, our results strongly suggest that FLLL12 is a potent curcumin analogue with more favorable pharmacokinetic properties that induces apoptosis of head and neck cancer cell lines by inhibition of survival proteins including EGFR, AKT, and Bcl-2 and increasing of the proapoptotic protein Bim. flll12 50-56 BCL2 like 11 Homo sapiens 301-304 28717678-6 2016 OS rates were significantly lower for patients with the Bim deletion polymorphism than for those with the wild-type sequence. Osmium 0-2 BCL2 like 11 Homo sapiens 56-59 26694174-0 2016 Bim directly antagonizes Bcl-xl in doxorubicin-induced prostate cancer cell apoptosis independently of p53. Doxorubicin 35-46 BCL2 like 11 Homo sapiens 0-3 26694174-10 2016 Finally, co-immunoprecipitation and siRNA analysis revealed that a BH3-only protein, Bim, is involved in doxorubicin-induced apoptosis by directly counteracting Bcl-xl. Doxorubicin 105-116 BCL2 like 11 Homo sapiens 85-88 26497683-5 2015 Expression analysis revealed that fluorizoline induced the upregulation of Noxa and Bim mRNA levels, which was not observed in PHB-depleted MEFs. Fluorizoline 34-46 BCL2 like 11 Homo sapiens 84-87 26497683-6 2015 Finally, Noxa(-/-)/Bim(-/-) MEFs and NOXA-downregulated HeLa cells were resistant to fluorizoline-induced apoptosis. Fluorizoline 85-97 BCL2 like 11 Homo sapiens 19-22 26473375-4 2015 Mechanistically, JNJ-26481585/Doxorubicin cotreatment causes upregulation of the BH3-only proteins Bim and Noxa as well as downregulation of the antiapoptotic proteins Mcl-1 and Bcl-xL. Doxorubicin 30-41 BCL2 like 11 Homo sapiens 99-102 26376801-4 2015 In response to dexamethasone, it was found that FOXO3a translocates into the nucleus, where it induces the expression of downstream targets, including p27Kip1 and Bim, important for proliferative arrest and cell death in the sensitive RS4;11 and SUP-B15 B-ALL cells. Dexamethasone 15-28 BCL2 like 11 Homo sapiens 163-166 26517515-8 2015 Supporting this, FOXO3a knockdown attenuated FasL and Bim upregulation and apoptosis induction in GOS+VPA-treated cells. Valproic Acid 102-105 BCL2 like 11 Homo sapiens 54-57 26473375-5 2015 These changes in the ratio of pro- and antiapoptotic Bcl-2 proteins contribute to JNJ-26481585/Doxorubicin-mediated apoptosis, since knockdown of Bim or Noxa significantly inhibits cell death. Doxorubicin 95-106 BCL2 like 11 Homo sapiens 146-149 26447615-0 2015 Targeting ERK1/2-bim signaling cascades by BH3-mimetic ABT-737 as an alternative therapeutic strategy for oral cancer. BH 3 43-46 BCL2 like 11 Homo sapiens 17-20 26447615-0 2015 Targeting ERK1/2-bim signaling cascades by BH3-mimetic ABT-737 as an alternative therapeutic strategy for oral cancer. ABT-737 55-62 BCL2 like 11 Homo sapiens 17-20 26447615-8 2015 In the present study, we observed that inactivation of the ERK1/2 signaling pathway using ABT-737 dramatically increased the expression of pro-apoptotic protein Bim via transcriptional and/or posttranslational regulation, in a cell type-dependent manner, inducing mitochondria-mediated apoptosis of human oral cancer cells. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 90-93 BCL2 like 11 Homo sapiens 161-164 26245900-3 2015 GDC-0623 was shown to potently up-regulate BIM expression to a greater extent versus other MEK inhibitors in isogenic KRAS HCT116 and mutant KRAS SW620 colon cancer cells. GDC-0623 0-8 BCL2 like 11 Homo sapiens 43-46 26397392-7 2015 Licochalcone C treatment reduced the levels of the anti-apoptotic mRNAs (Bcl-2, Bcl-w and Bcl-XL) and increased expression of the pro-apoptotic mRNAs (Bax and Bim). licochalcone C 0-14 BCL2 like 11 Homo sapiens 159-162 26528184-0 2015 Effect of cAMP signaling on expression of glucocorticoid receptor, Bim and Bad in glucocorticoid-sensitive and resistant leukemic and multiple myeloma cells. Cyclic AMP 10-14 BCL2 like 11 Homo sapiens 67-70 26528184-5 2015 This study shows that leukemic and multiple myeloma cells, including those resistant to glucocorticoids, can be induced to undergo apoptosis by stimulating the cAMP signaling pathway, with enhancement by glucocorticoids, and the mechanism by which this occurs may be related to changes in Bim and Bad expression, and in all cases, to activation of Bad. Cyclic AMP 160-164 BCL2 like 11 Homo sapiens 289-292 26318418-7 2015 The upregulation of pro-apoptotic Bak, Bax, Puma and Bim were accompanied with the decrease in Mcl-1 in HCT 116 and Bcl-xL expression profiles in HT-29 following 48h EBR treatment. EBR 166-169 BCL2 like 11 Homo sapiens 53-56 26318418-8 2015 We suggest that the upregulation of Bim expression levels might be related with one of the PI3K/AKT target transcription factor Foxo3a, which was dephosphorylated by EBR treatment in HCT 116 and HT-29 cells. EBR 166-169 BCL2 like 11 Homo sapiens 36-39 26254608-0 2015 The proapoptotic protein Bim is up regulated by 1alpha,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma. Calcitriol 48-77 BCL2 like 11 Homo sapiens 25-28 26254608-7 2015 On the other hand, Bortezomib (0.25-1nM), an inhibitor of NF-kappaB pathway highly activated in vGPCR cells, increased Bim protein levels and induced caspase-3 cleavage. Bortezomib 19-29 BCL2 like 11 Homo sapiens 119-122 26245900-8 2015 GDC-0623 plus ABT-263 induced a synergistic apoptosis by a mechanism that includes release of BIM from its sequestration by BCL-XL. GDC-0623 0-8 BCL2 like 11 Homo sapiens 94-97 26245900-8 2015 GDC-0623 plus ABT-263 induced a synergistic apoptosis by a mechanism that includes release of BIM from its sequestration by BCL-XL. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 14-17 BCL2 like 11 Homo sapiens 94-97 26245900-4 2015 ERK silencing enhanced BIM up-regulation by GDC-0623 that was due to its loss of phosphorylation at Ser(69), confirmed by a BIM-EL phosphorylation-defective mutant (S69G) that increased protein stability and blocked BIM induction. GDC-0623 44-52 BCL2 like 11 Homo sapiens 23-26 26245900-4 2015 ERK silencing enhanced BIM up-regulation by GDC-0623 that was due to its loss of phosphorylation at Ser(69), confirmed by a BIM-EL phosphorylation-defective mutant (S69G) that increased protein stability and blocked BIM induction. Serine 100-103 BCL2 like 11 Homo sapiens 23-26 25633717-0 2015 The tubulysin analogue KEMTUB10 induces apoptosis in breast cancer cells via p53, Bim and Bcl-2. kemtub10 23-31 BCL2 like 11 Homo sapiens 82-85 25753394-7 2015 Biochemically, treatment of DP thymcoytes with TrxR1 inhibitor alone or in conjunction with anti-CD3 resulted in enhanced phosphorylation of redox-sensitive ASK-1, JNK and p38 MAPK, and upregulated expression of Bim. dp 28-30 BCL2 like 11 Homo sapiens 212-215 25633717-8 2015 KEMTUB10-induced apoptosis involves p53 and Bim, and to some extent Bcl-2 phosphorylation. kemtub10 0-8 BCL2 like 11 Homo sapiens 44-47 25860284-2 2015 We have previously reported that the combination of the EGFR-TKI erlotinib and epigallocatechin-3-gallate (EGCG) exhibited synergistic chemopreventive effects in head and neck cancers by inducing the expression of Bim, p21, p27, and by inhibiting the phosphorylation of ERK and AKT and expression of Bcl-2. epigallocatechin gallate 107-111 BCL2 like 11 Homo sapiens 214-217 26296767-0 2015 HCV upregulates Bim through the ROS/JNK signalling pathway, leading to Bax-mediated apoptosis. Reactive Oxygen Species 32-35 BCL2 like 11 Homo sapiens 16-19 26296767-5 2015 The HCV-induced increase in the Bim mRNA and protein levels was significantly counteracted by treatment with NAC or SP600125, suggesting that the ROS/JNK signalling pathway is involved in Bim upregulation. Acetylcysteine 109-112 BCL2 like 11 Homo sapiens 32-35 26296767-5 2015 The HCV-induced increase in the Bim mRNA and protein levels was significantly counteracted by treatment with NAC or SP600125, suggesting that the ROS/JNK signalling pathway is involved in Bim upregulation. Acetylcysteine 109-112 BCL2 like 11 Homo sapiens 188-191 26296767-5 2015 The HCV-induced increase in the Bim mRNA and protein levels was significantly counteracted by treatment with NAC or SP600125, suggesting that the ROS/JNK signalling pathway is involved in Bim upregulation. pyrazolanthrone 116-124 BCL2 like 11 Homo sapiens 32-35 26296767-5 2015 The HCV-induced increase in the Bim mRNA and protein levels was significantly counteracted by treatment with NAC or SP600125, suggesting that the ROS/JNK signalling pathway is involved in Bim upregulation. pyrazolanthrone 116-124 BCL2 like 11 Homo sapiens 188-191 26296767-5 2015 The HCV-induced increase in the Bim mRNA and protein levels was significantly counteracted by treatment with NAC or SP600125, suggesting that the ROS/JNK signalling pathway is involved in Bim upregulation. Reactive Oxygen Species 146-149 BCL2 like 11 Homo sapiens 32-35 26296767-5 2015 The HCV-induced increase in the Bim mRNA and protein levels was significantly counteracted by treatment with NAC or SP600125, suggesting that the ROS/JNK signalling pathway is involved in Bim upregulation. Reactive Oxygen Species 146-149 BCL2 like 11 Homo sapiens 188-191 26296767-8 2015 Taken together, these observations suggest that HCV-induced ROS/JNK signalling transcriptionally activates Bim expression, which leads to Bax activation and apoptosis induction. Reactive Oxygen Species 60-63 BCL2 like 11 Homo sapiens 107-110 26550240-6 2015 The PCR chip detection found 13 up-regulating genes and 15 down-regulating genes, among which the expression of Bim, Caspase 9, Caspase 14, B-cell lymphoma-2 (BCL2) and BAX increased with the doses of sodium fluoride, while the expression of Caspase 3 down-regulated in 5 mg/L sodium fluoride but up-regulated at the concentration of sodium fluoride more than 10 mg/L. Sodium Fluoride 201-216 BCL2 like 11 Homo sapiens 112-115 26550240-6 2015 The PCR chip detection found 13 up-regulating genes and 15 down-regulating genes, among which the expression of Bim, Caspase 9, Caspase 14, B-cell lymphoma-2 (BCL2) and BAX increased with the doses of sodium fluoride, while the expression of Caspase 3 down-regulated in 5 mg/L sodium fluoride but up-regulated at the concentration of sodium fluoride more than 10 mg/L. Sodium Fluoride 277-292 BCL2 like 11 Homo sapiens 112-115 26550240-6 2015 The PCR chip detection found 13 up-regulating genes and 15 down-regulating genes, among which the expression of Bim, Caspase 9, Caspase 14, B-cell lymphoma-2 (BCL2) and BAX increased with the doses of sodium fluoride, while the expression of Caspase 3 down-regulated in 5 mg/L sodium fluoride but up-regulated at the concentration of sodium fluoride more than 10 mg/L. Sodium Fluoride 277-292 BCL2 like 11 Homo sapiens 112-115 26231047-16 2015 Finally, treatment of the multiple myeloma KMS11 cell model (dependent on Mcl-1 for survival) with dexamethasone induced Bim and Bim-dependent lethality. Dexamethasone 99-112 BCL2 like 11 Homo sapiens 121-124 26231047-16 2015 Finally, treatment of the multiple myeloma KMS11 cell model (dependent on Mcl-1 for survival) with dexamethasone induced Bim and Bim-dependent lethality. Dexamethasone 99-112 BCL2 like 11 Homo sapiens 129-132 25526094-7 2015 This complex forms as a result of Bim-EL phosphorylation on serine 59, and thus Bim-EL cannot localize to the mitochondria and cause anoikis. Serine 60-66 BCL2 like 11 Homo sapiens 34-37 25860284-0 2015 Combination of erlotinib and EGCG induces apoptosis of head and neck cancers through posttranscriptional regulation of Bim and Bcl-2. Erlotinib Hydrochloride 15-24 BCL2 like 11 Homo sapiens 119-122 25860284-0 2015 Combination of erlotinib and EGCG induces apoptosis of head and neck cancers through posttranscriptional regulation of Bim and Bcl-2. epigallocatechin gallate 29-33 BCL2 like 11 Homo sapiens 119-122 25860284-2 2015 We have previously reported that the combination of the EGFR-TKI erlotinib and epigallocatechin-3-gallate (EGCG) exhibited synergistic chemopreventive effects in head and neck cancers by inducing the expression of Bim, p21, p27, and by inhibiting the phosphorylation of ERK and AKT and expression of Bcl-2. Erlotinib Hydrochloride 65-74 BCL2 like 11 Homo sapiens 214-217 25860284-2 2015 We have previously reported that the combination of the EGFR-TKI erlotinib and epigallocatechin-3-gallate (EGCG) exhibited synergistic chemopreventive effects in head and neck cancers by inducing the expression of Bim, p21, p27, and by inhibiting the phosphorylation of ERK and AKT and expression of Bcl-2. epigallocatechin gallate 79-105 BCL2 like 11 Homo sapiens 214-217 25860284-4 2015 shRNA-mediated silencing of Bim significantly inhibited apoptosis induced by the combination of erlotinib and EGCG (p = 0.005). Erlotinib Hydrochloride 96-105 BCL2 like 11 Homo sapiens 28-31 25860284-4 2015 shRNA-mediated silencing of Bim significantly inhibited apoptosis induced by the combination of erlotinib and EGCG (p = 0.005). epigallocatechin gallate 110-114 BCL2 like 11 Homo sapiens 28-31 25860284-7 2015 Furthermore, we found that erlotinib or the combination of EGCG and erlotinib inhibited the phosphorylation of Bim and stabilized Bim after inhibition of protein translation by cycloheximide. Erlotinib Hydrochloride 27-36 BCL2 like 11 Homo sapiens 111-114 25860284-7 2015 Furthermore, we found that erlotinib or the combination of EGCG and erlotinib inhibited the phosphorylation of Bim and stabilized Bim after inhibition of protein translation by cycloheximide. Erlotinib Hydrochloride 27-36 BCL2 like 11 Homo sapiens 130-133 25860284-7 2015 Furthermore, we found that erlotinib or the combination of EGCG and erlotinib inhibited the phosphorylation of Bim and stabilized Bim after inhibition of protein translation by cycloheximide. epigallocatechin gallate 59-63 BCL2 like 11 Homo sapiens 111-114 25860284-7 2015 Furthermore, we found that erlotinib or the combination of EGCG and erlotinib inhibited the phosphorylation of Bim and stabilized Bim after inhibition of protein translation by cycloheximide. epigallocatechin gallate 59-63 BCL2 like 11 Homo sapiens 130-133 25860284-7 2015 Furthermore, we found that erlotinib or the combination of EGCG and erlotinib inhibited the phosphorylation of Bim and stabilized Bim after inhibition of protein translation by cycloheximide. Erlotinib Hydrochloride 68-77 BCL2 like 11 Homo sapiens 111-114 25860284-7 2015 Furthermore, we found that erlotinib or the combination of EGCG and erlotinib inhibited the phosphorylation of Bim and stabilized Bim after inhibition of protein translation by cycloheximide. Erlotinib Hydrochloride 68-77 BCL2 like 11 Homo sapiens 130-133 25860284-8 2015 Taken together, our results strongly suggest that the combination of erlotinib and EGCG induces apoptosis of SCCHN cells by regulating Bim and Bcl-2 at the posttranscriptional level. Erlotinib Hydrochloride 69-78 BCL2 like 11 Homo sapiens 135-138 25860284-8 2015 Taken together, our results strongly suggest that the combination of erlotinib and EGCG induces apoptosis of SCCHN cells by regulating Bim and Bcl-2 at the posttranscriptional level. epigallocatechin gallate 83-87 BCL2 like 11 Homo sapiens 135-138 25817195-6 2015 PTL treatment also induced the translocation of cytosolic Bim into the mitochondria and, more importantly, PTL-induced apoptosis was significantly attenuated, when the Bim expression was knockdown by siRNA transfection. parthenolide 0-3 BCL2 like 11 Homo sapiens 58-61 26084280-0 2015 PTK6 inhibition promotes apoptosis of Lapatinib-resistant Her2(+) breast cancer cells by inducing Bim. Lapatinib 38-47 BCL2 like 11 Homo sapiens 98-101 26084280-6 2015 RESULTS: Lapatinib treatment of "sensitive" Her2(+) cells induces apoptotic cell death and enhances transcript and protein levels of Bim, a pro-apoptotic Bcl2 family member. Lapatinib 9-18 BCL2 like 11 Homo sapiens 133-136 26084280-13 2015 CONCLUSIONS: PTK6 downregulation induces apoptosis of Lapatinib-resistant Her2(+) breast cancer cells by enhancing Bim expression via p38 activation. Lapatinib 54-63 BCL2 like 11 Homo sapiens 115-118 26117007-5 2015 In process of inducing effect of 20 mmol/L metformin on THP-1 cells, the expressions of BCL-XL and BIM did not significantly changed, while the expressions of BAX and caspase-3 significantly increased (P<0.01). Metformin 43-52 BCL2 like 11 Homo sapiens 99-102 25753156-5 2015 The potency of siIL-10RA was enhanced further by combining it with siRNA targeting TGF-beta receptor (siTGF-betaR), which was the next best option during the screening of this study, or the previously selected immunoadjuvant siRNA targeting phosphatase and tensin homologue deleted on chromosome 10 (PTEN) or Bcl-2-like protein 11 (BIM). siil-10ra 15-24 BCL2 like 11 Homo sapiens 309-330 26171069-6 2015 It was observed that combined administration of cisplatin and bortezomib induced upregulation of caspase-3, -8 and -9, B-cell lymphoma-2 (Bcl-2)-like 11 and Bcl-2-interacting killer, but downregulated Bcl-2 and Bcl-extra large protein expression levels in T24 cells in a dose-dependent manner. Cisplatin 48-57 BCL2 like 11 Homo sapiens 138-152 26171069-6 2015 It was observed that combined administration of cisplatin and bortezomib induced upregulation of caspase-3, -8 and -9, B-cell lymphoma-2 (Bcl-2)-like 11 and Bcl-2-interacting killer, but downregulated Bcl-2 and Bcl-extra large protein expression levels in T24 cells in a dose-dependent manner. Bortezomib 62-72 BCL2 like 11 Homo sapiens 138-152 25817195-6 2015 PTL treatment also induced the translocation of cytosolic Bim into the mitochondria and, more importantly, PTL-induced apoptosis was significantly attenuated, when the Bim expression was knockdown by siRNA transfection. parthenolide 0-3 BCL2 like 11 Homo sapiens 168-171 26019998-4 2015 Additionally, the molecular mechanisms of lappaconitine"s analgesic effects may be related to affect the expression levels of endogenous opioid system genes (POMC, PENK and MOR), as well as apoptosis-related genes (Xiap, Smac, Bim, NF-kappaB and p53). lappaconitine 42-55 BCL2 like 11 Homo sapiens 227-230 25612549-7 2015 As hsa-miR-32-5p was described to target genes being involved in the regulation of apoptosis, the effect of alpha-eleostearic acid on the expression of the apoptosis-associated genes BCL2L11, BCL-2, and BCL-XL was examined. eleostearic acid 108-130 BCL2 like 11 Homo sapiens 183-190 25576194-5 2015 Knockdown of BiP/GRP78 by siRNA and inhibition of BiP/GRP78 using EGCG both abolished the formation of the JNK-Bim complex, caspase-3 activation, and subsequent apoptosis induction by ARV S1133 efficiently. epigallocatechin gallate 66-70 BCL2 like 11 Homo sapiens 111-114 25711465-0 2015 Melatonin-mediated Bim up-regulation and cyclooxygenase-2 (COX-2) down-regulation enhances tunicamycin-induced apoptosis in MDA-MB-231 cells. Melatonin 0-9 BCL2 like 11 Homo sapiens 19-22 25711465-4 2015 Melatonin up-regulates pro-apoptotic protein Bim expression at the transcriptional levels in the presence of tunicamycin. Melatonin 0-9 BCL2 like 11 Homo sapiens 45-48 25711465-4 2015 Melatonin up-regulates pro-apoptotic protein Bim expression at the transcriptional levels in the presence of tunicamycin. Tunicamycin 109-120 BCL2 like 11 Homo sapiens 45-48 25711465-11 2015 Taken together, our results suggest that melatonin enhances antitumor function through up-regulation of Bim expression and down-regulation of COX-2 expression in tunicamycin-treated MDA-MB-231 cells. Melatonin 41-50 BCL2 like 11 Homo sapiens 104-107 25501496-10 2015 The chemical chaperone 4-phenylbutyrate acid antagonizes the induction of FOXO activation, Bim expression and caspase cleavage by rhein, indicating that protein misfolding may be involved in triggering these deleterious effects. 4-phenylbutyric acid 23-39 BCL2 like 11 Homo sapiens 91-94 25174872-6 2015 RESULTS: The pro-apoptotic molecule, Bim, was significantly elevated in DNTC. dntc 72-76 BCL2 like 11 Homo sapiens 37-40 25174872-8 2015 Strikingly, Bim levels in DNTC correlated significantly with serum IL-10 in ALPS patients, and IL-10 was sufficient to mildly induce Bim in normal and ALPS T cells via a Janus kinase/signal transducer and activator of transcription 3-dependent mechanism. dntc 26-30 BCL2 like 11 Homo sapiens 12-15 25174872-10 2015 CONCLUSION: Combined, these data show that an IL-10/Janus kinase/signal transducer and activator of transcription 3 pathway drives Bim expression in ALPS DNTC, which renders them sensitive to BH3 mimetics, uncovering a potentially novel therapeutic approach to ALPS. dntc 154-158 BCL2 like 11 Homo sapiens 131-134 25174872-10 2015 CONCLUSION: Combined, these data show that an IL-10/Janus kinase/signal transducer and activator of transcription 3 pathway drives Bim expression in ALPS DNTC, which renders them sensitive to BH3 mimetics, uncovering a potentially novel therapeutic approach to ALPS. BH 3 192-195 BCL2 like 11 Homo sapiens 131-134 25714678-7 2015 Furthermore, we show that binding of both cBid and Bim to membranes is facilitated by electrostatic interactions with anionic phospholipids. Phospholipids 126-139 BCL2 like 11 Homo sapiens 51-54 26054686-8 2015 Oridonin treatment upregulated the expression levels of Bim, Bax, cytosolic cytochrome c, cleaved caspase-9 and cleaved caspase-3 proteins, downregulated the expression levels of Bcl-2, procaspase-9 and procaspase-3 proteins, and meanwhile obviously activated caspase-9 and caspase-3 in a dose-dependent manner in HCT-116 and LoVo cells. oridonin 0-8 BCL2 like 11 Homo sapiens 56-59 25643632-4 2015 This conclusion is supported by the fact, that a selective PKC inhibitor, BIM, inhibits ERK1/2 and COX-2 signalings, MEK/ERK1/2 inhibitor, PD98059, nullifies COX-2 signaling, and COX-2 inhibitor, NS-398, attenuates the proliferation and invasiveness potential of the colonic cancer cells. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 139-146 BCL2 like 11 Homo sapiens 74-77 25643632-4 2015 This conclusion is supported by the fact, that a selective PKC inhibitor, BIM, inhibits ERK1/2 and COX-2 signalings, MEK/ERK1/2 inhibitor, PD98059, nullifies COX-2 signaling, and COX-2 inhibitor, NS-398, attenuates the proliferation and invasiveness potential of the colonic cancer cells. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 196-202 BCL2 like 11 Homo sapiens 74-77 25737542-4 2015 We found that high expression of the proapoptotic gene Bcl2-interacting mediator of cell death (BIM) predicts sensitivity to ABT-263. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 125-128 BCL2 like 11 Homo sapiens 55-94 25612549-8 2015 The qPCR results indicate that fatty acid-mediated downregulation of hsa-miR-32-5p is accompanied by a downregulation of BCL-2 and BCL2L11 mRNA whereas BCL-XL was shown to be simultaneously upregulated. Fatty Acids 31-41 BCL2 like 11 Homo sapiens 131-138 25336632-9 2015 ChIP sequencing analysis revealed a novel GR binding site in a BIM intronic region (IGR) that was engaged only in dexamethasone-sensitive PDXs. Dexamethasone 114-127 BCL2 like 11 Homo sapiens 63-66 25422052-0 2015 Imidazole inhibits autophagy flux by blocking autophagic degradation and triggers apoptosis via increasing FoxO3a-Bim expression. imidazole 0-9 BCL2 like 11 Homo sapiens 114-117 25422052-10 2015 In addition, siRNA-mediated silencing of FoxO3a effectively attenuated imidazole-induced Bim upregulation and cell death, indicating direct involvement of this pathway in the imidazole-induced apoptosis. imidazole 71-80 BCL2 like 11 Homo sapiens 89-92 25422052-10 2015 In addition, siRNA-mediated silencing of FoxO3a effectively attenuated imidazole-induced Bim upregulation and cell death, indicating direct involvement of this pathway in the imidazole-induced apoptosis. imidazole 175-184 BCL2 like 11 Homo sapiens 89-92 25437618-0 2015 Design, synthesis and evaluation of marinopyrrole derivatives as selective inhibitors of Mcl-1 binding to pro-apoptotic Bim and dual Mcl-1/Bcl-xL inhibitors. marinopyrrole 36-49 BCL2 like 11 Homo sapiens 120-123 25437618-5 2015 Among the most potent dual inhibitors is 42 which inhibited Mcl-1/Bim and Bcl-xL/Bim binding 15-fold (IC50 = 600 nM) and 33-fold (500 nM) more potently than (+-)-marinopyrrole A (1), respectively. marinopyrrole A 157-177 BCL2 like 11 Homo sapiens 66-69 25437618-5 2015 Among the most potent dual inhibitors is 42 which inhibited Mcl-1/Bim and Bcl-xL/Bim binding 15-fold (IC50 = 600 nM) and 33-fold (500 nM) more potently than (+-)-marinopyrrole A (1), respectively. marinopyrrole A 157-177 BCL2 like 11 Homo sapiens 81-84 25545058-0 2015 Oridonin induces apoptosis in uveal melanoma cells by upregulation of Bim and downregulation of Fatty Acid Synthase. oridonin 0-8 BCL2 like 11 Homo sapiens 70-73 25545058-6 2015 We found that oridonin markedly increased the expression of proapoptotic Bcl-2 family protein Bim in uveal melanoma cells, and knockdown Bim by small interfering RNA significantly attenuated oridonin-induced cell death, indicating an essential role of Bim in oridonin-mediated anticancer activity. oridonin 14-22 BCL2 like 11 Homo sapiens 94-97 25545058-6 2015 We found that oridonin markedly increased the expression of proapoptotic Bcl-2 family protein Bim in uveal melanoma cells, and knockdown Bim by small interfering RNA significantly attenuated oridonin-induced cell death, indicating an essential role of Bim in oridonin-mediated anticancer activity. oridonin 191-199 BCL2 like 11 Homo sapiens 137-140 25545058-6 2015 We found that oridonin markedly increased the expression of proapoptotic Bcl-2 family protein Bim in uveal melanoma cells, and knockdown Bim by small interfering RNA significantly attenuated oridonin-induced cell death, indicating an essential role of Bim in oridonin-mediated anticancer activity. oridonin 191-199 BCL2 like 11 Homo sapiens 137-140 25545058-6 2015 We found that oridonin markedly increased the expression of proapoptotic Bcl-2 family protein Bim in uveal melanoma cells, and knockdown Bim by small interfering RNA significantly attenuated oridonin-induced cell death, indicating an essential role of Bim in oridonin-mediated anticancer activity. oridonin 191-199 BCL2 like 11 Homo sapiens 137-140 25545058-6 2015 We found that oridonin markedly increased the expression of proapoptotic Bcl-2 family protein Bim in uveal melanoma cells, and knockdown Bim by small interfering RNA significantly attenuated oridonin-induced cell death, indicating an essential role of Bim in oridonin-mediated anticancer activity. oridonin 191-199 BCL2 like 11 Homo sapiens 137-140 25545058-8 2015 Taken together, we reported that oridonin displays potent anticancer effect against uveal melanoma cells through upregulation of Bim and inhibition of FAS. oridonin 33-41 BCL2 like 11 Homo sapiens 129-132 25336632-10 2015 The absence of GR binding at the BIM IGR was associated with BIM silencing and dexamethasone resistance. Dexamethasone 79-92 BCL2 like 11 Homo sapiens 33-36 25791936-4 2015 In this study, we attempt to determine the effect of Bim on Photofrin photodynamic treatment (PPT)-induced apoptosis in human lung adenocarcinoma ASTC-a-1 cells. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 94-97 BCL2 like 11 Homo sapiens 53-56 25756510-6 2015 Inhibition of EGFR by shRNA or erlotinib in Mcl(-)1 dependent NBs disrupts Bim binding to Mcl(-)1 and enhances its affinity for Bcl(-)2, restoring sensitivity to ABT-737 as well as cytotoxics in vitro. Erlotinib Hydrochloride 31-40 BCL2 like 11 Homo sapiens 75-78 25756510-7 2015 Mechanistically treatment of NBs with small molecule inhibitors of EGFR (erlotinib, cetuximab) and ERK (U0126) increases Noxa expression and dephosphorylates Bim to promote Bim binding to Bcl(-)2. Erlotinib Hydrochloride 73-82 BCL2 like 11 Homo sapiens 158-161 25756510-7 2015 Mechanistically treatment of NBs with small molecule inhibitors of EGFR (erlotinib, cetuximab) and ERK (U0126) increases Noxa expression and dephosphorylates Bim to promote Bim binding to Bcl(-)2. Erlotinib Hydrochloride 73-82 BCL2 like 11 Homo sapiens 173-176 25756510-7 2015 Mechanistically treatment of NBs with small molecule inhibitors of EGFR (erlotinib, cetuximab) and ERK (U0126) increases Noxa expression and dephosphorylates Bim to promote Bim binding to Bcl(-)2. U 0126 104-109 BCL2 like 11 Homo sapiens 158-161 25756510-7 2015 Mechanistically treatment of NBs with small molecule inhibitors of EGFR (erlotinib, cetuximab) and ERK (U0126) increases Noxa expression and dephosphorylates Bim to promote Bim binding to Bcl(-)2. U 0126 104-109 BCL2 like 11 Homo sapiens 173-176 25791936-9 2015 The effect of Bim on PPT-induced apoptosis was determined by RNAi. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 21-24 BCL2 like 11 Homo sapiens 14-17 25791936-11 2015 PPT increased the level of Bim and activated caspase-3 in cells and that knockdown of Bim by RNAi significantly protected against caspase-3 activity. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 0-3 BCL2 like 11 Homo sapiens 27-30 25791936-12 2015 PPT-induced apoptosis were suppressed in cells transfected with shRNA-Bim. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 0-3 BCL2 like 11 Homo sapiens 70-73 25791936-13 2015 CONCLUSION: We demonstrated the involvement of Bim in PPT-induced apoptosis in human ASTC-a-1 lung adenocarcinoma cells and suggested that enhancing Bim activity might be a potential strategy for treating human cancers. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 54-57 BCL2 like 11 Homo sapiens 47-50 25791936-13 2015 CONCLUSION: We demonstrated the involvement of Bim in PPT-induced apoptosis in human ASTC-a-1 lung adenocarcinoma cells and suggested that enhancing Bim activity might be a potential strategy for treating human cancers. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 54-57 BCL2 like 11 Homo sapiens 149-152 25220073-5 2014 L-carnitine suppress the endoplasmic reticulum dilation and activation of ER stress-associated proteins including glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein-homologous protein (CHOP), JNK, Bax and Bim induced by H2O2 or TM. Carnitine 0-11 BCL2 like 11 Homo sapiens 223-226 25339540-6 2015 In addition, treatment of K562/ADR cells with quercetin alone or in combination with ADR resulted in loss of mitochondrial membrane potential, activation of caspase-8, -9 and -3, reduced expression of the anti-apoptotic proteins B-cell lymphoma (Bcl)-2 and Bcl-extra large and enhanced expression of the pro-apoptotic proteins Bcl-2-interacting mediator of cell death, Bcl-2-associated death promoter and Bcl-2-associated X protein in the cells. Quercetin 46-55 BCL2 like 11 Homo sapiens 327-367 25220073-8 2014 CHOP/Bim or JNK/Bim-dependent ER stress signaling pathways maybe related to the neuroprotective effects of L-carnitine against H2O2-induced apoptosis and oxidative injury. Carnitine 107-118 BCL2 like 11 Homo sapiens 5-8 25220073-8 2014 CHOP/Bim or JNK/Bim-dependent ER stress signaling pathways maybe related to the neuroprotective effects of L-carnitine against H2O2-induced apoptosis and oxidative injury. Carnitine 107-118 BCL2 like 11 Homo sapiens 16-19 25220073-8 2014 CHOP/Bim or JNK/Bim-dependent ER stress signaling pathways maybe related to the neuroprotective effects of L-carnitine against H2O2-induced apoptosis and oxidative injury. Hydrogen Peroxide 127-131 BCL2 like 11 Homo sapiens 5-8 25220073-8 2014 CHOP/Bim or JNK/Bim-dependent ER stress signaling pathways maybe related to the neuroprotective effects of L-carnitine against H2O2-induced apoptosis and oxidative injury. Hydrogen Peroxide 127-131 BCL2 like 11 Homo sapiens 16-19 25128467-0 2014 FoxO proteins" nuclear retention and BH3-only protein Bim induction evoke mitochondrial dysfunction-mediated apoptosis in berberine-treated HepG2 cells. Berberine 122-131 BCL2 like 11 Homo sapiens 54-57 25289048-3 2014 The results revealed that casticin significantly induced apoptosis of HT-29, HCT-116, SW480 and Caco-2 cells, induced the accumulation of reactive oxygen species (ROS) and increased the protein levels of apoptosis signal-regulating kinase 1 (ASK1), c-Jun N-terminal kinase (JNK) and B-cell lymphoma 2-interacting mediator of cell death (Bim) in HT-29 cells. casticin 26-34 BCL2 like 11 Homo sapiens 337-340 25375379-0 2014 Cafestol overcomes ABT-737 resistance in Mcl-1-overexpressed renal carcinoma Caki cells through downregulation of Mcl-1 expression and upregulation of Bim expression. cafestol 0-8 BCL2 like 11 Homo sapiens 151-154 25375379-7 2014 Moreover, cafestol increased Bim expression, and siRNA-mediated suppression of Bim expression reduced the apoptosis induced by cafestol plus ABT-737. cafestol 10-18 BCL2 like 11 Homo sapiens 29-32 25375379-7 2014 Moreover, cafestol increased Bim expression, and siRNA-mediated suppression of Bim expression reduced the apoptosis induced by cafestol plus ABT-737. cafestol 127-135 BCL2 like 11 Homo sapiens 79-82 25375379-7 2014 Moreover, cafestol increased Bim expression, and siRNA-mediated suppression of Bim expression reduced the apoptosis induced by cafestol plus ABT-737. ABT-737 141-148 BCL2 like 11 Homo sapiens 79-82 25375379-8 2014 Taken together, cafestol may be effectively used to enhance ABT-737 sensitivity in cancer therapy via downregulation of Mcl-1 expression and upregulation of Bim expression. cafestol 16-24 BCL2 like 11 Homo sapiens 157-160 25289048-4 2014 Pretreatment with N-acetylcysteine, an antioxidant chemical compound, inhibited the activation of ASK1, JNK and Bim, as well as the apoptosis induced by casticin. Acetylcysteine 18-34 BCL2 like 11 Homo sapiens 112-115 25289048-6 2014 SP600125, a specific JNK inhibitor, attenuated Bim activation and apoptosis, but did not alter ASK1 phosphorylation levels. pyrazolanthrone 0-8 BCL2 like 11 Homo sapiens 47-50 25289048-8 2014 These results suggest that casticin significantly induced apoptosis by the activation of the ASK1-JNK-Bim signaling cascade and the accumulation of ROS in colon cancer cells. casticin 27-35 BCL2 like 11 Homo sapiens 102-105 25128467-9 2014 The pivotal role of Bim in berberine-mediated cytotoxicity was further corroborated by knockdown experiments where Bim-silencing partially restored HepG2 cell viability during berberine exposure. Berberine 27-36 BCL2 like 11 Homo sapiens 20-23 25128467-9 2014 The pivotal role of Bim in berberine-mediated cytotoxicity was further corroborated by knockdown experiments where Bim-silencing partially restored HepG2 cell viability during berberine exposure. Berberine 27-36 BCL2 like 11 Homo sapiens 115-118 25128467-9 2014 The pivotal role of Bim in berberine-mediated cytotoxicity was further corroborated by knockdown experiments where Bim-silencing partially restored HepG2 cell viability during berberine exposure. Berberine 176-185 BCL2 like 11 Homo sapiens 115-118 25128467-11 2014 Thus, our findings suggest that the antiproliferative effect of berberine may in part be due to mitochondria-mediated apoptosis with Bim acting as a pivotal downstream factor of FoxO-induced transcriptional activation. Berberine 64-73 BCL2 like 11 Homo sapiens 133-136 25343522-8 2014 Furthermore, the 1,10-PT blocked the cleavage of Bcl-xL, Mcl-1, PARP, caspase-3, and caspase-9, as well as the release of cytochrome c into the cytosol, and it significantly increased the association levels of the Bcl-xL/Bim and Mcl-1/Bim protein complexes, returning them to normal levels. 1,10-phenanthroline 17-24 BCL2 like 11 Homo sapiens 235-238 25187648-5 2014 Hsp27 depletion induced by oxidative stress using hydrogen peroxide (H2O2) correlated with bim gene activation and subsequent neuronal death, whereas enhanced Hsp27 expression prevented these. Hydrogen Peroxide 50-67 BCL2 like 11 Homo sapiens 91-94 25187648-5 2014 Hsp27 depletion induced by oxidative stress using hydrogen peroxide (H2O2) correlated with bim gene activation and subsequent neuronal death, whereas enhanced Hsp27 expression prevented these. Hydrogen Peroxide 69-73 BCL2 like 11 Homo sapiens 91-94 26767045-8 2014 Additionally, we found that the BIM deletion polymorphism was an effective predictor of short progression-free survival in individuals with EGFR-mutant NSCLC and treated with chemotherapy containing pemetrexed (3.32 vs. 5.30, P = 0.012) or second-/beyond-line chemotherapy containing taxanes (1.53 vs. 2.61 months, P = 0.025). Pemetrexed 199-209 BCL2 like 11 Homo sapiens 32-35 26767045-8 2014 Additionally, we found that the BIM deletion polymorphism was an effective predictor of short progression-free survival in individuals with EGFR-mutant NSCLC and treated with chemotherapy containing pemetrexed (3.32 vs. 5.30, P = 0.012) or second-/beyond-line chemotherapy containing taxanes (1.53 vs. 2.61 months, P = 0.025). Taxoids 284-291 BCL2 like 11 Homo sapiens 32-35 25343522-8 2014 Furthermore, the 1,10-PT blocked the cleavage of Bcl-xL, Mcl-1, PARP, caspase-3, and caspase-9, as well as the release of cytochrome c into the cytosol, and it significantly increased the association levels of the Bcl-xL/Bim and Mcl-1/Bim protein complexes, returning them to normal levels. 1,10-phenanthroline 17-24 BCL2 like 11 Homo sapiens 221-224 25443417-8 2014 In addition, DMF suppressed B-cell lymphoma extra-large (Bcl-xL) and X-linked inhibitor of apoptosis (XIAP) expression whereas Bcl-2, survivin, Bcl-2-associated X protein (Bax), and Bim levels did not change. Dimethyl Fumarate 13-16 BCL2 like 11 Homo sapiens 182-185 24596063-9 2014 Decreased Bim levels after loss of HSulf-1 were due to increased p-ERK, because inhibition of ERK activity with PD98059 resulted in increased Bim expression. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 112-119 BCL2 like 11 Homo sapiens 142-145 25219883-2 2014 Proteasome inhibitors and melatonin are both intimately involved in the regulation of major signal transduction proteins including p53, cyclin p27, transcription factor NF-kappaB, apoptotic factors Bax and Bim, caspase 3, caspase 9, anti-apoptotic factor Bcl-2, TRAIL, NRF2 and transcription factor beta-catenin. Melatonin 26-35 BCL2 like 11 Homo sapiens 206-209 25090024-6 2014 Underlying the lack of prognostic significance, we found that the chemotherapy agents used in our cohort (vincristine, L-asparaginase, and methotrexate) were each able to induce ALL cell death in a BIM-independent fashion, and resensitize BIM deletion-containing cells to GCs. Vincristine 106-117 BCL2 like 11 Homo sapiens 198-201 25096914-5 2014 Auranofin treatment activates the pro-apoptotic caspase-3, increases protein levels of apoptosis-inducing proteins Bax and Bim and reduces the expression of the anti-apoptotic mediator Bcl-2 in SKOV3 cells. Auranofin 0-9 BCL2 like 11 Homo sapiens 123-126 25096993-0 2014 Enhanced apoptosis by pemetrexed and simvastatin in malignant mesothelioma and lung cancer cells by reactive oxygen species-dependent mitochondrial dysfunction and Bim induction. Pemetrexed 22-32 BCL2 like 11 Homo sapiens 164-167 25096993-0 2014 Enhanced apoptosis by pemetrexed and simvastatin in malignant mesothelioma and lung cancer cells by reactive oxygen species-dependent mitochondrial dysfunction and Bim induction. Simvastatin 37-48 BCL2 like 11 Homo sapiens 164-167 25096993-9 2014 In addition, Bim siRNA conferred protection against apoptosis induced by pemetrexed and simvastatin. Pemetrexed 73-83 BCL2 like 11 Homo sapiens 13-16 25096993-9 2014 In addition, Bim siRNA conferred protection against apoptosis induced by pemetrexed and simvastatin. Simvastatin 88-99 BCL2 like 11 Homo sapiens 13-16 24814195-6 2014 More importantly, cisplatin significantly inhibited FOXO3a phosphorylation (at Thr32, AKT phosphorylation site) and induced FOXO3a nuclear accumulation, which in turn increased the expression of FOXO3a-dependent apoptotic protein Bim. Cisplatin 18-27 BCL2 like 11 Homo sapiens 230-233 25232279-8 2014 The regulatory targets of miR-106b~25 cluster namely p21 (cyclin-dependent kinase inhibitor) and BIM (pro-apoptotic gene) were elevated, and apoptotic cell death was observed, in RB tumor cells treated with the specific antagomirs of the miR-106b~25 cluster. mir-106b 26-34 BCL2 like 11 Homo sapiens 58-100 25232279-8 2014 The regulatory targets of miR-106b~25 cluster namely p21 (cyclin-dependent kinase inhibitor) and BIM (pro-apoptotic gene) were elevated, and apoptotic cell death was observed, in RB tumor cells treated with the specific antagomirs of the miR-106b~25 cluster. mir-106b 238-246 BCL2 like 11 Homo sapiens 58-100 25090024-6 2014 Underlying the lack of prognostic significance, we found that the chemotherapy agents used in our cohort (vincristine, L-asparaginase, and methotrexate) were each able to induce ALL cell death in a BIM-independent fashion, and resensitize BIM deletion-containing cells to GCs. Vincristine 106-117 BCL2 like 11 Homo sapiens 239-242 25090024-6 2014 Underlying the lack of prognostic significance, we found that the chemotherapy agents used in our cohort (vincristine, L-asparaginase, and methotrexate) were each able to induce ALL cell death in a BIM-independent fashion, and resensitize BIM deletion-containing cells to GCs. Methotrexate 139-151 BCL2 like 11 Homo sapiens 198-201 25090024-6 2014 Underlying the lack of prognostic significance, we found that the chemotherapy agents used in our cohort (vincristine, L-asparaginase, and methotrexate) were each able to induce ALL cell death in a BIM-independent fashion, and resensitize BIM deletion-containing cells to GCs. Methotrexate 139-151 BCL2 like 11 Homo sapiens 239-242 24830786-15 2014 Taken together, these data demonstrated that H2AX phosphorylation regulated by p38 is involved in Bim expression and apoptosis in CML cells induced by imatinib. Imatinib Mesylate 151-159 BCL2 like 11 Homo sapiens 98-101 25134536-8 2014 Capric acid also increased apoptosis in mature osteoclasts through the induction of Bim expression and the suppression of ERK activation by M-CSF. decanoic acid 0-11 BCL2 like 11 Homo sapiens 84-87 24830786-0 2014 H2AX phosphorylation regulated by p38 is involved in Bim expression and apoptosis in chronic myelogenous leukemia cells induced by imatinib. Imatinib Mesylate 131-139 BCL2 like 11 Homo sapiens 53-56 24536031-8 2014 The 14-3-3epsilon gene silencing resulted in downregulation of Bim expression after PD98059 treatment. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 84-91 BCL2 like 11 Homo sapiens 63-66 24759597-7 2014 Co-treatment with SAHA and S116838 repressed the expressions of anti-apoptosis proteins, such as Mcl-1 and XIAP, but promoted Bim expression and mitochondrial damage. Vorinostat 18-22 BCL2 like 11 Homo sapiens 126-129 24947039-5 2014 Our results demonstrated that LH induced autophagy and downregulated Bad and Bim in hepatocellular carcinoma cells. Luteinizing Hormone 30-32 BCL2 like 11 Homo sapiens 77-80 24947039-7 2014 Furthermore, Bad and Bim were also significantly downregulated by autophagy during the process that LH promoted the chemoresistance of hepatocellular carcinoma cells. Luteinizing Hormone 100-102 BCL2 like 11 Homo sapiens 21-24 24927938-0 2014 Combination treatment with doxorubicin and gamitrinib synergistically augments anticancer activity through enhanced activation of Bim. Doxorubicin 27-38 BCL2 like 11 Homo sapiens 130-133 24927938-0 2014 Combination treatment with doxorubicin and gamitrinib synergistically augments anticancer activity through enhanced activation of Bim. Gamitrinib 43-53 BCL2 like 11 Homo sapiens 130-133 25076060-0 2014 Marinopyrrole derivatives with sulfide spacers as selective disruptors of Mcl-1 binding to pro-apoptotic protein Bim. marinopyrrole 0-13 BCL2 like 11 Homo sapiens 113-116 25076060-0 2014 Marinopyrrole derivatives with sulfide spacers as selective disruptors of Mcl-1 binding to pro-apoptotic protein Bim. Sulfides 31-38 BCL2 like 11 Homo sapiens 113-116 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. 7-methoxy-6-(2'-methoxy-3'-hydroxy-3'-methyl butyl) 19-26 BCL2 like 11 Homo sapiens 96-99 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. 7-methoxy-6-(2'-methoxy-3'-hydroxy-3'-methyl butyl) 19-26 BCL2 like 11 Homo sapiens 111-114 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. 7-methoxy-6-(2'-methoxy-3'-hydroxy-3'-methyl butyl) 19-26 BCL2 like 11 Homo sapiens 111-114 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. 7-methoxy-6-(2'-methoxy-3'-hydroxy-3'-methyl butyl) 19-26 BCL2 like 11 Homo sapiens 111-114 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. containing sulfide 27-45 BCL2 like 11 Homo sapiens 96-99 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. containing sulfide 27-45 BCL2 like 11 Homo sapiens 111-114 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. containing sulfide 27-45 BCL2 like 11 Homo sapiens 111-114 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. containing sulfide 27-45 BCL2 like 11 Homo sapiens 111-114 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. Sulfides 38-45 BCL2 like 11 Homo sapiens 96-99 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. Sulfides 38-45 BCL2 like 11 Homo sapiens 111-114 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. Sulfides 38-45 BCL2 like 11 Homo sapiens 111-114 25076060-4 2014 Benzyl- and benzyl methoxy-containing sulfide derivatives 4 and 5 were highly potent dual Mcl-1/Bim and Bcl-xL/Bim disruptors (IC50 values of 600 and 700 nM), whereas carboxylate-containing sulfide derivative 9 exhibited 16.4-fold more selectivity for disrupting Mcl-1/Bim over Bcl-xL/Bim binding. Sulfides 38-45 BCL2 like 11 Homo sapiens 111-114 25076060-5 2014 In addition, a nonsymmetrical marinopyrrole 12 is as equally potent as the parent marinopyrrole A (1) for disrupting both Mcl-1/Bim and Bcl-xL/Bim binding. marinopyrrole 12 30-46 BCL2 like 11 Homo sapiens 128-131 25076060-5 2014 In addition, a nonsymmetrical marinopyrrole 12 is as equally potent as the parent marinopyrrole A (1) for disrupting both Mcl-1/Bim and Bcl-xL/Bim binding. marinopyrrole 12 30-46 BCL2 like 11 Homo sapiens 143-146 25076060-5 2014 In addition, a nonsymmetrical marinopyrrole 12 is as equally potent as the parent marinopyrrole A (1) for disrupting both Mcl-1/Bim and Bcl-xL/Bim binding. marinopyrrole A 82-97 BCL2 like 11 Homo sapiens 128-131 25076060-5 2014 In addition, a nonsymmetrical marinopyrrole 12 is as equally potent as the parent marinopyrrole A (1) for disrupting both Mcl-1/Bim and Bcl-xL/Bim binding. marinopyrrole A 82-97 BCL2 like 11 Homo sapiens 143-146 24594907-5 2014 Analogous events were observed in both drug-naive and acquired bortezomib-resistant MM cells displaying increased Mcl-1 but diminished Bim expression, or cells ectopically expressing Mcl-1. Bortezomib 63-73 BCL2 like 11 Homo sapiens 135-138 24959385-9 2014 FL118 was found to not only inhibit multiple antiapoptotic proteins (survivin, XIAP, cIAP2) in the inhibitor of apoptosis (IAP) family, but to also inhibit the antiapoptotic protein Mcl-1 in the Bcl-2 family, while inducing the pro-apoptotic proteins Bax and Bim expression. 7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione 0-5 BCL2 like 11 Homo sapiens 259-262 24854555-0 2014 [MiR-192 confers cisplatin resistance by targeting Bim in lung cancer]. Cisplatin 17-26 BCL2 like 11 Homo sapiens 51-54 24854555-9 2014 CONCLUSIONS: Our data suggested that miR-192 induced Cisplatin-resistance and inhibited cell apoptosis in lung cancer via negative targeting Bim expression. Cisplatin 53-62 BCL2 like 11 Homo sapiens 141-144 24375836-0 2014 MiR-92a mediates AZD6244 induced apoptosis and G1-phase arrest of lymphoma cells by targeting Bim. mir-92a 0-7 BCL2 like 11 Homo sapiens 94-97 24375836-0 2014 MiR-92a mediates AZD6244 induced apoptosis and G1-phase arrest of lymphoma cells by targeting Bim. AZD 6244 17-24 BCL2 like 11 Homo sapiens 94-97 24375836-6 2014 A luciferase reporter assay showed that miR-92a directly targetsthe 3"-UTRs of Bim. mir-92a 40-47 BCL2 like 11 Homo sapiens 79-82 24375836-8 2014 Silencing Bim decreases AZD6244-induced apoptosis and G1-phase arrest, suggesting that Bim contributes to the growth arrest. AZD 6244 24-31 BCL2 like 11 Homo sapiens 10-13 24375836-8 2014 Silencing Bim decreases AZD6244-induced apoptosis and G1-phase arrest, suggesting that Bim contributes to the growth arrest. AZD 6244 24-31 BCL2 like 11 Homo sapiens 87-90 24375836-9 2014 Thus, miR-92a mediates AZD6244-induced cytotoxicity of lymphoma cells by targeting Bim. mir-92a 6-13 BCL2 like 11 Homo sapiens 83-86 24375836-9 2014 Thus, miR-92a mediates AZD6244-induced cytotoxicity of lymphoma cells by targeting Bim. AZD 6244 23-30 BCL2 like 11 Homo sapiens 83-86 24608970-0 2014 Cyclic marinopyrrole derivatives as disruptors of Mcl-1 and Bcl-x(L) binding to Bim. cyclic marinopyrrole derivatives 0-32 BCL2 like 11 Homo sapiens 80-83 24402163-4 2014 Here we show that in lymphoid cells, ABT-199 specifically causes Bax/Bak-mediated apoptosis that is triggered principally by the initiator BH3-only protein Bim. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 37-40 BCL2 like 11 Homo sapiens 156-159 24825889-6 2014 BH3-mimetic compounds recapitulated the effect of Bim not only in the adenomas but also in human CRC organoids that had lost responsiveness to TGF-beta-induced apoptosis. BH 3 0-3 BCL2 like 11 Homo sapiens 50-53 24567336-9 2014 Our results thus suggest that Puma is activated by both p53 and PI3K/Akt/FoxO3a pathways and cooperates with Bim to induce neuron death in response to Abeta(1-42). UNII-042A8N37WH 151-156 BCL2 like 11 Homo sapiens 109-112 24495951-5 2014 Among highly methylated genes, the combination of DHA and butyrate significantly reduced methylation of the proapoptotic Bcl2l11, Cideb, Dapk1, Ltbr, and Tnfrsf25 genes compared to untreated control cells. Docosahexaenoic Acids 50-53 BCL2 like 11 Homo sapiens 121-128 24495951-5 2014 Among highly methylated genes, the combination of DHA and butyrate significantly reduced methylation of the proapoptotic Bcl2l11, Cideb, Dapk1, Ltbr, and Tnfrsf25 genes compared to untreated control cells. Butyrates 58-66 BCL2 like 11 Homo sapiens 121-128 24419059-2 2014 Capsaicin treatment phosphorylated c-jun-NH2-kinase (JNK); forkhead box transcription factor, class O (FOXO1); and BIM in BxPC-3, AsPC-1, and L3.6PL cells. Capsaicin 0-9 BCL2 like 11 Homo sapiens 115-118 24419059-3 2014 The expression of BIM increased in response to capsaicin treatment. Capsaicin 47-56 BCL2 like 11 Homo sapiens 18-21 24419059-5 2014 Antioxidants tiron and PEG-catalase blocked capsaicin-mediated JNK/FOXO/BIM activation and protected the cells from apoptosis. 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt 13-18 BCL2 like 11 Homo sapiens 72-75 24419059-5 2014 Antioxidants tiron and PEG-catalase blocked capsaicin-mediated JNK/FOXO/BIM activation and protected the cells from apoptosis. Capsaicin 44-53 BCL2 like 11 Homo sapiens 72-75 24419059-7 2014 Capsaicin-mediated expression of BIM was found to be directly dependent on the acetylation of FOXO-1. Capsaicin 0-9 BCL2 like 11 Homo sapiens 33-36 24419059-11 2014 Moreover, silencing FOXO1 by siRNA blocked capsaicin-mediated activation of BIM and apoptosis, whereas overexpression of FOXO-1 augmented its effects. Capsaicin 43-52 BCL2 like 11 Homo sapiens 76-79 24419059-12 2014 Silencing Bim drastically reduced capsaicin-mediated cleavage of caspase-3 and PARP, indicating the role of BIM in apoptosis. Capsaicin 34-43 BCL2 like 11 Homo sapiens 10-13 24419059-12 2014 Silencing Bim drastically reduced capsaicin-mediated cleavage of caspase-3 and PARP, indicating the role of BIM in apoptosis. Capsaicin 34-43 BCL2 like 11 Homo sapiens 108-111 24525736-13 2014 Bim knockdown blunts the stimulatory effect of salubrinal on TRAIL-induced apoptosis. salubrinal 47-57 BCL2 like 11 Homo sapiens 0-3 24600487-11 2014 Furthermore, our study showed that the expression profiles of various BH3-only proteins including Bid, Bad, and Bim, apoptosis regulatory protein cleaved caspase3 was up regulated in a time-dependent manner in Hep-2 cells treated with AZD8055. (5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol 235-242 BCL2 like 11 Homo sapiens 112-115 25551567-7 2014 The administration of the autophagy inhibitor chloroquine significantly increased the expression of proapoptotic genes (Trp53, Bax, Bak1, Pmaip1, Bcl2l11, Cdkn1a, and Cdkn1b) and DNA fragmentation in the frontal brain region of olanzapine-exposed animals. Chloroquine 46-57 BCL2 like 11 Homo sapiens 146-153 24166139-0 2014 Prometaphase arrest-dependent phosphorylation of Bcl-2 and Bim reduces the association of Bcl-2 with Bak or Bim, provoking Bak activation and mitochondrial apoptosis in nocodazole-treated Jurkat T cells. Nocodazole 169-179 BCL2 like 11 Homo sapiens 59-62 24166139-0 2014 Prometaphase arrest-dependent phosphorylation of Bcl-2 and Bim reduces the association of Bcl-2 with Bak or Bim, provoking Bak activation and mitochondrial apoptosis in nocodazole-treated Jurkat T cells. Nocodazole 169-179 BCL2 like 11 Homo sapiens 108-111 24166139-8 2014 NOC-induced phosphorylation of Bcl-2 and Bim, Deltapsim loss, and mitochondria-dependent apoptotic events were significantly suppressed by a Cdk1 inhibitor roscovitine, but not by the JNK inhibitor SP600125 or the p38 MAPK inhibitor SB203580. Roscovitine 156-167 BCL2 like 11 Homo sapiens 41-44 24239173-0 2014 By inhibiting Src, verapamil and dasatinib overcome multidrug resistance via increased expression of Bim and decreased expressions of MDR1 and survivin in human multidrug-resistant myeloma cells. Verapamil 19-28 BCL2 like 11 Homo sapiens 101-104 24117987-0 2014 Transcriptional and post-translational regulation of Bim controls apoptosis in melatonin-treated human renal cancer Caki cells. Melatonin 79-88 BCL2 like 11 Homo sapiens 53-56 24117987-3 2014 Treatment with melatonin induced apoptosis and upregulated the expression of the pro-apoptotic protein Bcl-2-interacting mediator of cell death (Bim) in renal cancer Caki cells. Melatonin 15-24 BCL2 like 11 Homo sapiens 103-143 24117987-3 2014 Treatment with melatonin induced apoptosis and upregulated the expression of the pro-apoptotic protein Bcl-2-interacting mediator of cell death (Bim) in renal cancer Caki cells. Melatonin 15-24 BCL2 like 11 Homo sapiens 145-148 24117987-4 2014 Furthermore, downregulation of Bim expression by siRNA markedly reduced melatonin-mediated apoptosis. Melatonin 72-81 BCL2 like 11 Homo sapiens 31-34 24117987-5 2014 Melatonin increased Bim mRNA expression through the induction of Sp1 and E2F1 expression and transcriptional activity. Melatonin 0-9 BCL2 like 11 Homo sapiens 20-23 24117987-6 2014 We found that melatonin also modulated Bim protein stability through the inhibition of proteasome activity. Melatonin 14-23 BCL2 like 11 Homo sapiens 39-42 24117987-7 2014 However, melatonin-induced Bim upregulation was independent of melatonin"s antioxidant properties and the melatonin receptor. Melatonin 9-18 BCL2 like 11 Homo sapiens 27-30 24117987-8 2014 Taken together, our results suggest that melatonin induces apoptosis through the upregulation of Bim expression at the transcriptional level and at the post-translational level. Melatonin 41-50 BCL2 like 11 Homo sapiens 97-100 24239173-0 2014 By inhibiting Src, verapamil and dasatinib overcome multidrug resistance via increased expression of Bim and decreased expressions of MDR1 and survivin in human multidrug-resistant myeloma cells. Dasatinib 33-42 BCL2 like 11 Homo sapiens 101-104 24239173-4 2014 We found that verapamil suppresses MDR1 and survivin expressions and increases Bim expression via suppression of Src activation. Verapamil 14-23 BCL2 like 11 Homo sapiens 79-82 23802642-10 2014 RESULTS: HPFs exposed to TEGDMA showed significant increases in multiple pro-apoptotic proteins such as Bid, Bim, Caspase 3, Caspase 8, and Cytochrome c at 24 hours. triethylene glycol dimethacrylate 25-31 BCL2 like 11 Homo sapiens 109-112 24002658-3 2013 We recently had demonstrated that the beta-adrenoceptor/cAMP-PKA pathway triggers apoptosis through the transcriptional induction of the pro-apoptotic BH3-only Bcl-2 family member BIM in tissues, such as the thymus and the heart. Cyclic AMP 56-60 BCL2 like 11 Homo sapiens 180-183 24097825-7 2013 Importantly, binding of endogenous Bcl-2 to Bim also increased during mitosis, when Bcl-2 is endogenously phosphorylated, and disruption of this mitotic Bcl-2/Bim binding with navitoclax or ABT-199, like Bcl-2 downregulation, enhanced the cytotoxicity of paclitaxel. navitoclax 176-186 BCL2 like 11 Homo sapiens 44-47 24097825-7 2013 Importantly, binding of endogenous Bcl-2 to Bim also increased during mitosis, when Bcl-2 is endogenously phosphorylated, and disruption of this mitotic Bcl-2/Bim binding with navitoclax or ABT-199, like Bcl-2 downregulation, enhanced the cytotoxicity of paclitaxel. navitoclax 176-186 BCL2 like 11 Homo sapiens 159-162 24097825-7 2013 Importantly, binding of endogenous Bcl-2 to Bim also increased during mitosis, when Bcl-2 is endogenously phosphorylated, and disruption of this mitotic Bcl-2/Bim binding with navitoclax or ABT-199, like Bcl-2 downregulation, enhanced the cytotoxicity of paclitaxel. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 190-193 BCL2 like 11 Homo sapiens 44-47 24097825-7 2013 Importantly, binding of endogenous Bcl-2 to Bim also increased during mitosis, when Bcl-2 is endogenously phosphorylated, and disruption of this mitotic Bcl-2/Bim binding with navitoclax or ABT-199, like Bcl-2 downregulation, enhanced the cytotoxicity of paclitaxel. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 190-193 BCL2 like 11 Homo sapiens 159-162 24097825-7 2013 Importantly, binding of endogenous Bcl-2 to Bim also increased during mitosis, when Bcl-2 is endogenously phosphorylated, and disruption of this mitotic Bcl-2/Bim binding with navitoclax or ABT-199, like Bcl-2 downregulation, enhanced the cytotoxicity of paclitaxel. Paclitaxel 255-265 BCL2 like 11 Homo sapiens 44-47 24097825-7 2013 Importantly, binding of endogenous Bcl-2 to Bim also increased during mitosis, when Bcl-2 is endogenously phosphorylated, and disruption of this mitotic Bcl-2/Bim binding with navitoclax or ABT-199, like Bcl-2 downregulation, enhanced the cytotoxicity of paclitaxel. Paclitaxel 255-265 BCL2 like 11 Homo sapiens 159-162 24223824-3 2013 The present study aimed at identifying mutations in the BIM sequence that could lead to imatinib resistance independently of BCR-ABL mutations. Imatinib Mesylate 88-96 BCL2 like 11 Homo sapiens 56-59 24223824-4 2013 EXPERIMENTAL DESIGN: BIM coding sequence analysis was performed in 72 imatinib-treated CML patients from a French population of our centre and in 29 healthy controls (reference population) as a case-control study. Imatinib Mesylate 70-78 BCL2 like 11 Homo sapiens 21-24 24223824-12 2013 CONCLUSION: These results suggest that the analysis of the c465C>T SNP of BIM could be useful for predicting the outcome of imatinib-treated CML patients. Imatinib Mesylate 127-135 BCL2 like 11 Homo sapiens 77-80 23920411-9 2013 Overexpression of FoxO3a also increased the level of the pro-apoptotic protein Bim, whereas FoxO3a silencing downregulated H2O2 induced Bim expression. Hydrogen Peroxide 123-127 BCL2 like 11 Homo sapiens 136-139 24095762-0 2013 Design and application of a rigid quinazolone scaffold based on two-face Bim alpha-helix mimicking. quinazolone 34-45 BCL2 like 11 Homo sapiens 73-76 24095762-1 2013 Based on our previous discovery of an anthraquinone scaffold mimicking two faces of Bim alpha-helix, we derived a quinazolone scaffold through structure simplification and optimization. Anthraquinones 38-51 BCL2 like 11 Homo sapiens 84-87 24095762-1 2013 Based on our previous discovery of an anthraquinone scaffold mimicking two faces of Bim alpha-helix, we derived a quinazolone scaffold through structure simplification and optimization. quinazolone 114-125 BCL2 like 11 Homo sapiens 84-87 24331535-6 2013 Western blotting revealed that resveratrol significantly decreased the expression of antiapoptotic proteins (Mcl-1 and Bcl-2) and increased the expression of proapoptotic proteins (Bax, Bim, and Bad), and induced cleaved-caspase-3 in a time-dependent manner. Resveratrol 31-42 BCL2 like 11 Homo sapiens 186-189 24120870-3 2013 Employing a "BCL-XL-addiction" model, we show that neutralization of BCL-XL by the BH3 mimetic ABT-737 resulted in death only when cells were reconstituted with BCL-XL:BAK, but not BCL-2/ BCL-XL:BIM complexes. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 95-98 BCL2 like 11 Homo sapiens 195-198 23888996-7 2013 Moreover, we demonstrate that MAPK1 is a novel target of MIR335, and that MEK/ERK inhibitor treatment enhanced prednisolone-induced cell death through the activation of BIM (BCL2L11). Prednisolone 111-123 BCL2 like 11 Homo sapiens 174-181 23054486-6 2013 In addition, dieckol induced increased expression of truncated Bid and Bim. dieckol 13-20 BCL2 like 11 Homo sapiens 71-74 23908358-9 2013 CONCLUSIONS: Increased expression of prosurvival Mcl1 and presence of Bim isoforms lacking proapoptotic function might explain marked reduction of OS in a disease and dose-dependent manner in ALL patients carrying Bim- and Mcl1-risk genotypes. Osmium 147-149 BCL2 like 11 Homo sapiens 70-73 23908358-9 2013 CONCLUSIONS: Increased expression of prosurvival Mcl1 and presence of Bim isoforms lacking proapoptotic function might explain marked reduction of OS in a disease and dose-dependent manner in ALL patients carrying Bim- and Mcl1-risk genotypes. Osmium 147-149 BCL2 like 11 Homo sapiens 214-217 23579242-4 2013 Here we demonstrate that the beta-adrenoceptor/cAMP/PKA pathway triggers apoptosis through the transcriptional induction of the pro-apoptotic BH3-only Bcl-2 family member Bim in tissues such as the thymus and the heart. Cyclic AMP 47-51 BCL2 like 11 Homo sapiens 171-174 23579242-5 2013 In these cell types, the catecholamine-mediated apoptosis is abrogated by loss of Bim. Catecholamines 25-38 BCL2 like 11 Homo sapiens 82-85 23394612-0 2013 The roles of epigenetic modifications of proapoptotic BID and BIM genes in imatinib-resistant chronic myeloid leukemia cells. Imatinib Mesylate 75-83 BCL2 like 11 Homo sapiens 62-65 23394612-3 2013 We detected higher expression levels of BIM and BID genes and lower expression levels of EZH2, EED2, SIRT1, and SUZ12 genes in imatinib-resistant K562/IMA-3 cells compared to imatinib-non-resistant K562 cells. Imatinib Mesylate 127-135 BCL2 like 11 Homo sapiens 40-43 23912711-7 2013 Notably, we observed that knockdown of Bim significantly increased resistance of cells to the Aurora A inhibitor MLN8054. MLN8054 113-120 BCL2 like 11 Homo sapiens 39-42 23916707-3 2013 In the present study we found that photo-oxidative (phox)-ER stress induced by hypericin-based photodynamic therapy is associated with activation of PERK (an ER sessile, stress sensor), robust induction of CHOP (a pro-apoptotic transcription factor) and induction of Bim and Noxa (accompanied by an eventual drop in Mcl-1 levels). hypericin 79-88 BCL2 like 11 Homo sapiens 267-270 23956326-0 2013 Sirtuin 2 (SIRT2) enhances 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigrostriatal damage via deacetylating forkhead box O3a (Foxo3a) and activating Bim protein. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 27-71 BCL2 like 11 Homo sapiens 167-170 23956326-0 2013 Sirtuin 2 (SIRT2) enhances 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigrostriatal damage via deacetylating forkhead box O3a (Foxo3a) and activating Bim protein. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 73-77 BCL2 like 11 Homo sapiens 167-170 23648111-5 2013 In this study, we examined whether Zn(2+) affects the expression of Bim in human neuroblastoma SH-SY5Y cells. Zinc 35-37 BCL2 like 11 Homo sapiens 68-71 23648111-6 2013 Zn(2+) triggered alterations in Bim splicing and induced preferential generation of BimS, but not BimEL and BimL, in a dose- and time-dependent manner. Zinc 0-2 BCL2 like 11 Homo sapiens 32-35 23648111-8 2013 To address the mechanism of Zn(2+)-induced preferential generation of BimS, which lacks exon 4, we developed a Bim mini-gene construct. Zinc 28-31 BCL2 like 11 Homo sapiens 70-73 23624712-0 2013 4-Chlorobenzoyl berbamine, a novel berbamine derivative, induces apoptosis in multiple myeloma cells through the IL-6 signal transduction pathway and increases FOXO3a-Bim expression. 4-chlorobenzoylberbamine 0-25 BCL2 like 11 Homo sapiens 167-170 23624712-13 2013 These results suggest that BBD9 induces apoptosis in MM cells through the inhibition of the IL-6 signaling pathway, leading to FOXO3a activation and upregulation of pro-apoptotic Bim. bbd9 27-31 BCL2 like 11 Homo sapiens 179-182 23624712-0 2013 4-Chlorobenzoyl berbamine, a novel berbamine derivative, induces apoptosis in multiple myeloma cells through the IL-6 signal transduction pathway and increases FOXO3a-Bim expression. berbamine 16-25 BCL2 like 11 Homo sapiens 167-170 23801966-5 2013 Cellular ROS levels are affected by the FOXO-targets Bim, BclxL, and Survivin. Reactive Oxygen Species 9-12 BCL2 like 11 Homo sapiens 53-56 23801966-9 2013 This ability distinguishes Survivin from other anti-apoptotic proteins such as BclxL, which inhibits ROS by inactivating Bim but does not alter mitochondrial function. Reactive Oxygen Species 101-104 BCL2 like 11 Homo sapiens 121-124 23801966-7 2013 Bim-activation by FOXO3 causes mitochondrial depolarization resulting in a transitory decrease of respiration and ROS production. Reactive Oxygen Species 114-117 BCL2 like 11 Homo sapiens 0-3 23801966-11 2013 In this paper we discuss the hypothesis that the delicate balance between ROS-accumulation by Bim-triggered mitochondrial damage, mitochondrial architecture and ROS-detoxifying proteins determines cell fate. Reactive Oxygen Species 74-77 BCL2 like 11 Homo sapiens 94-97 23681223-0 2013 BECN1 and BIM interactions with MCL-1 determine fludarabine resistance in leukemic B cells. fludarabine 48-59 BCL2 like 11 Homo sapiens 10-13 23801206-6 2013 RESULTS: After treatment of different oxaliplatin concentrations in human colon carcinoma cells SW480 line, the cell growth was inhibited in a dose-dependent manner, while Bim and PUMA expressions were significantly up-regulated. Oxaliplatin 38-49 BCL2 like 11 Homo sapiens 172-175 23801206-11 2013 Induction of apoptosis of colon cancer cells by oxaliplatin may be associated with the up-regulation of BH3-only proteins, Bim and PUMA. Oxaliplatin 48-59 BCL2 like 11 Homo sapiens 123-126 23270470-0 2013 Gefitinib-resistance is related to BIM expression in non-small cell lung cancer cell lines. Gefitinib 0-9 BCL2 like 11 Homo sapiens 35-38 23403163-0 2013 Combination of a novel HDAC inhibitor OBP-801/YM753 and a PI3K inhibitor LY294002 synergistically induces apoptosis in human endometrial carcinoma cells due to increase of Bim with accumulation of ROS. YM753 compound 46-51 BCL2 like 11 Homo sapiens 172-175 23403163-0 2013 Combination of a novel HDAC inhibitor OBP-801/YM753 and a PI3K inhibitor LY294002 synergistically induces apoptosis in human endometrial carcinoma cells due to increase of Bim with accumulation of ROS. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 73-81 BCL2 like 11 Homo sapiens 172-175 23403163-0 2013 Combination of a novel HDAC inhibitor OBP-801/YM753 and a PI3K inhibitor LY294002 synergistically induces apoptosis in human endometrial carcinoma cells due to increase of Bim with accumulation of ROS. Reactive Oxygen Species 197-200 BCL2 like 11 Homo sapiens 172-175 23403163-8 2013 RESULTS: The combination of OBP-801/YM753 and LY294002 significantly inhibited the cell growth on comparison with each agent alone and synergistically increased apoptosis with the induction of Bim, a well-known apoptosis inducer. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 46-54 BCL2 like 11 Homo sapiens 193-196 23633923-3 2013 We show that BIM is epigenetically silenced in cell lines and lymph node specimens and that treatment with the deacetylase inhibitor trichostatin A restores the histone acetylation, strongly upregulates BIM expression, and induces cell death. trichostatin A 133-147 BCL2 like 11 Homo sapiens 13-16 23633923-3 2013 We show that BIM is epigenetically silenced in cell lines and lymph node specimens and that treatment with the deacetylase inhibitor trichostatin A restores the histone acetylation, strongly upregulates BIM expression, and induces cell death. trichostatin A 133-147 BCL2 like 11 Homo sapiens 203-206 23633923-5 2013 This event requires BIM CpG methylation/demethylation with 5-azacytidine that leads to detachment of the MeCP2 corepressor complex and reacetylation of the histone tails. Azacitidine 59-72 BCL2 like 11 Homo sapiens 20-23 23262244-0 2013 Heroin activates Bim via c-Jun N-terminal kinase/c-Jun pathway to mediate neuronal apoptosis. Heroin 0-6 BCL2 like 11 Homo sapiens 17-20 23262244-2 2013 In the present study, we found that heroin could induce apoptosis of primary cultured cerebellar granule cells (CGCs) and Bim was upregulated both transcriptionally and post transcriptionally during CGCs apoptosis. Heroin 36-42 BCL2 like 11 Homo sapiens 122-125 23262244-4 2013 Genetic knockdown of Bim using lentiviruses significantly prevented neuronal apoptosis induced by heroin. Heroin 98-104 BCL2 like 11 Homo sapiens 21-24 23262244-7 2013 These results indicate that Bim plays a critical role in the neurotoxic process by heroin and JNK/c-Jun pathway acts upstream of Bim in regulating heroin-induced neuronal death. Heroin 83-89 BCL2 like 11 Homo sapiens 28-31 23262244-7 2013 These results indicate that Bim plays a critical role in the neurotoxic process by heroin and JNK/c-Jun pathway acts upstream of Bim in regulating heroin-induced neuronal death. Heroin 147-153 BCL2 like 11 Homo sapiens 28-31 23262244-7 2013 These results indicate that Bim plays a critical role in the neurotoxic process by heroin and JNK/c-Jun pathway acts upstream of Bim in regulating heroin-induced neuronal death. Heroin 147-153 BCL2 like 11 Homo sapiens 129-132 23234544-0 2013 The BH3 mimetic ABT-263 synergizes with the MEK1/2 inhibitor selumetinib/AZD6244 to promote BIM-dependent tumour cell death and inhibit acquired resistance. BH 3 4-7 BCL2 like 11 Homo sapiens 92-95 23234544-0 2013 The BH3 mimetic ABT-263 synergizes with the MEK1/2 inhibitor selumetinib/AZD6244 to promote BIM-dependent tumour cell death and inhibit acquired resistance. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 16-19 BCL2 like 11 Homo sapiens 92-95 23234544-0 2013 The BH3 mimetic ABT-263 synergizes with the MEK1/2 inhibitor selumetinib/AZD6244 to promote BIM-dependent tumour cell death and inhibit acquired resistance. AZD 6244 61-72 BCL2 like 11 Homo sapiens 92-95 23234544-0 2013 The BH3 mimetic ABT-263 synergizes with the MEK1/2 inhibitor selumetinib/AZD6244 to promote BIM-dependent tumour cell death and inhibit acquired resistance. AZD 6244 73-80 BCL2 like 11 Homo sapiens 92-95 23274910-4 2013 Although Mcl-1 dominance renders SCC cells resistant to the BH3-mimetic ABT-737, vorinostat primes them for sensitivity to ABT-737 by shuttling Bim from Mcl-1 to Bcl-2/Bcl-xl, resulting in dramatic synergy for this combination and sustained tumor regression in vivo. Vorinostat 81-91 BCL2 like 11 Homo sapiens 144-147 23270470-3 2013 In this study, we found that in Gefitinib-sensitive cell lines, Gefitinib could induce tumor cell apoptosis via upregulation of a proapoptotic protein BIM. Gefitinib 32-41 BCL2 like 11 Homo sapiens 151-154 23270470-3 2013 In this study, we found that in Gefitinib-sensitive cell lines, Gefitinib could induce tumor cell apoptosis via upregulation of a proapoptotic protein BIM. Gefitinib 64-73 BCL2 like 11 Homo sapiens 151-154 23270470-4 2013 Small interfering RNA results showed that silencing of BIM could alleviate apoptosis induced by Gefitinib. Gefitinib 96-105 BCL2 like 11 Homo sapiens 55-58 23270470-6 2013 As expected, the combination substantially induced apoptosis and restored the sensitivity to Gefitinib by increasing the expression of BIM. Gefitinib 93-102 BCL2 like 11 Homo sapiens 135-138 23102022-8 2013 Given the well-established functions of Bcl-2 family proteins and ER calcium in drug resistance, our results suggest that the down-regulation of Mcl-1 and the up-regulation of Noxa and Bim along with the decrease in ER calcium content are likely responsible for CXL017-induced resensitization of MDR cancer cells. Calcium 69-76 BCL2 like 11 Homo sapiens 185-188 23425937-0 2013 Regulation of the FOXO3a/Bim signaling pathway by 5,7-dihydroxy-8-nitrochrysin in MDA-MB-453 breast cancer cells. 5,7-dihydroxy-8-nitrochrysin 50-78 BCL2 like 11 Homo sapiens 25-28 23266503-7 2013 We also showed that the down-regulation of Bcl-2 and concurrent increase in Bax and Bim levels contribute to the apoptosis induced by baicalein. baicalein 134-143 BCL2 like 11 Homo sapiens 84-87 23102022-8 2013 Given the well-established functions of Bcl-2 family proteins and ER calcium in drug resistance, our results suggest that the down-regulation of Mcl-1 and the up-regulation of Noxa and Bim along with the decrease in ER calcium content are likely responsible for CXL017-induced resensitization of MDR cancer cells. Calcium 219-226 BCL2 like 11 Homo sapiens 185-188 23000344-4 2013 Salubrinal inhibits ursolic acid-induced CHOP expression, Bim ER accumulation and caspase-3 activation in T24 cells. salubrinal 0-10 BCL2 like 11 Homo sapiens 58-61 23243017-13 2013 Together, these findings suggest that antileukemic synergism between PI3K/AKT/mTOR inhibitors and BH3 mimetics involves multiple mechanisms, including Mcl-1 downregulation, release of Bim from Bcl-2/Bcl-xL as well as Bak and Bax from Mcl-1/Bcl-2/Bcl-xL, and GSK3alpha/beta, culminating in Bax/Bak activation and apoptosis. BH 3 98-101 BCL2 like 11 Homo sapiens 184-187 23283967-4 2013 We also found a direct interaction between Bim, PUMA, or Noxa with either Bax or Bak during apoptosis induction. bakuchiol 81-84 BCL2 like 11 Homo sapiens 43-46 23257900-0 2013 Melatonin induces transcriptional regulation of Bim by FoxO3a in HepG2 cells. Melatonin 0-9 BCL2 like 11 Homo sapiens 48-51 23257900-4 2013 In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate whether melatonin treatment induces Bim through regulation by the transcription factor FoxO3a. Melatonin 98-107 BCL2 like 11 Homo sapiens 126-129 23257900-12 2013 During melatonin treatment, we observed increased transcriptional activity of the forkhead-responsive element and could demonstrate that FoxO3a binds to a specific sequence within the Bim promoter. Melatonin 7-16 BCL2 like 11 Homo sapiens 184-187 23257900-15 2013 CONCLUSION: This study shows that melatonin can induce apoptosis in HepG2 hepatocarcinoma cells through the upregulation of proapoptotic Bim mediated by nuclear translocation and activation of the transcription factor FoxO3a. Melatonin 34-43 BCL2 like 11 Homo sapiens 137-140 23085435-0 2013 Nitrogen-containing bisphosphonates induce apoptosis of hematopoietic tumor cells via inhibition of Ras signaling pathways and Bim-mediated activation of the intrinsic apoptotic pathway. Nitrogen 0-8 BCL2 like 11 Homo sapiens 127-130 23085435-0 2013 Nitrogen-containing bisphosphonates induce apoptosis of hematopoietic tumor cells via inhibition of Ras signaling pathways and Bim-mediated activation of the intrinsic apoptotic pathway. Diphosphonates 20-35 BCL2 like 11 Homo sapiens 127-130 23085435-4 2013 Furthermore, N-BPs decreased the levels of phosphorylated extracellular signal-regulated kinase (ERK) and mTOR via suppression of Ras prenylation and enhanced Bim expression. n-bps 13-18 BCL2 like 11 Homo sapiens 159-162 23085435-5 2013 The present results indicated that N-BPs induce apoptosis by decreasing the mitochondrial transmembrane potential, increasing the activation of caspase-9 and caspase-3, and enhancing Bim expression through inhibition of the Ras/MEK/ERK and Ras/mTOR pathways. n-bps 35-40 BCL2 like 11 Homo sapiens 183-186 23116058-0 2013 The BCL2L11 (BIM) deletion polymorphism is a possible criterion for discontinuation of imatinib in chronic myeloid leukaemia patients. Imatinib Mesylate 87-95 BCL2 like 11 Homo sapiens 4-11 23144237-8 2013 Knockdown of Bim using siRNA decreased apoptosis induced by treatment with saracatinib, suggesting that Bim has an important role in saracatinib-induced apoptosis. saracatinib 75-86 BCL2 like 11 Homo sapiens 13-16 23330014-6 2013 DHA down-regulates the protein expression of Bcl-2 and Bim mRNA level, and up-regulates caspase-3 activity and Bax expression level. Docosahexaenoic Acids 0-3 BCL2 like 11 Homo sapiens 55-58 23138847-0 2013 Involvement of the mitochondrial pathway and Bim/Bcl-2 balance in dihydroartemisinin-induced apoptosis in human breast cancer in vitro. artenimol 66-84 BCL2 like 11 Homo sapiens 45-48 23138847-5 2013 In addition, the apoptotic action of DHA was associated with the increased expression of the pro-apoptotic gene Bim and a decreased expression of the anti-apoptotic gene Bcl-2. artenimol 37-40 BCL2 like 11 Homo sapiens 124-127 23144237-8 2013 Knockdown of Bim using siRNA decreased apoptosis induced by treatment with saracatinib, suggesting that Bim has an important role in saracatinib-induced apoptosis. saracatinib 75-86 BCL2 like 11 Homo sapiens 104-107 23144237-8 2013 Knockdown of Bim using siRNA decreased apoptosis induced by treatment with saracatinib, suggesting that Bim has an important role in saracatinib-induced apoptosis. saracatinib 133-144 BCL2 like 11 Homo sapiens 13-16 23144237-8 2013 Knockdown of Bim using siRNA decreased apoptosis induced by treatment with saracatinib, suggesting that Bim has an important role in saracatinib-induced apoptosis. saracatinib 133-144 BCL2 like 11 Homo sapiens 104-107 23152053-3 2012 We investigated here whether prevention of Bim degradation by a proteasomal inhibitor, MG132, would induce apoptosis in mast cells with the D816V mutation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 87-92 BCL2 like 11 Homo sapiens 43-46 23254290-0 2012 TRAIL enhances paracetamol-induced liver sinusoidal endothelial cell death in a Bim- and Bid-dependent manner. Acetaminophen 15-26 BCL2 like 11 Homo sapiens 80-83 23254290-9 2012 TRAIL appears to enhance paracetamol-induced LSEC death via the activation of the pro-apoptotic BH3-only proteins Bid and Bim, which initiate the mitochondrial apoptotic pathway. Acetaminophen 25-36 BCL2 like 11 Homo sapiens 122-125 23533616-8 2013 Knockdown of CHOP attenuated MMC-induced apoptosis by increasing the ratio of BCL-2/BAX and decreasing BIM expression, suggesting that ER stress is involved in MMC-induced fibroblast apoptosis. Mitomycin 29-32 BCL2 like 11 Homo sapiens 103-106 23533616-10 2013 Reactive oxygen species (ROS) scavenging also decreased the expression of GRP78, phospho-PERK, CHOP, and BIM. Reactive Oxygen Species 0-23 BCL2 like 11 Homo sapiens 105-108 23533616-10 2013 Reactive oxygen species (ROS) scavenging also decreased the expression of GRP78, phospho-PERK, CHOP, and BIM. Reactive Oxygen Species 25-28 BCL2 like 11 Homo sapiens 105-108 23441183-0 2013 Pramanicin analog induces apoptosis in human colon cancer cells: critical roles for Bcl-2, Bim, and p38 MAPK signaling. pramanicin 0-10 BCL2 like 11 Homo sapiens 91-94 23001407-0 2012 miR-17-5p inhibitor enhances chemosensitivity to gemcitabine via upregulating Bim expression in pancreatic cancer cells. gemcitabine 49-60 BCL2 like 11 Homo sapiens 78-81 23152053-5 2012 MG132 at 1 muM induced apoptosis in all cell types, an effect accompanied by increased BH3-only proapoptotic protein Bim. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-5 BCL2 like 11 Homo sapiens 117-120 23152053-6 2012 The raise of Bim was accompanied by caspase-3 activation, and a caspase-3 inhibitor reduced MG132-induced apoptosis. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 92-97 BCL2 like 11 Homo sapiens 13-16 23152053-7 2012 Further, MG132 caused a reduction of activated Erk, a negative regulator of Bim expression, and thus Bim upregulation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 9-14 BCL2 like 11 Homo sapiens 76-79 23152053-7 2012 Further, MG132 caused a reduction of activated Erk, a negative regulator of Bim expression, and thus Bim upregulation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 9-14 BCL2 like 11 Homo sapiens 101-104 23152057-7 2012 We also noted that patients with a have high level of phospho-Bad and phospho-Bim displayed a lower OS. Osmium 100-102 BCL2 like 11 Homo sapiens 78-81 22539004-2 2012 We have previously shown that ATP depletion and activation of AMP-activated protein kinase (AMPK) during excitotoxic injury induces neuronal apoptosis by transcription of the pro-apoptotic BH3-only protein, Bim. Adenosine Triphosphate 30-33 BCL2 like 11 Homo sapiens 207-210 22539004-8 2012 Inhibition of this phosphorylation prevented Bim expression and protected neurons against excitotoxic and oxygen/glucose deprivation-induced injury. Oxygen 106-112 BCL2 like 11 Homo sapiens 45-48 22732497-0 2012 Fenofibrate-induced nuclear translocation of FoxO3A triggers Bim-mediated apoptosis in glioblastoma cells in vitro. Fenofibrate 0-11 BCL2 like 11 Homo sapiens 61-64 22465296-1 2012 The anti-cancer effects of bryostatin-1, a potent diacylglycerol analogue, have traditionally been attributed to its action on protein kinase C. However, we previously documented apoptosis in a B non-Hodgkin lymphoma cell line involving diacylglycerol analogue stimulation of Ras guanyl-releasing protein, a Ras activator, and Bim, a proapoptotic Bcl-2 family protein. bryostatin 1 27-39 BCL2 like 11 Homo sapiens 327-330 22825467-3 2012 BIM (BCL-2-interacting mediator of cell death), a BCL-2 homology 3-only pro-apoptotic protein, is upregulated by dexamethasone (Dex) treatment in acute lymphoblastic leukemia cells and has an essential role in Dex-induced apoptosis. Dexamethasone 113-126 BCL2 like 11 Homo sapiens 0-3 22825467-3 2012 BIM (BCL-2-interacting mediator of cell death), a BCL-2 homology 3-only pro-apoptotic protein, is upregulated by dexamethasone (Dex) treatment in acute lymphoblastic leukemia cells and has an essential role in Dex-induced apoptosis. Dexamethasone 113-126 BCL2 like 11 Homo sapiens 5-45 22825467-3 2012 BIM (BCL-2-interacting mediator of cell death), a BCL-2 homology 3-only pro-apoptotic protein, is upregulated by dexamethasone (Dex) treatment in acute lymphoblastic leukemia cells and has an essential role in Dex-induced apoptosis. Dexamethasone 128-131 BCL2 like 11 Homo sapiens 0-3 22825467-3 2012 BIM (BCL-2-interacting mediator of cell death), a BCL-2 homology 3-only pro-apoptotic protein, is upregulated by dexamethasone (Dex) treatment in acute lymphoblastic leukemia cells and has an essential role in Dex-induced apoptosis. Dexamethasone 128-131 BCL2 like 11 Homo sapiens 5-45 22825467-3 2012 BIM (BCL-2-interacting mediator of cell death), a BCL-2 homology 3-only pro-apoptotic protein, is upregulated by dexamethasone (Dex) treatment in acute lymphoblastic leukemia cells and has an essential role in Dex-induced apoptosis. Dexamethasone 210-213 BCL2 like 11 Homo sapiens 0-3 22825467-3 2012 BIM (BCL-2-interacting mediator of cell death), a BCL-2 homology 3-only pro-apoptotic protein, is upregulated by dexamethasone (Dex) treatment in acute lymphoblastic leukemia cells and has an essential role in Dex-induced apoptosis. Dexamethasone 210-213 BCL2 like 11 Homo sapiens 5-45 22825467-4 2012 It has been indicated that Dex-induced BIM is regulated mainly by transcription, however, the molecular mechanisms including responsible transcription factors are unclear. Dexamethasone 27-30 BCL2 like 11 Homo sapiens 39-42 22825467-5 2012 In this study, we found that Dex treatment induced transcription factor Runx2 and c-Jun in parallel with BIM induction. Dexamethasone 29-32 BCL2 like 11 Homo sapiens 105-108 22825467-6 2012 Dex-induced BIM and apoptosis were decreased in cells harboring dominant-negative c-Jun and were increased in cells with c-Jun overexpression. Dexamethasone 0-3 BCL2 like 11 Homo sapiens 12-15 22825467-9 2012 Treatment with RU486, a GC receptor antagonist, blocked Dex-induced Runx2, c-Jun and BIM induction, as well as apoptosis. Mifepristone 15-20 BCL2 like 11 Homo sapiens 85-88 22825467-9 2012 Treatment with RU486, a GC receptor antagonist, blocked Dex-induced Runx2, c-Jun and BIM induction, as well as apoptosis. Dexamethasone 56-59 BCL2 like 11 Homo sapiens 85-88 22825467-10 2012 Furthermore, pretreatment with SB203580, a p38-mitogen-activated protein kinase (MAPK) inhibitor, decreased Dex-induced Runx2, c-Jun and BIM, suggesting that p38-MAPK activation is upstream of the induction of these molecules. SB 203580 31-39 BCL2 like 11 Homo sapiens 137-140 22825467-10 2012 Furthermore, pretreatment with SB203580, a p38-mitogen-activated protein kinase (MAPK) inhibitor, decreased Dex-induced Runx2, c-Jun and BIM, suggesting that p38-MAPK activation is upstream of the induction of these molecules. Dexamethasone 108-111 BCL2 like 11 Homo sapiens 137-140 22391963-3 2012 In this study, we investigated the function of Bim during DHA-induced apoptosis in ASTC-a-1 and another human lung adenocarcinoma (A549) cell lines. Dihydroalprenolol 58-61 BCL2 like 11 Homo sapiens 47-50 22391963-4 2012 Confocal imaging of single living cell expressing GFP-BimL showed the translocation of Bim to endoplasmic reticulum (ER) rather than mitochondria during DHA-induced apoptosis. Dihydroalprenolol 153-156 BCL2 like 11 Homo sapiens 54-57 22391963-5 2012 Moreover, we also found that DHA induced ER stress and an increase of Bim protein levels. Dihydroalprenolol 29-32 BCL2 like 11 Homo sapiens 70-73 22391963-7 2012 Taken together, our results demonstrate for the first time that DHA induces Bim translocation to ER, but DHA-induced apoptosis is not dependent on Bim in ASTC-a-1 and A549 cell lines. Dihydroalprenolol 64-67 BCL2 like 11 Homo sapiens 76-79 22693249-6 2012 Mechanistic investigations revealed that flavopiridol inhibited Mcl-1 transcription but increased transcription of Bim and its binding to Bcl-2/Bcl-xL. alvocidib 41-53 BCL2 like 11 Homo sapiens 115-118 22693249-9 2012 Notably, short hairpin RNA knockdown of Bim or Noxa abrogated lethality triggered by the flavopiridol/obatoclax combination in vitro and in vivo. alvocidib 89-101 BCL2 like 11 Homo sapiens 40-43 22589275-5 2012 The Bcl-2/Bcl-xL/Bcl-w inhibitor ABT-737 showed single-agent activity against only Bim:Bcl-2 primed tumor xenografts. ABT-737 33-40 BCL2 like 11 Homo sapiens 83-86 21739479-0 2012 Bim contributes to phenethyl isothiocyanate-induced apoptosis in breast cancer cells. phenethyl isothiocyanate 19-43 BCL2 like 11 Homo sapiens 0-3 22576693-6 2012 Furthermore, DNA methylation analysis showed that the BPA exposure induced the hypermethylation of BCL2L11, PARD6G, FOXP1 and SFRS11, as well as the hypomethylation of NUP98 and CtIP (RBBP8). bisphenol A 54-57 BCL2 like 11 Homo sapiens 99-106 22261340-3 2012 Fisetin enhanced caspase-3 activation, downregulation of Bcl-2 and Mcl-1(L), and upregulation of Bax, Bim and Bad. fisetin 0-7 BCL2 like 11 Homo sapiens 102-105 22446485-0 2012 Inhibition of Bcl-2 antiapoptotic members by obatoclax potently enhances sorafenib-induced apoptosis in human myeloid leukemia cells through a Bim-dependent process. Sorafenib 73-82 BCL2 like 11 Homo sapiens 143-146 22446485-3 2012 Sorafenib triggered rapid and pronounced Mcl-1 down-regulation accompanied by enhanced binding of Bim to Bcl-2 and Bcl-xL, effects that were abolished by obatoclax coadministration. Sorafenib 0-9 BCL2 like 11 Homo sapiens 98-101 22446485-4 2012 Notably, shRNA knockdown of Bim, Bak, or Bax, but not Noxa, significantly attenuated obatoclax/sorafenib lethality, whereas ectopic expression of Mcl-1 exerted a protective effect. Sorafenib 95-104 BCL2 like 11 Homo sapiens 28-31 22525702-3 2012 Compared with parental cells, cells that have developed acquired resistance to ABT-737 showed increased expression of Mcl-1 in addition to posttranslational modifications that facilitated both Mcl-1 stabilization and its interaction with the BH3-only protein Bim. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 79-82 BCL2 like 11 Homo sapiens 259-262 22538851-4 2012 Moreover, we show that increasing Bcl-2 sensitized normal and transformed lymphoid cells to ABT-737 by elevating proapoptotic Bim. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 92-95 BCL2 like 11 Homo sapiens 126-129 22538851-6 2012 Cell-based protein redistribution assays unexpectedly revealed that ABT-737 disrupts Bcl-2/Bim complexes more readily than Bcl-x(L)/Bim or Bcl-w/Bim complexes. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 68-71 BCL2 like 11 Homo sapiens 91-94 22622039-4 2012 We harnessed the natural killing activity of BCL-2-interacting mediator of cell death (BIM), which contains one of the most potent BH3 death domains of the BCL-2 protein family, to restore BH3-dependent cell death in resistant hematologic cancers. BH 3 131-134 BCL2 like 11 Homo sapiens 45-85 21986940-6 2012 BH3-only members, Bim and Bmf, were upregulated by 2DG, and shRNAs targeting Bim protected from 2DG toxicity demonstrating that Bim is a critical mediator of 2DG toxicity. Deoxyglucose 51-54 BCL2 like 11 Homo sapiens 18-21 21986940-6 2012 BH3-only members, Bim and Bmf, were upregulated by 2DG, and shRNAs targeting Bim protected from 2DG toxicity demonstrating that Bim is a critical mediator of 2DG toxicity. Deoxyglucose 96-99 BCL2 like 11 Homo sapiens 77-80 21986940-6 2012 BH3-only members, Bim and Bmf, were upregulated by 2DG, and shRNAs targeting Bim protected from 2DG toxicity demonstrating that Bim is a critical mediator of 2DG toxicity. Deoxyglucose 96-99 BCL2 like 11 Homo sapiens 77-80 21986940-6 2012 BH3-only members, Bim and Bmf, were upregulated by 2DG, and shRNAs targeting Bim protected from 2DG toxicity demonstrating that Bim is a critical mediator of 2DG toxicity. Deoxyglucose 96-99 BCL2 like 11 Homo sapiens 77-80 21986940-6 2012 BH3-only members, Bim and Bmf, were upregulated by 2DG, and shRNAs targeting Bim protected from 2DG toxicity demonstrating that Bim is a critical mediator of 2DG toxicity. Deoxyglucose 96-99 BCL2 like 11 Homo sapiens 77-80 21986940-7 2012 2DG also induced GADD153/CHOP expression, a marker of endoplasmic reticulum (ER) stress and a known activator of Bim. Deoxyglucose 0-3 BCL2 like 11 Homo sapiens 113-116 22351689-9 2012 Although response to RAF265 did not correlate with pERK1/2 reduction, RAF265 responders did exhibit reduced pMEK1, reduced proliferation based upon reduced Ki-67, cyclin D1 and polo-like kinase1 levels, and induction of the apoptosis mediator BCL2-like 11. RAF265 70-76 BCL2 like 11 Homo sapiens 243-255 21732363-0 2012 18beta-glycyrrhetinic acid induces apoptosis through modulation of Akt/FOXO3a/Bim pathway in human breast cancer MCF-7 cells. 18alpha-glycyrrhetinic acid 0-26 BCL2 like 11 Homo sapiens 78-81 21732363-6 2012 GRA induced an increase in Bax:Bcl-2 ratio along with a significant increase in the protein level of the BH3 protein Bim. 18alpha-glycyrrhetinic acid 0-3 BCL2 like 11 Homo sapiens 117-120 22211565-6 2012 Treatment with CR2408 results in increased protein levels of Bim and pJNK and downregulation of Bad and Bcl-xL and activation of Caspases 3, 8 and 9. CR2408 15-21 BCL2 like 11 Homo sapiens 61-64 22402663-5 2012 Accordingly, lysine methylation reduces oxidative stress-induced and FOXO3-mediated Bim expression and neuronal apoptosis in neurons. Lysine 13-19 BCL2 like 11 Homo sapiens 84-87 22549588-2 2012 Using a cell-based kinase inhibitor screening assay, we identified the compound bisindoylmaleimide I (BIM) as a potent agonist of the cytosolic beta-catenin accumulation in preosteoblast cells. bisindolylmaleimide I 80-100 BCL2 like 11 Homo sapiens 102-105 22235114-9 2012 Forkhead Box Protein O3a (FoxO3a), a well defined transcriptional activator of Bim, was phosphorylated at Ser-253 and inactivated after FSH stimulation. Serine 106-109 BCL2 like 11 Homo sapiens 79-82 22245094-0 2012 Skin mild hypoxia enhances killing of UVB-damaged keratinocytes through reactive oxygen species-mediated apoptosis requiring Noxa and Bim. Reactive Oxygen Species 72-95 BCL2 like 11 Homo sapiens 134-137 22245094-6 2012 Prolonged exposure of UVB-treated NHKs to hypoxia triggers a sustained and reactive oxygen species-dependent activation of the stress kinases p38(MAPK) and JNKs, which in turn, engage the activation of Noxa and Bim proapoptotic proteins. Reactive Oxygen Species 75-98 BCL2 like 11 Homo sapiens 211-214 22349704-3 2012 After knockdown of FOXO3 or expression of a dominant-negative FOXO3 mutant we observed that etoposide- and doxorubicin-induced elevation of cellular ROS depends on FOXO3 activation and induction of its transcriptional target BCL2L11 (Bim). Etoposide 92-101 BCL2 like 11 Homo sapiens 225-232 22349704-3 2012 After knockdown of FOXO3 or expression of a dominant-negative FOXO3 mutant we observed that etoposide- and doxorubicin-induced elevation of cellular ROS depends on FOXO3 activation and induction of its transcriptional target BCL2L11 (Bim). Doxorubicin 107-118 BCL2 like 11 Homo sapiens 225-232 22349704-0 2012 FOXO3-induced reactive oxygen species are regulated by BCL2L11 (Bim) and SESN3. Reactive Oxygen Species 14-37 BCL2 like 11 Homo sapiens 55-62 22349704-3 2012 After knockdown of FOXO3 or expression of a dominant-negative FOXO3 mutant we observed that etoposide- and doxorubicin-induced elevation of cellular ROS depends on FOXO3 activation and induction of its transcriptional target BCL2L11 (Bim). Reactive Oxygen Species 149-152 BCL2 like 11 Homo sapiens 225-232 22624338-6 2012 Western blot analysis demonstrated that oxaliplatin could induce apoptosis of L02 cells by reducing the Bcl-2/Bim ratio, stimulating the cytochrome c release, and activating caspase-3. Oxaliplatin 40-51 BCL2 like 11 Homo sapiens 110-113 22038922-6 2012 Iron and BCL2-interacting mediator of cell death (BIM) protein were involved in LCN2-induced cell death sensitization, based on the studies using iron donor, chelator, siderophore, and short hairpin RNA (shRNA)-mediated knockdown of bim expression. Iron 0-4 BCL2 like 11 Homo sapiens 50-53 22038922-6 2012 Iron and BCL2-interacting mediator of cell death (BIM) protein were involved in LCN2-induced cell death sensitization, based on the studies using iron donor, chelator, siderophore, and short hairpin RNA (shRNA)-mediated knockdown of bim expression. Iron 0-4 BCL2 like 11 Homo sapiens 233-236 22038922-6 2012 Iron and BCL2-interacting mediator of cell death (BIM) protein were involved in LCN2-induced cell death sensitization, based on the studies using iron donor, chelator, siderophore, and short hairpin RNA (shRNA)-mediated knockdown of bim expression. Iron 146-150 BCL2 like 11 Homo sapiens 50-53 22399804-9 2012 The pro-apoptotic protein BIM (also known as BCL2L11) is recruited to mitochondria in response to vinorelbine, where it can inhibit the anti-apoptotic protein BCL2, suggesting that BIM mediates vinorelbine-induced cell death. Vinorelbine 98-109 BCL2 like 11 Homo sapiens 45-52 22399804-9 2012 The pro-apoptotic protein BIM (also known as BCL2L11) is recruited to mitochondria in response to vinorelbine, where it can inhibit the anti-apoptotic protein BCL2, suggesting that BIM mediates vinorelbine-induced cell death. Vinorelbine 194-205 BCL2 like 11 Homo sapiens 45-52 23300762-2 2012 We have previously found that resistance to the proteasome inhibitor bortezomib in 3D can be explained by a lack of upregulation of Noxa, the pro-apoptotic BH3 sensitizer that acts via displacement of the Bak/Bax-activator BH3-only protein, Bim. Bortezomib 69-79 BCL2 like 11 Homo sapiens 241-244 22131152-8 2012 The apoptotic effects on BL cell lines of NaB/VP-16 and NaB/CDDP were followed by upregulation of Bim protein (P < 0.05), activation of caspase-3 and caspase-9, followed by Mcl-1 downregulation (P < 0.05). nab 42-45 BCL2 like 11 Homo sapiens 98-101 22131152-8 2012 The apoptotic effects on BL cell lines of NaB/VP-16 and NaB/CDDP were followed by upregulation of Bim protein (P < 0.05), activation of caspase-3 and caspase-9, followed by Mcl-1 downregulation (P < 0.05). Cisplatin 60-64 BCL2 like 11 Homo sapiens 98-101 21965604-8 2012 Further investigation revealed that post-translationally myristoylated ctPKCepsilon localized to membranes and increased Erk signaling and degradation of the proapoptotic protein Bim, which prevented a significant loss of mitochondrial potential of 17% over nonmyristoylated ctPKCepsilon in HeLa cells in the presence of apoptotic stimuli. ctpkcepsilon 71-83 BCL2 like 11 Homo sapiens 179-182 21965604-8 2012 Further investigation revealed that post-translationally myristoylated ctPKCepsilon localized to membranes and increased Erk signaling and degradation of the proapoptotic protein Bim, which prevented a significant loss of mitochondrial potential of 17% over nonmyristoylated ctPKCepsilon in HeLa cells in the presence of apoptotic stimuli. ctpkcepsilon 275-287 BCL2 like 11 Homo sapiens 179-182 23285061-0 2012 ABT-737 induces Bim expression via JNK signaling pathway and its effect on the radiation sensitivity of HeLa cells. ABT-737 0-7 BCL2 like 11 Homo sapiens 16-19 23285061-1 2012 ABT-737 is a BH3 mimetic small molecule inhibitor that can effectively inhibit the activity of antiapoptotic Bcl-2 family proteins including Bcl2, Bcl-xL and Bcl-w, and further enhances the effect of apoptosis by activating the proapoptotic proteins (t-Bid, Bad, Bim). ABT-737 0-7 BCL2 like 11 Homo sapiens 263-266 23285061-3 2012 Our results show that ABT-737 inhibited HeLa cell proliferation and activated JNK and its downstream target c-Jun, which caused the up-regulation of Bim expression. ABT-737 22-29 BCL2 like 11 Homo sapiens 149-152 22391178-9 2012 The expression levels of caspase-3 mRNA and Bim mRNA in KM3 cells treated with Bor plus As(2)O(3) were higher than that in KM3 cells treated with Bor alone. Bortezomib 79-82 BCL2 like 11 Homo sapiens 44-47 22391178-11 2012 It is concluded that As(2)O(3) can enhance the apoptosis-inducing effect of Bor on multiple myeloma cell line KM3, which is associated with decreasing the expression of Bcl-xl mRNA and increasing the expression of Caspase-3 and Bim mRNA. (2)o(3) 23-30 BCL2 like 11 Homo sapiens 228-231 22391178-11 2012 It is concluded that As(2)O(3) can enhance the apoptosis-inducing effect of Bor on multiple myeloma cell line KM3, which is associated with decreasing the expression of Bcl-xl mRNA and increasing the expression of Caspase-3 and Bim mRNA. Bortezomib 76-79 BCL2 like 11 Homo sapiens 228-231 22048238-0 2012 Phenylarsine oxide induces apoptosis in Bax- and Bak-deficient cells through upregulation of Bim. oxophenylarsine 0-18 BCL2 like 11 Homo sapiens 93-96 22048238-11 2012 PAO augmented the expression of Bim and strengthened the interaction between Bim and Bcl-2. oxophenylarsine 0-3 BCL2 like 11 Homo sapiens 32-35 22048238-11 2012 PAO augmented the expression of Bim and strengthened the interaction between Bim and Bcl-2. oxophenylarsine 0-3 BCL2 like 11 Homo sapiens 77-80 21897270-0 2012 Oleanen induces apoptosis of cervical cancer cells by up-regulation of Bim. oleanen 0-7 BCL2 like 11 Homo sapiens 71-74 21897270-10 2012 Furthermore, the increase in the expression of Bim was the most significant among the Bcl-2 family after oleanen treatment. 12-oleanene-3beta,6alpha-diol 105-112 BCL2 like 11 Homo sapiens 47-50 21897270-11 2012 CONCLUSION: Oleanen up-regulates the expression of Bim and other proapoptotic molecules to activate the endogenous apoptosis pathway, thus promoting apoptosis and inhibiting proliferation of human cervical cancer HeLa cells in vitro. oleanen 12-19 BCL2 like 11 Homo sapiens 51-54 23285061-4 2012 Blockade of JNK/c-Jun signaling pathway resulted in significant down-regulation of ABT-737-induced Bim mRNA and protein expression level. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 83-86 BCL2 like 11 Homo sapiens 99-102 23285061-5 2012 Also, ABT-737 could evoke the Bim promoter activity, and enhance the radiation sensitivity of HeLa cells via JNK/c-Jun and Bim signaling pathway. ABT-737 6-13 BCL2 like 11 Homo sapiens 30-33 23285061-5 2012 Also, ABT-737 could evoke the Bim promoter activity, and enhance the radiation sensitivity of HeLa cells via JNK/c-Jun and Bim signaling pathway. ABT-737 6-13 BCL2 like 11 Homo sapiens 123-126 23300762-5 2012 The ability of vorinostat to reverse resistance was ablated by knockdown of Noxa or Bim, confirming the essential role of the Noxa/Bim axis in the response to vorinostat. Vorinostat 15-25 BCL2 like 11 Homo sapiens 84-87 23300762-5 2012 The ability of vorinostat to reverse resistance was ablated by knockdown of Noxa or Bim, confirming the essential role of the Noxa/Bim axis in the response to vorinostat. Vorinostat 15-25 BCL2 like 11 Homo sapiens 131-134 23300762-5 2012 The ability of vorinostat to reverse resistance was ablated by knockdown of Noxa or Bim, confirming the essential role of the Noxa/Bim axis in the response to vorinostat. Vorinostat 159-169 BCL2 like 11 Homo sapiens 131-134 22355769-1 2012 Recently we reported that the BH3-only proteins Bim and Noxa bind tightly but transiently to the BH3-binding groove of Bak to initiate Bak homo-oligomerization. BH 3 30-33 BCL2 like 11 Homo sapiens 48-51 22355769-4 2012 In particular, upon binding to the BH3-binding groove, Bim and Noxa induce a large conformational change of the loop between helices 1 and 2 and in turn partially expose a remote groove between helices 1 and 6 in Bak. BH 3 35-38 BCL2 like 11 Homo sapiens 55-58 20697841-4 2011 The significant up-regulation of BIM in CEM-C7 cells induced by DEX was also observed, but no up-regulation of BIM was detected in DEX-induced CEM-C1 cells. Dextromethorphan 64-67 BCL2 like 11 Homo sapiens 33-36 22157681-5 2011 We showed that these miRNAs have important roles in gefitinib-induced apoptosis and epithelial-mesenchymal transition of NSCLC cells in vitro and in vivo by inhibiting the expression of the genes encoding BCL2-like 11 (BIM), apoptotic peptidase activating factor 1 (APAF-1), protein kinase C e (PKC-e) and sarcoma viral oncogene homolog (SRC). Gefitinib 52-61 BCL2 like 11 Homo sapiens 205-217 22115332-0 2011 Flavokawain B induces apoptosis of human oral adenoid cystic cancer ACC-2 cells via up-regulation of Bim and down-regulation of Bcl-2 expression. flavokawain B 0-13 BCL2 like 11 Homo sapiens 101-104 22115332-6 2011 Among them, Bim expression was significantly induced by FKB, and knockdown of Bim expression by short-hairpin RNAs attenuated the inhibitory effect induced by FKB on ACC-2 cells. flavokawain B 56-59 BCL2 like 11 Homo sapiens 12-15 22101335-7 2011 Cytochrome c release from mitochondria to the cytosol in curcumin-treated cells was associated with upregulation of proapoptotic proteins such as Bax, Bak, Bid, and Bim. Curcumin 57-65 BCL2 like 11 Homo sapiens 165-168 22101335-8 2011 Crosslinking experiments demonstrated Bax oligomerization during curcumin-induced apoptosis, suggesting that induced expression of Bax, Bid, and Bim causes Bax-channel formation on the mitochondrial membrane. Curcumin 65-73 BCL2 like 11 Homo sapiens 145-148 20697841-5 2011 When treated with DEX plus RU486, a glucocorticoid receptor blocker, the apoptosis and BIM expression of CEM-C7 cells were canceled. Dextromethorphan 18-21 BCL2 like 11 Homo sapiens 87-90 20697841-5 2011 When treated with DEX plus RU486, a glucocorticoid receptor blocker, the apoptosis and BIM expression of CEM-C7 cells were canceled. Mifepristone 27-32 BCL2 like 11 Homo sapiens 87-90 20697841-6 2011 P38MAPK-blocking pharmacon SB203580 also significantly inhibited the up-regulation of BIM in CEM-C7 cells. SB 203580 27-35 BCL2 like 11 Homo sapiens 86-89 21787858-6 2011 Pretreatment with 1 muM CdCl2 also attenuated the decrease in Mcl-1 and the increases in Bim, Noxa and tBid induced by 50 muM CdCl2. Cadmium Chloride 24-29 BCL2 like 11 Homo sapiens 89-92 21787858-6 2011 Pretreatment with 1 muM CdCl2 also attenuated the decrease in Mcl-1 and the increases in Bim, Noxa and tBid induced by 50 muM CdCl2. Cadmium Chloride 126-131 BCL2 like 11 Homo sapiens 89-92 21710254-5 2011 The susceptibility of cells toward WFA-induced apoptosis correlated with low Bcl-2/Bax and Bcl-2/Bim ratios. withaferin A 35-38 BCL2 like 11 Homo sapiens 97-100 21958719-9 2011 Silencing of Bim using siRNA transfected into hepatocytes also prevented cell death resulting from 8-OHEFV-treatment. 8-ohefv 99-106 BCL2 like 11 Homo sapiens 13-16 22071694-2 2011 Here we report that the pro-apoptotic BH3-only family member Bim undergoes phosphorylation in K562 cells following treatment with the microtubule targeting agents Taxol and Nocodazole. Paclitaxel 163-168 BCL2 like 11 Homo sapiens 61-64 22071694-2 2011 Here we report that the pro-apoptotic BH3-only family member Bim undergoes phosphorylation in K562 cells following treatment with the microtubule targeting agents Taxol and Nocodazole. Nocodazole 173-183 BCL2 like 11 Homo sapiens 61-64 22071694-3 2011 The phosphorylation of two Bim isoforms, BimEL and BimL, at the mitochondria correlates with mitotic arrest and precedes cell death induced by Taxol. Paclitaxel 143-148 BCL2 like 11 Homo sapiens 27-30 22071694-5 2011 In addition, siRNA silencing of Bim reduces sensitivity to Taxol-induced cell death. Paclitaxel 59-64 BCL2 like 11 Homo sapiens 32-35 22071694-7 2011 The Cdk1 inhibitors, RO-3306 and Purvalanol A, block Bim phosphorylation in mitotically arrested cells. RO 3306 21-28 BCL2 like 11 Homo sapiens 53-56 22071694-7 2011 The Cdk1 inhibitors, RO-3306 and Purvalanol A, block Bim phosphorylation in mitotically arrested cells. 6-((3-chloro)anilino)-2-(isopropyl-2-hydroxyethylamino)-9-isopropylpurine 33-45 BCL2 like 11 Homo sapiens 53-56 21673341-4 2011 Tipifarnib caused dose-dependent up-regulation of Bim in lymphoid cell lines (Jurkat, Molt3, H9, DoHH2, and RL) that undergo tipifarnib-induced apoptosis but not in lines (SKW6.4 and Hs445) that resist tipifarnib-induced apoptosis. tipifarnib 0-10 BCL2 like 11 Homo sapiens 50-53 21673341-4 2011 Tipifarnib caused dose-dependent up-regulation of Bim in lymphoid cell lines (Jurkat, Molt3, H9, DoHH2, and RL) that undergo tipifarnib-induced apoptosis but not in lines (SKW6.4 and Hs445) that resist tipifarnib-induced apoptosis. tipifarnib 125-135 BCL2 like 11 Homo sapiens 50-53 21673341-4 2011 Tipifarnib caused dose-dependent up-regulation of Bim in lymphoid cell lines (Jurkat, Molt3, H9, DoHH2, and RL) that undergo tipifarnib-induced apoptosis but not in lines (SKW6.4 and Hs445) that resist tipifarnib-induced apoptosis. tipifarnib 202-212 BCL2 like 11 Homo sapiens 50-53 21673341-7 2011 These results not only trace a pathway through c-Raf to Bim that contributes to tipifarnib cytotoxicity in human lymphoid cells but also identify potential determinants of sensitivity to this agent. tipifarnib 80-90 BCL2 like 11 Homo sapiens 56-59 21697949-7 2011 ABT-737 was active in spheroids grown from those tumors (5/7, ~70%) with elevated levels of Bim. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 0-3 BCL2 like 11 Homo sapiens 92-95 21816906-0 2011 MicroRNA-32 upregulation by 1,25-dihydroxyvitamin D3 in human myeloid leukemia cells leads to Bim targeting and inhibition of AraC-induced apoptosis. Calcitriol 28-52 BCL2 like 11 Homo sapiens 94-97 21597002-8 2011 Overlapping the gene expression profiles of MV human diaphragm and H2O2-treated muscle cells, we identify Fos, FoxO1, and Stat3 as regulators of Bim expression as well as of expression of the catabolic markers atrogin and LC3. Hydrogen Peroxide 67-71 BCL2 like 11 Homo sapiens 145-148 21659544-5 2011 Consistent with these findings, acquired resistance to ABT-737 results in loss of codependence through redistribution of Bim to Mcl-1. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 55-58 BCL2 like 11 Homo sapiens 121-124 21762482-5 2011 RESULTS: We report that U0126, an inhibitor of the prosurvival MEK-ERK pathway, increases bim mRNA levels in sympathetic neurons in the presence of NGF. U 0126 24-29 BCL2 like 11 Homo sapiens 90-93 21825007-5 2011 Signaling studies indicated that increased expression of Bim protein and reduced X-linked inhibitor of apoptosis protein and Mcl-1(L) levels were involved in nocodazole-induced apoptosis. Nocodazole 158-168 BCL2 like 11 Homo sapiens 57-60 21499301-4 2011 Lapatinib induced apoptosis in association with upregulation of the pro-apoptotic protein Bcl-2 interacting mediator of cell death (BIM) through inhibition of the MEK-ERK signaling pathway in breast cancer cells with HER2 amplification. Lapatinib 0-9 BCL2 like 11 Homo sapiens 132-135 21499301-5 2011 RNA interference (RNAi)-mediated depletion of BIM inhibited lapatinib-induced apoptosis, implicating BIM induction in this process. Lapatinib 60-69 BCL2 like 11 Homo sapiens 46-49 21628457-4 2011 We show that ABT-737 is the only BH3 mimetic that inhibits BCL2 as assessed by displacement of BAD and BIM from BCL2. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 13-16 BCL2 like 11 Homo sapiens 103-106 21628457-4 2011 We show that ABT-737 is the only BH3 mimetic that inhibits BCL2 as assessed by displacement of BAD and BIM from BCL2. BH 3 33-36 BCL2 like 11 Homo sapiens 103-106 22093624-9 2011 With exposure to tunicamycin (3 micromol/L) for 12, 24, 36 hours the Bim protein levels were not increased in Mel-RM and MM200 cells. Tunicamycin 17-28 BCL2 like 11 Homo sapiens 69-72 21561860-0 2011 Bim protein degradation contributes to cisplatin resistance. Cisplatin 39-48 BCL2 like 11 Homo sapiens 0-3 21561860-3 2011 Here we show that degradation of the Bcl-2 homology 3-only proapoptotic protein Bim plays an important role in cisplatin resistance in ovarian cancer. Cisplatin 111-120 BCL2 like 11 Homo sapiens 80-83 21561860-4 2011 Specifically, we show that treatment of ovarian cancer cells with cisplatin caused Bim phosphorylation and subsequent degradation and that its degradation is associated with cisplatin resistance. Cisplatin 66-75 BCL2 like 11 Homo sapiens 83-86 21561860-5 2011 We also show that cisplatin treatment caused the activation of ERK, which correlated with Bim phosphorylation and degradation. Cisplatin 18-27 BCL2 like 11 Homo sapiens 90-93 21561860-6 2011 By inhibiting ERK phosphorylation with the MEK inhibitor and knocking down ERK expression with siRNA, we show that Bim phosphorylation and degradation were blocked, which suggests that Bim is phosphorylated by ERK and that such phosphorylation is responsible for cisplatin-induced Bim degradation. Cisplatin 263-272 BCL2 like 11 Homo sapiens 115-118 21561860-6 2011 By inhibiting ERK phosphorylation with the MEK inhibitor and knocking down ERK expression with siRNA, we show that Bim phosphorylation and degradation were blocked, which suggests that Bim is phosphorylated by ERK and that such phosphorylation is responsible for cisplatin-induced Bim degradation. Cisplatin 263-272 BCL2 like 11 Homo sapiens 185-188 21561860-6 2011 By inhibiting ERK phosphorylation with the MEK inhibitor and knocking down ERK expression with siRNA, we show that Bim phosphorylation and degradation were blocked, which suggests that Bim is phosphorylated by ERK and that such phosphorylation is responsible for cisplatin-induced Bim degradation. Cisplatin 263-272 BCL2 like 11 Homo sapiens 185-188 21561860-8 2011 We also show that Bim was phosphorylated and degraded in cisplatin-resistant OV433 cells but not in the parental OV433 cells. Cisplatin 57-66 BCL2 like 11 Homo sapiens 18-21 21561860-9 2011 Importantly, we show that inhibition of Bim degradation by the proteasome inhibitor MG132 sensitized resistant OV433 cells to cisplatin-induced death. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 84-89 BCL2 like 11 Homo sapiens 40-43 21561860-9 2011 Importantly, we show that inhibition of Bim degradation by the proteasome inhibitor MG132 sensitized resistant OV433 cells to cisplatin-induced death. Cisplatin 126-135 BCL2 like 11 Homo sapiens 40-43 21561860-10 2011 Taken together, our data indicate that degradation of Bim via ERK-mediated phosphorylation can lead to cisplatin resistance. Cisplatin 103-112 BCL2 like 11 Homo sapiens 54-57 21130142-0 2011 BIM is a prognostic biomarker for early prednisolone response in pediatric acute lymphoblastic leukemia. Prednisolone 40-52 BCL2 like 11 Homo sapiens 0-3 20237869-4 2011 Gefitinib provoked apoptosis of caspase activation via the intrinsic pathways and significantly up-regulated expression of BIM protein in drug-sensitive PC-9 cell line, but not resistant PC-9/BB4 cell line. Gefitinib 0-9 BCL2 like 11 Homo sapiens 123-126 20237869-5 2011 The knockdown of BIM expression by RNA interference virtually eliminated gefitinib-induced cell killing in PC-9 cells in vitro. Gefitinib 73-82 BCL2 like 11 Homo sapiens 17-20 21148306-0 2011 The BH3 alpha-helical mimic BH3-M6 disrupts Bcl-X(L), Bcl-2, and MCL-1 protein-protein interactions with Bax, Bak, Bad, or Bim and induces apoptosis in a Bax- and Bim-dependent manner. BH 3 4-7 BCL2 like 11 Homo sapiens 123-126 21148306-0 2011 The BH3 alpha-helical mimic BH3-M6 disrupts Bcl-X(L), Bcl-2, and MCL-1 protein-protein interactions with Bax, Bak, Bad, or Bim and induces apoptosis in a Bax- and Bim-dependent manner. BH 3 4-7 BCL2 like 11 Homo sapiens 163-166 21148306-3 2011 We designed a BH3 alpha-helical mimetic BH3-M6 that binds to Bcl-X(L) and Mcl-1 and prevents their binding to fluorescently labeled Bak- or Bim-BH3 peptides in vitro. BH 3 14-17 BCL2 like 11 Homo sapiens 140-143 21148306-3 2011 We designed a BH3 alpha-helical mimetic BH3-M6 that binds to Bcl-X(L) and Mcl-1 and prevents their binding to fluorescently labeled Bak- or Bim-BH3 peptides in vitro. bh3-m6 40-46 BCL2 like 11 Homo sapiens 140-143 21367852-6 2011 ABT-737-induced Bax activation and apoptosis were also observed in Bid/Bim-deficient platelets. ABT-737 0-7 BCL2 like 11 Homo sapiens 71-74 21415216-7 2011 Depletion of BIM and overexpression of survivin each inhibited TAE684-induced apoptosis, suggesting that both upregulation of BIM and downregulation of survivin contribute to TAE684-induced apoptosis in EML4-ALK-positive lung cancer cells. NVP-TAE684 63-69 BCL2 like 11 Homo sapiens 13-16 21415216-7 2011 Depletion of BIM and overexpression of survivin each inhibited TAE684-induced apoptosis, suggesting that both upregulation of BIM and downregulation of survivin contribute to TAE684-induced apoptosis in EML4-ALK-positive lung cancer cells. NVP-TAE684 63-69 BCL2 like 11 Homo sapiens 126-129 21415216-7 2011 Depletion of BIM and overexpression of survivin each inhibited TAE684-induced apoptosis, suggesting that both upregulation of BIM and downregulation of survivin contribute to TAE684-induced apoptosis in EML4-ALK-positive lung cancer cells. NVP-TAE684 175-181 BCL2 like 11 Homo sapiens 126-129 21375523-0 2011 Bortezomib interacts synergistically with belinostat in human acute myeloid leukaemia and acute lymphoblastic leukaemia cells in association with perturbations in NF-kappaB and Bim. Bortezomib 0-10 BCL2 like 11 Homo sapiens 177-180 21375523-5 2011 Moreover, belinostat/bortezomib co-exposure induced up-regulation of the BH3-only pro-death protein Bim. belinostat 10-20 BCL2 like 11 Homo sapiens 100-103 21375523-5 2011 Moreover, belinostat/bortezomib co-exposure induced up-regulation of the BH3-only pro-death protein Bim. Bortezomib 21-31 BCL2 like 11 Homo sapiens 100-103 21375523-6 2011 Significantly, shRNA knock-down of Bim substantially reduced the lethality of belinostat/bortezomib regimens. belinostat 78-88 BCL2 like 11 Homo sapiens 35-38 21375523-6 2011 Significantly, shRNA knock-down of Bim substantially reduced the lethality of belinostat/bortezomib regimens. Bortezomib 89-99 BCL2 like 11 Homo sapiens 35-38 21375523-9 2011 Together, these findings indicate that belinostat and bortezomib interact synergistically in both cultured and primary AML and ALL cells, and raise the possibilities that up-regulation of Bim and interference with NF-kappaB pathways contribute to this phenomenon. belinostat 39-49 BCL2 like 11 Homo sapiens 188-191 21375523-9 2011 Together, these findings indicate that belinostat and bortezomib interact synergistically in both cultured and primary AML and ALL cells, and raise the possibilities that up-regulation of Bim and interference with NF-kappaB pathways contribute to this phenomenon. Bortezomib 54-64 BCL2 like 11 Homo sapiens 188-191 21148306-4 2011 Using several approaches, we demonstrate that BH3-M6 is a pan-Bcl-2 antagonist that inhibits the binding of Bcl-X(L), Bcl-2, and Mcl-1 to multi-domain Bax or Bak, or BH3-only Bim or Bad in cell-free systems and in intact human cancer cells, freeing up pro-apoptotic proteins to induce apoptosis. bh3-m6 46-52 BCL2 like 11 Homo sapiens 175-178 21858169-5 2011 Lysine acetylation of Foxo4 is required for Foxo4 binding and transcription of Bcl2l11 in podocytes treated with AGE-BSA. Lysine 0-6 BCL2 like 11 Homo sapiens 79-86 21047686-7 2011 The effect of the LEN and DEX combination on apoptotic induction was mainly through mitochondrial signaling pathways, as demonstrated by phosphorylation of bcl-2 and up-regulation of proapoptotic proteins Bax, Bad and Bim, and the subsequent activation of caspase-9, caspase-3, and cleavage of PARP. Dexamethasone 26-29 BCL2 like 11 Homo sapiens 218-221 21053278-0 2011 Role of Bim in diallyl trisulfide-induced cytotoxicity in human cancer cells. diallyl trisulfide 15-33 BCL2 like 11 Homo sapiens 8-11 21053278-8 2011 SP600125, a JNK inhibitor, inhibited DATS-induced Bim phosphorylation and protected cells from DATS-induced cytotoxicity. pyrazolanthrone 0-8 BCL2 like 11 Homo sapiens 50-53 21053278-8 2011 SP600125, a JNK inhibitor, inhibited DATS-induced Bim phosphorylation and protected cells from DATS-induced cytotoxicity. diallyl trisulfide 37-41 BCL2 like 11 Homo sapiens 50-53 21053278-9 2011 Our results indicate that the cytotoxicity caused by DATS is mediated by the generation of ROS and subsequent activation of the ASK1-JNK-Bim signal transduction pathway in human breast carcinoma MDA-MB-231 cells. diallyl trisulfide 53-57 BCL2 like 11 Homo sapiens 137-140 21156403-3 2010 We aimed at investigating if the pro-apoptotic members Bad, Bax, Bim and Bid are involved in cisplatin-resistance. Cisplatin 93-102 BCL2 like 11 Homo sapiens 65-68 21179458-15 2010 Inhibition of FOXO transcription factors by shRNA blocked resveratrol-induced upregulation of Bim, TRAIL, DR4, DR5, p27/KIP1 and apoptosis, and inhibition of cyclin D1 by resveratrol. Resveratrol 58-69 BCL2 like 11 Homo sapiens 94-97 20889917-8 2010 Further, VPA induced Bim expression and short hairpin RNA knockdown of Bim resulted in significantly decreased apoptosis induced by cytarabine and by cytarabine plus VPA. Cytarabine 132-142 BCL2 like 11 Homo sapiens 71-74 20889917-8 2010 Further, VPA induced Bim expression and short hairpin RNA knockdown of Bim resulted in significantly decreased apoptosis induced by cytarabine and by cytarabine plus VPA. Cytarabine 150-160 BCL2 like 11 Homo sapiens 71-74 20889917-8 2010 Further, VPA induced Bim expression and short hairpin RNA knockdown of Bim resulted in significantly decreased apoptosis induced by cytarabine and by cytarabine plus VPA. Valproic Acid 9-12 BCL2 like 11 Homo sapiens 21-24 21121775-7 2010 RESULTS: The simulations were in good agreement with the observed experimental data suggesting that Bim was induced between 6 and 10 h after the addition of the synthetic glucocorticoid dexamethasone, possibly through rapid glucocorticoid dependent modulation of an unknown factor. Dexamethasone 186-199 BCL2 like 11 Homo sapiens 100-103 21655183-0 2011 BIM-mediated AKT phosphorylation is a key modulator of arsenic trioxide-induced apoptosis in cisplatin-sensitive and -resistant ovarian cancer cells. Arsenic Trioxide 55-71 BCL2 like 11 Homo sapiens 0-3 21655183-0 2011 BIM-mediated AKT phosphorylation is a key modulator of arsenic trioxide-induced apoptosis in cisplatin-sensitive and -resistant ovarian cancer cells. Cisplatin 93-102 BCL2 like 11 Homo sapiens 0-3 21655183-10 2011 CONCLUSIONS: We demonstrated the roles of BIM in ATO-induced apoptosis and the molecular mechanisms of BIM expression regulated by ATO during ovarian cancer cell apoptosis. Arsenic Trioxide 49-52 BCL2 like 11 Homo sapiens 42-45 21655183-11 2011 Our findings suggest that BIM plays an important role in regulating p-AKT by activating caspase-3 and that BIM mediates the level of AKT phosphorylation to determine the threshold for overcoming cisplatin resistance in ovarian cancer cells. Cisplatin 195-204 BCL2 like 11 Homo sapiens 107-110 20647567-5 2010 Moreover, the histone deacetylase inhibitor vorinostat relieved BIM repression and exerted synergistic antileukemic efficacy with dexamethasone in vitro and in vivo. Vorinostat 44-54 BCL2 like 11 Homo sapiens 64-67 20438634-6 2010 Interestingly, although withaferin A and quercetin treatments both decrease intracellular protein levels of Bcl2, Bim and P-Bad, only withaferin A decreases protein levels of cytoskeletal tubulin, concomitantly with potent PARP cleavage, caspase 3 activation and apoptosis, at least in part via a direct thiol oxidation mechanism. withaferin A 24-36 BCL2 like 11 Homo sapiens 114-117 20885957-4 2010 We found that AZD6244 elicited a large increase of Bim proteins and a smaller increase of PUMA and NOXA proteins, and induced cell death in sensitive lung cancer cell lines, but had no effect on other Bcl-2 related proteins in those cell lines. AZD 6244 14-21 BCL2 like 11 Homo sapiens 51-54 20885957-5 2010 Knockdown of Bim by siRNA greatly increased the IC(50) and reduced apoptosis for AZD6244 treated cells. AZD 6244 81-88 BCL2 like 11 Homo sapiens 13-16 20885957-7 2010 In the sensitive cells, AZD6244 induced FOXO3a nuclear translocation required for Bim activation. AZD 6244 24-31 BCL2 like 11 Homo sapiens 82-85 20877573-7 2010 CXCL12 producing carcinomas cultured on poly-HEMA displayed heightened Bim and loss of Mcl-1 and Bcl-2 preceding cytochrome c release, and caspase-9 activation. poly-hema 40-49 BCL2 like 11 Homo sapiens 71-74 20804592-5 2010 Furthermore, taurine exerted its protective effect through down-regulation of expression of GRP 78, CHOP, Bim and caspase 12. Taurine 13-20 BCL2 like 11 Homo sapiens 106-109 20188077-8 2010 In Jurkat cells simultaneous silencing of Bim and PUMA was necessary to reduce doxorubicin-induced apoptosis. Doxorubicin 79-90 BCL2 like 11 Homo sapiens 42-45 20188077-9 2010 In U937 cells silencing of Bim or Noxa reduced sensitivity to doxorubicin. Doxorubicin 62-73 BCL2 like 11 Homo sapiens 27-30 20223826-4 2010 The pro-apoptotic members Bak, Bad, Bim, and Noxa were required for apoptosis induced by DNA damaging agents camptothecin and UV. Camptothecin 109-121 BCL2 like 11 Homo sapiens 36-39 20231287-0 2010 Role for the proapoptotic factor BIM in mediating imatinib-induced apoptosis in a c-KIT-dependent gastrointestinal stromal tumor cell line. Imatinib Mesylate 50-58 BCL2 like 11 Homo sapiens 33-36 20231287-4 2010 Here, we show that inhibition of c-KIT with imatinib in gastrointestinal stromal tumors (GISTs) triggered the up-regulation of the proapoptotic protein BIM via both transcriptional and post-translational mechanisms. Imatinib Mesylate 44-52 BCL2 like 11 Homo sapiens 152-155 20231287-5 2010 The inhibition of c-KIT by imatinib increased levels of the dephosphorylated and deubiquitinated form of BIM as well as triggered the accumulation of the transcription factor FOXO3a on the BIM promoter to activate transcription of BIM mRNA. Imatinib Mesylate 27-35 BCL2 like 11 Homo sapiens 105-108 20231287-5 2010 The inhibition of c-KIT by imatinib increased levels of the dephosphorylated and deubiquitinated form of BIM as well as triggered the accumulation of the transcription factor FOXO3a on the BIM promoter to activate transcription of BIM mRNA. Imatinib Mesylate 27-35 BCL2 like 11 Homo sapiens 189-192 20231287-5 2010 The inhibition of c-KIT by imatinib increased levels of the dephosphorylated and deubiquitinated form of BIM as well as triggered the accumulation of the transcription factor FOXO3a on the BIM promoter to activate transcription of BIM mRNA. Imatinib Mesylate 27-35 BCL2 like 11 Homo sapiens 189-192 20231287-6 2010 Furthermore, using RNA interference directed against BIM, we demonstrated that BIM knockdown attenuated the effects of imatinib, suggesting that BIM functionally contributes to imatinib-induced apoptosis in GIST. Imatinib Mesylate 119-127 BCL2 like 11 Homo sapiens 79-82 20231287-6 2010 Furthermore, using RNA interference directed against BIM, we demonstrated that BIM knockdown attenuated the effects of imatinib, suggesting that BIM functionally contributes to imatinib-induced apoptosis in GIST. Imatinib Mesylate 119-127 BCL2 like 11 Homo sapiens 79-82 20231287-6 2010 Furthermore, using RNA interference directed against BIM, we demonstrated that BIM knockdown attenuated the effects of imatinib, suggesting that BIM functionally contributes to imatinib-induced apoptosis in GIST. Imatinib Mesylate 177-185 BCL2 like 11 Homo sapiens 79-82 20231287-6 2010 Furthermore, using RNA interference directed against BIM, we demonstrated that BIM knockdown attenuated the effects of imatinib, suggesting that BIM functionally contributes to imatinib-induced apoptosis in GIST. Imatinib Mesylate 177-185 BCL2 like 11 Homo sapiens 79-82 20676138-6 2010 In vitro, Y2R antagonist (BIIE0246) prevented activation of p44/42 mitogen-activated protein kinase (MAPK) induced by endogenous NPY, which resulted in decreased proliferation and induction of Bim-mediated apoptosis. BIIE 0246 26-34 BCL2 like 11 Homo sapiens 193-196 20885957-9 2010 In addition, we found that transfection of constitutively active AKT up-regulated p-Thr32-FOXO3a and p-Ser253-FOXO3a expression and inhibited AZD6244-induced Bim expression in sensitive cells. AZD 6244 142-149 BCL2 like 11 Homo sapiens 158-161 20885957-10 2010 These results show that Bim plays an important role in AZD6244-induced apoptosis in lung cancer cells and that the PI3K/AKT/FOXO3a pathway is involved in Bim regulation and susceptibility of lung cancer cells to AZD6244. AZD 6244 55-62 BCL2 like 11 Homo sapiens 24-27 20885957-10 2010 These results show that Bim plays an important role in AZD6244-induced apoptosis in lung cancer cells and that the PI3K/AKT/FOXO3a pathway is involved in Bim regulation and susceptibility of lung cancer cells to AZD6244. AZD 6244 212-219 BCL2 like 11 Homo sapiens 154-157 19904742-7 2010 Additionally, SYUNZ-16 partially attenuated the phosphorylation levels of FKHR and FKHRL1 in a dose-dependent and time-dependent fashion, and led to an increase in the nuclear accumulation of exogenous FKHR, and upregulated the mRNA expression of Bim and TRADD in cancer cells. syunz-16 14-22 BCL2 like 11 Homo sapiens 247-250 20348947-0 2010 The proapoptotic BH3-only protein Bim is downregulated in a subset of colorectal cancers and is repressed by antiapoptotic COX-2/PGE(2) signalling in colorectal adenoma cells. Prostaglandins E 129-132 BCL2 like 11 Homo sapiens 34-37 20348947-3 2010 Here, we have shown that PGE(2) suppresses apoptosis via repression of the proapoptotic BH3-only protein Bim in human colorectal adenoma cells. Dinoprostone 25-31 BCL2 like 11 Homo sapiens 105-108 20348947-4 2010 Repression of Bim expression was dependent upon PGE(2)-mediated activation of the Raf-MEK-ERK1/2 pathway, which promoted Bim phosphorylation and proteasomal degradation. Dinoprostone 48-54 BCL2 like 11 Homo sapiens 14-17 20348947-4 2010 Repression of Bim expression was dependent upon PGE(2)-mediated activation of the Raf-MEK-ERK1/2 pathway, which promoted Bim phosphorylation and proteasomal degradation. Dinoprostone 48-54 BCL2 like 11 Homo sapiens 121-124 20348947-5 2010 Reduction of Bim expression using RNA interference reduced spontaneous apoptosis in adenoma cells and abrogated PGE(2)-dependent apoptosis suppression. Dinoprostone 112-118 BCL2 like 11 Homo sapiens 13-16 20348947-6 2010 Treatment of COX-2-expressing colorectal carcinoma cells with COX-2-selective NSAIDs-induced Bim expression, suggesting that Bim repression via PGE(2) signalling may be opposed by COX-2 inhibition. Prostaglandins E 144-147 BCL2 like 11 Homo sapiens 125-128 20348947-9 2010 These observations highlight the COX-2/PGE(2) pathway as an important negative regulator of Bim expression in colorectal tumours and suggest that Bim repression may be an important step during colorectal cancer tumorigenesis. Dinoprostone 39-45 BCL2 like 11 Homo sapiens 92-95 20438634-6 2010 Interestingly, although withaferin A and quercetin treatments both decrease intracellular protein levels of Bcl2, Bim and P-Bad, only withaferin A decreases protein levels of cytoskeletal tubulin, concomitantly with potent PARP cleavage, caspase 3 activation and apoptosis, at least in part via a direct thiol oxidation mechanism. Quercetin 41-50 BCL2 like 11 Homo sapiens 114-117 20379528-1 2010 A coordination polymer, [Co(II)(bIM)(acetate)] (bIM = benzimidazole) was synthesized using a solvothermal method; the complex has a two dimensional non-interpenetrated network structure and exhibits a spin-canted antiferromagnetic behaviour at low temperature and a high coercive field. Polymers 15-22 BCL2 like 11 Homo sapiens 32-35 20074640-5 2010 However, we demonstrate that a region consisting of the ERK1/2 docking domain, ERK1/2 phosphorylation sites and either of the two potential ubiquitin-acceptor lysine residues is sufficient to allow poly-ubiquitination and turnover of BIM. Lysine 159-165 BCL2 like 11 Homo sapiens 234-237 20074640-6 2010 In the process we demonstrate that the C-terminal hydrophobic domain, previously suggested to be important in membrane localisation, is as important as the BH3 domain for BIM to induce cell death; similarly, the pro-death BH3-domain can also confer correct mitochondrial localisation in the absence of the C-terminus. BH 3 156-159 BCL2 like 11 Homo sapiens 171-174 20379528-1 2010 A coordination polymer, [Co(II)(bIM)(acetate)] (bIM = benzimidazole) was synthesized using a solvothermal method; the complex has a two dimensional non-interpenetrated network structure and exhibits a spin-canted antiferromagnetic behaviour at low temperature and a high coercive field. Polymers 15-22 BCL2 like 11 Homo sapiens 48-51 20379528-1 2010 A coordination polymer, [Co(II)(bIM)(acetate)] (bIM = benzimidazole) was synthesized using a solvothermal method; the complex has a two dimensional non-interpenetrated network structure and exhibits a spin-canted antiferromagnetic behaviour at low temperature and a high coercive field. benzimidazole 54-67 BCL2 like 11 Homo sapiens 32-35 20379528-1 2010 A coordination polymer, [Co(II)(bIM)(acetate)] (bIM = benzimidazole) was synthesized using a solvothermal method; the complex has a two dimensional non-interpenetrated network structure and exhibits a spin-canted antiferromagnetic behaviour at low temperature and a high coercive field. benzimidazole 54-67 BCL2 like 11 Homo sapiens 48-51 20160166-5 2010 Knockdown of Bim dramatically inhibited apoptosis induced by JAK2 inhibition, which was reversed by the BH3 mimetic agent ABT-737. BH 3 104-107 BCL2 like 11 Homo sapiens 13-16 20160166-5 2010 Knockdown of Bim dramatically inhibited apoptosis induced by JAK2 inhibition, which was reversed by the BH3 mimetic agent ABT-737. ABT-737 122-129 BCL2 like 11 Homo sapiens 13-16 20086250-5 2010 Treatment of cells with the histone deacetylase inhibitor LBH589 resulted in a clear up-regulation in the expression of Bim. Panobinostat 58-64 BCL2 like 11 Homo sapiens 120-123 20067466-6 2010 Dexamethasone-induced p38-MAPK and Bim activation were concomitantly suppressed. Dexamethasone 0-13 BCL2 like 11 Homo sapiens 35-38 19698762-6 2010 Bad and Bim are pro-apoptotic proteins that cause mitochondrial dysfunction characterized by excessive ROS formation, mitochnondrial DNA (mtDNA) damage, and release of mitochondrial apoptotic proteins including cytochrome c, apoptosis inducing factor (AIF), endonuclease G and Smac. ros 103-106 BCL2 like 11 Homo sapiens 8-11 20067466-8 2010 Inhibition of NF-kappaB by the pharmacological agent BAY11-7082 greatly enhanced the sensitivity of the GSTM1-expressing CEM to dexamethasone and was accompanied by an increase in Bim expression. 3-(4-methylphenylsulfonyl)-2-propenenitrile 53-63 BCL2 like 11 Homo sapiens 180-183 20067466-9 2010 Thus, we propose that GSTM1, a novel regulator of dexamethasone-induced apoptosis, causes dexamethasone resistance by suppression of Bim through dual mechanisms of both downregulation of p38-MAPK and upregulation of NF-kappaB p50. Dexamethasone 50-63 BCL2 like 11 Homo sapiens 133-136 20067466-9 2010 Thus, we propose that GSTM1, a novel regulator of dexamethasone-induced apoptosis, causes dexamethasone resistance by suppression of Bim through dual mechanisms of both downregulation of p38-MAPK and upregulation of NF-kappaB p50. Dexamethasone 90-103 BCL2 like 11 Homo sapiens 133-136 19881544-8 2010 Using gamma-secretase inhibitor and erlotinib in a xenograft model, Bim induction and tumor inhibition were observed to be enhanced compared with either agent alone, consistent with our previous observation of significant synergism between Notch and EGFR-ras-MAPK signaling. Erlotinib Hydrochloride 36-45 BCL2 like 11 Homo sapiens 68-71 20038611-5 2010 However, expression of the pro-apoptotic protein Bim, and the extent of its association with Bcl-2, significantly correlated with in vivo ABT-737 sensitivity. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 138-141 BCL2 like 11 Homo sapiens 49-52 20128807-8 2010 Furthermore, the pro-apoptotic protein Bim was up-regulated by SZ-685C treatment consistent with FOXO dephosphorylation. SZ 685C 63-70 BCL2 like 11 Homo sapiens 39-42 19914305-0 2010 Bim is the key mediator of glucocorticoid-induced apoptosis and of its potentiation by rapamycin in human myeloma cells. Sirolimus 87-96 BCL2 like 11 Homo sapiens 0-3 19914305-5 2010 Apoptotic gene expression profiling showed an increase in mRNA levels of Bim in MM.1S cells after Dex treatment and further increases in both cell lines when co-treated with rapamycin. Dexamethasone 98-101 BCL2 like 11 Homo sapiens 73-76 19914305-8 2010 Upon treatment with Dex, and specially Dex plus rapamycin, Bim-Mcl-1 complex was disrupted and Bim was found associated to a CHAPS-insoluble fraction. Dexamethasone 20-23 BCL2 like 11 Homo sapiens 59-62 19914305-8 2010 Upon treatment with Dex, and specially Dex plus rapamycin, Bim-Mcl-1 complex was disrupted and Bim was found associated to a CHAPS-insoluble fraction. Dexamethasone 20-23 BCL2 like 11 Homo sapiens 95-98 19914305-8 2010 Upon treatment with Dex, and specially Dex plus rapamycin, Bim-Mcl-1 complex was disrupted and Bim was found associated to a CHAPS-insoluble fraction. Dexamethasone 39-42 BCL2 like 11 Homo sapiens 59-62 19914305-8 2010 Upon treatment with Dex, and specially Dex plus rapamycin, Bim-Mcl-1 complex was disrupted and Bim was found associated to a CHAPS-insoluble fraction. Dexamethasone 39-42 BCL2 like 11 Homo sapiens 95-98 19914305-9 2010 Overexpression of Mcl-1 stabilized Bim-Mcl-1 complexes upon treatment with Dex or Dex+rapamycin and fully prevented apoptosis. Dexamethasone 75-78 BCL2 like 11 Homo sapiens 35-38 19914305-9 2010 Overexpression of Mcl-1 stabilized Bim-Mcl-1 complexes upon treatment with Dex or Dex+rapamycin and fully prevented apoptosis. dex+rapamycin 82-95 BCL2 like 11 Homo sapiens 35-38 19914305-10 2010 Gene silencing of Bim inhibited for the most part Dex-induced apoptosis and, to a large extent, apoptosis induced by Dex plus rapamycin. Dexamethasone 50-53 BCL2 like 11 Homo sapiens 18-21 19914305-10 2010 Gene silencing of Bim inhibited for the most part Dex-induced apoptosis and, to a large extent, apoptosis induced by Dex plus rapamycin. Dexamethasone 117-120 BCL2 like 11 Homo sapiens 18-21 19914305-10 2010 Gene silencing of Bim inhibited for the most part Dex-induced apoptosis and, to a large extent, apoptosis induced by Dex plus rapamycin. Sirolimus 126-135 BCL2 like 11 Homo sapiens 18-21 19914305-11 2010 These results, taken together, indicate that Bim protein is the key mediator of apoptosis induced by Dex and also responsible for the potentiating effect of rapamycin, providing molecular criteria for the use of glucocorticoids combined with mTOR inhibitors in myeloma therapy. Dexamethasone 101-104 BCL2 like 11 Homo sapiens 45-48 19914305-11 2010 These results, taken together, indicate that Bim protein is the key mediator of apoptosis induced by Dex and also responsible for the potentiating effect of rapamycin, providing molecular criteria for the use of glucocorticoids combined with mTOR inhibitors in myeloma therapy. Sirolimus 157-166 BCL2 like 11 Homo sapiens 45-48 19559478-0 2009 Dexamethasone-induced apoptosis and up-regulation of Bim is dependent on glycogen synthase kinase-3. Dexamethasone 0-13 BCL2 like 11 Homo sapiens 53-56 19946262-6 2010 FI-700 induced proteasome-mediated degradation of Mcl-1, resulting in the reduced ability of Mcl-1 to sequester proapoptotic Bim. FI-700 0-6 BCL2 like 11 Homo sapiens 125-128 19850739-6 2009 The KIT D816-induced down-regulation of Bim was rescued by the KIT-targeting drug PKC412/midostaurin. midostaurin 89-100 BCL2 like 11 Homo sapiens 40-43 19850739-7 2009 Both PKC412 and the proteasome-inhibitor bortezomib were found to decrease growth and promote expression of Bim in MC leukemia cell lines HMC-1.1 (D816V negative) and HMC-1.2 (D816V positive). Bortezomib 41-51 BCL2 like 11 Homo sapiens 108-111 19850739-11 2009 Our data show that KIT D816V suppresses expression of proapoptotic Bim in neoplastic MCs. d816v 23-28 BCL2 like 11 Homo sapiens 67-70 21364639-4 2010 In CHO cells, it inhibited apoptosis induced by the overexpression of human proapoptotic proteins, Bim and Bax. cho 3-6 BCL2 like 11 Homo sapiens 99-102 19559478-5 2009 Inhibition of GSK3 attenuated Dex-induced up-regulation of Bim, loss of mitochondrial membrane potential, release of cyt c and DNA fragmentation. Dexamethasone 30-33 BCL2 like 11 Homo sapiens 59-62 19559478-6 2009 These results indicate that GSK3 contributes to Dex-induced apoptosis by controlling up-regulation of Bim. Dexamethasone 48-51 BCL2 like 11 Homo sapiens 102-105 19805519-3 2009 Expression profiling of BH3-only proteins indicated that SBHA increased Bim, Puma, and Noxa expression, while SBHA concentrations that upregulated Bim significantly potentiated ABT-737 lethality. suberoyl bis-hydroxamic acid 57-61 BCL2 like 11 Homo sapiens 72-75 19805519-3 2009 Expression profiling of BH3-only proteins indicated that SBHA increased Bim, Puma, and Noxa expression, while SBHA concentrations that upregulated Bim significantly potentiated ABT-737 lethality. suberoyl bis-hydroxamic acid 110-114 BCL2 like 11 Homo sapiens 147-150 19805519-0 2009 Bim upregulation by histone deacetylase inhibitors mediates interactions with the Bcl-2 antagonist ABT-737: evidence for distinct roles for Bcl-2, Bcl-xL, and Mcl-1. ABT-737 99-106 BCL2 like 11 Homo sapiens 0-3 19805519-3 2009 Expression profiling of BH3-only proteins indicated that SBHA increased Bim, Puma, and Noxa expression, while SBHA concentrations that upregulated Bim significantly potentiated ABT-737 lethality. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 177-180 BCL2 like 11 Homo sapiens 147-150 19805519-1 2009 The Bcl-2 antagonist ABT-737 kills transformed cells in association with displacement of Bim from Bcl-2. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 21-24 BCL2 like 11 Homo sapiens 89-92 19934277-6 2009 Imatinib, gefitinib, bortezomib, and Bim protein itself are spotlighted as current and future Bim-targeting therapeutic agents. Imatinib Mesylate 0-8 BCL2 like 11 Homo sapiens 94-97 19934277-6 2009 Imatinib, gefitinib, bortezomib, and Bim protein itself are spotlighted as current and future Bim-targeting therapeutic agents. Gefitinib 10-19 BCL2 like 11 Homo sapiens 94-97 19805519-4 2009 Concordance between SBHA-mediated Bim upregulation and interactions with ABT-737 was observed in various human leukemia and myeloma cells. suberoyl bis-hydroxamic acid 20-24 BCL2 like 11 Homo sapiens 34-37 19934277-6 2009 Imatinib, gefitinib, bortezomib, and Bim protein itself are spotlighted as current and future Bim-targeting therapeutic agents. Bortezomib 21-31 BCL2 like 11 Homo sapiens 94-97 19805519-5 2009 SBHA-induced Bim was largely sequestered by Bcl-2 and Bcl-x(L), rather than Mcl-1; ABT-737 attenuated these interactions, thereby triggering Bak/Bax activation and mitochondrial outer membrane permeabilization. suberoyl bis-hydroxamic acid 0-4 BCL2 like 11 Homo sapiens 13-16 19805519-5 2009 SBHA-induced Bim was largely sequestered by Bcl-2 and Bcl-x(L), rather than Mcl-1; ABT-737 attenuated these interactions, thereby triggering Bak/Bax activation and mitochondrial outer membrane permeabilization. bakuchiol 141-144 BCL2 like 11 Homo sapiens 13-16 19805519-7 2009 Notably, ectopic expression of these antiapoptotic proteins disabled death signaling by sequestering different proapoptotic proteins, i.e., Bim by Bcl-2, both Bim and Bak by Bcl-x(L), and Bak by Mcl-1. bakuchiol 188-191 BCL2 like 11 Homo sapiens 140-143 19773546-6 2009 Notably, knockdown of Bim, but not Bad, blocked Bak and Bax conformational change, inhibited Bax membrane translocation, diminished Bax/Bak binding, and sharply attenuated perifosine/PD184352-induced apoptosis. 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide 183-191 BCL2 like 11 Homo sapiens 22-25 19773546-6 2009 Notably, knockdown of Bim, but not Bad, blocked Bak and Bax conformational change, inhibited Bax membrane translocation, diminished Bax/Bak binding, and sharply attenuated perifosine/PD184352-induced apoptosis. perifosine 172-182 BCL2 like 11 Homo sapiens 22-25 19641525-4 2009 In vitro sensitivity to ABT-737 could not be simply predicted by the patients" clinical features, including response to prior therapy or known prognostic markers (CD38 expression, 17p deletion), or the relative expression of BCL2 family proteins (BCL2, MCL1, BAX, BIM). 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 24-27 BCL2 like 11 Homo sapiens 264-267 19808980-0 2009 BH3-only proteins Mcl-1 and Bim as well as endonuclease G are targeted in spongistatin 1-induced apoptosis in breast cancer cells. spongistatin 1 74-88 BCL2 like 11 Homo sapiens 28-31 19404317-3 2009 We and others have shown that BIM (BCL-2 interacting mediator of cell death), a BH3-only pro-apoptotic protein, is up-regulated by dexamethasone (Dex) treatment in acute lymphoblastic leukemia (ALL) cells and plays an essential role in Dex-induced apoptosis. Dexamethasone 131-144 BCL2 like 11 Homo sapiens 35-75 19404317-3 2009 We and others have shown that BIM (BCL-2 interacting mediator of cell death), a BH3-only pro-apoptotic protein, is up-regulated by dexamethasone (Dex) treatment in acute lymphoblastic leukemia (ALL) cells and plays an essential role in Dex-induced apoptosis. Dexamethasone 146-149 BCL2 like 11 Homo sapiens 35-75 19404317-3 2009 We and others have shown that BIM (BCL-2 interacting mediator of cell death), a BH3-only pro-apoptotic protein, is up-regulated by dexamethasone (Dex) treatment in acute lymphoblastic leukemia (ALL) cells and plays an essential role in Dex-induced apoptosis. Dexamethasone 236-239 BCL2 like 11 Homo sapiens 35-75 19557009-4 2009 provides the first biophysical evidence for a direct interaction between a BH3 domain, that of Bim, with Bax. BH 3 75-78 BCL2 like 11 Homo sapiens 95-98 19737956-0 2009 Induction of Bim expression contributes to the antitumor synergy between sorafenib and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase inhibitor CI-1040 in hepatocellular carcinoma. Sorafenib 73-82 BCL2 like 11 Homo sapiens 13-16 19737956-0 2009 Induction of Bim expression contributes to the antitumor synergy between sorafenib and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase inhibitor CI-1040 in hepatocellular carcinoma. 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide 175-182 BCL2 like 11 Homo sapiens 13-16 19737956-10 2009 Knockdown of Bim expression by small interfering RNA partially abrogated the synergistic proapoptotic effects of sorafenib and CI-1040. Sorafenib 113-122 BCL2 like 11 Homo sapiens 13-16 19737956-10 2009 Knockdown of Bim expression by small interfering RNA partially abrogated the synergistic proapoptotic effects of sorafenib and CI-1040. 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide 127-134 BCL2 like 11 Homo sapiens 13-16 19106608-7 2009 Recently, we demonstrated that, in addition to its transcriptional effects on Bim, TGFbeta induces a MAPK phosphatase (MKP), MKP2/DUSP4, to rapidly increase BimEL levels by inactivation of Erk1/2, resulting in dephosphorylation and escape of BimEL from ubiquitin-mediated degradation. bimel 157-162 BCL2 like 11 Homo sapiens 78-81 19555760-0 2009 BDNF regulates BIM expression levels in 3-nitropropionic acid-treated cortical neurons. 3-nitropropionic acid 40-61 BCL2 like 11 Homo sapiens 15-18 19541822-0 2009 Forodesine has high antitumor activity in chronic lymphocytic leukemia and activates p53-independent mitochondrial apoptosis by induction of p73 and BIM. forodesine 0-10 BCL2 like 11 Homo sapiens 149-152 19541822-6 2009 Forodesine activates the mitochondrial apoptotic pathway by decreasing the levels of antiapoptotic MCL-1 protein and induction of proapoptotic BIM protein. forodesine 0-10 BCL2 like 11 Homo sapiens 143-146 19622774-5 2009 Depletion of Drg1 by small interfering RNA induced up-regulation of Bim and its accumulation in the mitochondria, which correlated with loss of mitochondrial membrane potential and induction of apoptosis in cells exposed to SN-38. Irinotecan 224-229 BCL2 like 11 Homo sapiens 68-71 19403302-0 2009 Epigenetic down-regulation of BIM expression is associated with reduced optimal responses to imatinib treatment in chronic myeloid leukaemia. Imatinib Mesylate 93-101 BCL2 like 11 Homo sapiens 30-33 19403302-1 2009 BACKGROUND: Expression of the pro-apoptotic BCL-2-interacting mediator (BIM) has recently been implicated in imatinib-induced apoptosis of BCR-ABL1(+) cells. Imatinib Mesylate 109-117 BCL2 like 11 Homo sapiens 72-75 19403302-6 2009 RESULTS: We demonstrated that down-regulation of BIM expression was present in 36% of the patients and was significantly associated with a lack of optimal response to imatinib as indicated by the decrease in cytogenetic and molecular responses at 6, 12 and 18 months in comparison with patients with normal BIM expression (p<0.05). Imatinib Mesylate 167-175 BCL2 like 11 Homo sapiens 49-52 19403302-7 2009 Expression of BIM was mediated by promoter hypermethylation as demonstrated by restoration of BIM expression after treatment of CML cells with 5-aza-2"-deoxycytidine. Decitabine 143-165 BCL2 like 11 Homo sapiens 14-17 19403302-8 2009 Using CML cell lines with low and normal expression of BIM we further demonstrated that the expression of BIM is required for imatinib-induced CML apoptosis. Imatinib Mesylate 126-134 BCL2 like 11 Homo sapiens 55-58 19403302-8 2009 Using CML cell lines with low and normal expression of BIM we further demonstrated that the expression of BIM is required for imatinib-induced CML apoptosis. Imatinib Mesylate 126-134 BCL2 like 11 Homo sapiens 106-109 19557159-6 2009 Consistent with this, methylation-specific PCR (MSP) and bisulphite sequencing of regions within the large CpG island located at the 5" end of Bim revealed significant methylation of CpG dinucleotides in all EBV-positive, but not EBV-negative B cells examined. hydrogen sulfite 57-67 BCL2 like 11 Homo sapiens 143-146 19293378-5 2009 A point mutation that lost the ability to bind Bak retained its ability to bind Bim and to protect cells. bakuchiol 47-50 BCL2 like 11 Homo sapiens 80-83 19308286-0 2009 Acetylation of FoxO1 activates Bim expression to induce apoptosis in response to histone deacetylase inhibitor depsipeptide treatment. Depsipeptides 111-123 BCL2 like 11 Homo sapiens 31-34 19308286-4 2009 Further study showed that Bim, a BH3-only proapoptotic protein, was significantly upregulated by depsipeptide in cancer cells, and Bim"s function in depsipeptide-induced apoptosis was confirmed by knockdown of Bim with RNAi. Depsipeptides 97-109 BCL2 like 11 Homo sapiens 26-29 19308286-5 2009 In addition, we found that depsipeptide-induced expression of Bim was directly dependent on acetylation of forkhead box class O1 (FoxO1) that is catalyzed by cyclic adenosine monophosphate-responsive element-binding protein-binding protein, and indirectly induced by a decreased four-and-a-half LIM-domain protein 2. Depsipeptides 27-39 BCL2 like 11 Homo sapiens 62-65 19308286-5 2009 In addition, we found that depsipeptide-induced expression of Bim was directly dependent on acetylation of forkhead box class O1 (FoxO1) that is catalyzed by cyclic adenosine monophosphate-responsive element-binding protein-binding protein, and indirectly induced by a decreased four-and-a-half LIM-domain protein 2. Cyclic AMP 158-188 BCL2 like 11 Homo sapiens 62-65 19308286-6 2009 Moreover, our results demonstrated that FoxO1 acetylation is required for the depsipeptide-induced activation of Bim and apoptosis, using transfection with a plasmid containing FoxO1 mutated at lysine sites and a luciferase reporter assay. Depsipeptides 78-90 BCL2 like 11 Homo sapiens 113-116 19199036-5 2009 During the induction of apoptosis in cell suspensions by safingol, there was an increase of the pro-apoptotic BH-3 only protein Bim and decrease of pro-survival Bcl-2 family proteins Bcl-xL and mitochondrial pro-apoptogenic factor endonuclease G translocated to the nucleus. safingol 57-65 BCL2 like 11 Homo sapiens 128-131 19199036-8 2009 These results suggest that Bim, Bcl-xL, FAK and endonuclease G are involved in safingol-induced apoptosis of detached oral SCC cells. safingol 79-87 BCL2 like 11 Homo sapiens 27-30 19343038-6 2009 The survival of MPM cells can be reversed by activating SAPK/JNK with anisomycin, according to a Bim-dependent mitochondrial pathway. Anisomycin 70-80 BCL2 like 11 Homo sapiens 97-100 18715233-8 2008 Re-activation of BRAF-->MEK-->ERK signaling led to phosphorylation of BIM-EL on serine 69 and its subsequent degradation. Serine 86-92 BCL2 like 11 Homo sapiens 76-79 18794804-5 2008 Inhibition of either Bim or Puma expression in Hus1-knockout cells confers significant resistance to etoposide-induced apoptosis, whereas knockdown of both proteins results in further resistance, suggesting that Bim and Puma cooperate in sensitizing Hus1-deficient cells to etoposide treatment. Etoposide 274-283 BCL2 like 11 Homo sapiens 212-215 18794804-6 2008 Moreover, we found that Rad9 collaborates with Bim and Puma to sensitize Hus1-deficient cells to etoposide-induced apoptosis. Etoposide 97-106 BCL2 like 11 Homo sapiens 47-50 18794804-8 2008 Taken together, these results suggest that loss of Hus1 sensitizes cells to etoposide-induced apoptosis not only by inducing Bim and Puma expressions but also by releasing Rad9 into the cytosol to augment mitochondrial apoptosis. Etoposide 76-85 BCL2 like 11 Homo sapiens 125-128 18843207-2 2008 This work focuses on the development of a novel peptidic molecule based on the BH3 domain of Bim. BH 3 79-82 BCL2 like 11 Homo sapiens 93-96 18843207-4 2008 According to a rational study of the structural interactions between wt Bim-BH3 and Bcl-X(L), we replaced specific residues of Bim-BH3 with natural and non-natural aminoacids and added an internalizing sequence, thus increasing dramatically the inhibitory activity of our modified Bim-BH3 peptide, called 072RB. BH 3 76-79 BCL2 like 11 Homo sapiens 72-75 18843207-4 2008 According to a rational study of the structural interactions between wt Bim-BH3 and Bcl-X(L), we replaced specific residues of Bim-BH3 with natural and non-natural aminoacids and added an internalizing sequence, thus increasing dramatically the inhibitory activity of our modified Bim-BH3 peptide, called 072RB. BH 3 131-134 BCL2 like 11 Homo sapiens 127-130 18843207-4 2008 According to a rational study of the structural interactions between wt Bim-BH3 and Bcl-X(L), we replaced specific residues of Bim-BH3 with natural and non-natural aminoacids and added an internalizing sequence, thus increasing dramatically the inhibitory activity of our modified Bim-BH3 peptide, called 072RB. BH 3 131-134 BCL2 like 11 Homo sapiens 127-130 18593821-0 2008 Patupilone-induced apoptosis is mediated by mitochondrial reactive oxygen species through Bim relocalization to mitochondria. epothilone B 0-10 BCL2 like 11 Homo sapiens 90-93 18593821-0 2008 Patupilone-induced apoptosis is mediated by mitochondrial reactive oxygen species through Bim relocalization to mitochondria. Reactive Oxygen Species 58-81 BCL2 like 11 Homo sapiens 90-93 18593821-8 2008 It is noteworthy that ROS inhibition prevented Bim relocalization to mitochondria and mitochondrial membrane changes induced by patupilone. Reactive Oxygen Species 22-25 BCL2 like 11 Homo sapiens 47-50 18593821-8 2008 It is noteworthy that ROS inhibition prevented Bim relocalization to mitochondria and mitochondrial membrane changes induced by patupilone. epothilone B 128-138 BCL2 like 11 Homo sapiens 47-50 18593821-9 2008 Altogether, our data reveal that patupilone-mediated ROS production by mitochondria initiates the intrinsic signaling cascade by inducing Bim accumulation in mitochondria. epothilone B 33-43 BCL2 like 11 Homo sapiens 138-141 18593821-9 2008 Altogether, our data reveal that patupilone-mediated ROS production by mitochondria initiates the intrinsic signaling cascade by inducing Bim accumulation in mitochondria. Reactive Oxygen Species 53-56 BCL2 like 11 Homo sapiens 138-141 19100522-6 2009 RESULTS: Stimulation of B cells with DAG analogues results in activation of protein kinase C/RasGRP-Ras-Raf-Mek-Erk signaling and phosphorylation of the proapoptotic BH3-only protein Bim. Diglycerides 37-40 BCL2 like 11 Homo sapiens 183-186 19088028-8 2008 ABT-737 unsequestered the BH3-only protein Bim from its complex with Bcl-xL or Bcl-2 and disrupted the interaction of Bcl-xL with Bak. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 0-3 BCL2 like 11 Homo sapiens 43-46 18794804-4 2008 Here, we report that etoposide treatment dramatically upregulates the BH3-only proteins, Bim and Puma, in Hus1-deficient cells. Etoposide 21-30 BCL2 like 11 Homo sapiens 89-92 18794804-5 2008 Inhibition of either Bim or Puma expression in Hus1-knockout cells confers significant resistance to etoposide-induced apoptosis, whereas knockdown of both proteins results in further resistance, suggesting that Bim and Puma cooperate in sensitizing Hus1-deficient cells to etoposide treatment. Etoposide 101-110 BCL2 like 11 Homo sapiens 21-24 18794804-5 2008 Inhibition of either Bim or Puma expression in Hus1-knockout cells confers significant resistance to etoposide-induced apoptosis, whereas knockdown of both proteins results in further resistance, suggesting that Bim and Puma cooperate in sensitizing Hus1-deficient cells to etoposide treatment. Etoposide 101-110 BCL2 like 11 Homo sapiens 212-215 19641506-2 2008 Although Bim has been implicated in the regulation of cell death induction in multiple cell types and tissues in response to a large number of stimuli, including growth factor or cytokine deprivation, calcium flux, ligation of antigen receptors on T and B cells, glucocorticoid or loss of adhesion, Bmf seems to play a more restricted role by supporting Bim in some of these cell death processes. Calcium 201-208 BCL2 like 11 Homo sapiens 9-12 18695355-11 2008 Taken together, our results suggest that AG490 inhibited cytochrome c release into the cytosol at least partly by inhibiting the pro-apoptotic proteins Bad and Bim, which in turn suppressed caspase-9 and -3 activation, thereby inhibiting osteoclast apoptosis. alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide 41-46 BCL2 like 11 Homo sapiens 160-163 18452209-13 2008 Residues from this helix interact with an Arg residue in Bad and Bim peptides. Arginine 42-45 BCL2 like 11 Homo sapiens 65-68 18794155-0 2008 Withaferin A causes FOXO3a- and Bim-dependent apoptosis and inhibits growth of human breast cancer cells in vivo. withaferin A 0-12 BCL2 like 11 Homo sapiens 32-35 18583568-4 2008 In MM cells, irrespective of p53 status, the combined PD/ATO treatment increases the level of the proapoptotic protein Bim (PD-mediated) and decreases antiapoptotic protein Mcl-1 (ATO-mediated). Arsenic Trioxide 57-60 BCL2 like 11 Homo sapiens 119-122 18345036-1 2008 We previously reported that actin damage by treatment with an actin-depolymerizing agent including pectenotoxin-2 induces Bim-mediated apoptosis in p53-deficient human tumors. pectenotoxin 2 99-113 BCL2 like 11 Homo sapiens 122-125 18515658-1 2008 The mechanism by which the glucocorticoid (GC) dexamethasone induces apoptosis in multiple myeloma (MM) cells is unknown, although previous work suggests that either transactivation through the glucocorticoid response element (GRE), transrepression of NF-kappaB, phosphorylation of RAFTK (Pyk2), or induction of Bim is important. Dexamethasone 47-60 BCL2 like 11 Homo sapiens 312-315 18515658-8 2008 Dexamethasone treatment of MM1R cells expressing a mutant incapable of inducing apoptosis successfully resulted in RAFTK (Pyk2) phosphorylation and Bim induction indicating the latter GR-mediated events were not sufficient to induce apoptosis. Dexamethasone 0-13 BCL2 like 11 Homo sapiens 148-151 18549468-4 2008 In HEK293 cells, this novel candidate promoter originates BCL2L11 transcripts whose expression can be modulated by a known modulator of BCL2L11 expression (Trichostatin A) and by E2F, a characterized transcriptional regulator of BCL2L11 expression. trichostatin A 156-170 BCL2 like 11 Homo sapiens 58-65 18467496-8 2008 Combining information from the alanine, lysine, and glutamic acid scans has enabled us to identify Bim BH3 domain mutants containing only two or three sequence changes that bind very selectively either to Bcl-x(L) or Mcl-1. Alanine 31-38 BCL2 like 11 Homo sapiens 99-102 18467496-8 2008 Combining information from the alanine, lysine, and glutamic acid scans has enabled us to identify Bim BH3 domain mutants containing only two or three sequence changes that bind very selectively either to Bcl-x(L) or Mcl-1. Lysine 40-46 BCL2 like 11 Homo sapiens 99-102 18467496-8 2008 Combining information from the alanine, lysine, and glutamic acid scans has enabled us to identify Bim BH3 domain mutants containing only two or three sequence changes that bind very selectively either to Bcl-x(L) or Mcl-1. Glutamic Acid 52-65 BCL2 like 11 Homo sapiens 99-102 18549468-4 2008 In HEK293 cells, this novel candidate promoter originates BCL2L11 transcripts whose expression can be modulated by a known modulator of BCL2L11 expression (Trichostatin A) and by E2F, a characterized transcriptional regulator of BCL2L11 expression. trichostatin A 156-170 BCL2 like 11 Homo sapiens 136-143 18549468-4 2008 In HEK293 cells, this novel candidate promoter originates BCL2L11 transcripts whose expression can be modulated by a known modulator of BCL2L11 expression (Trichostatin A) and by E2F, a characterized transcriptional regulator of BCL2L11 expression. trichostatin A 156-170 BCL2 like 11 Homo sapiens 136-143 18566236-0 2008 Bortezomib induces apoptosis via Bim and Bik up-regulation and synergizes with cisplatin in the killing of head and neck squamous cell carcinoma cells. Bortezomib 0-10 BCL2 like 11 Homo sapiens 33-36 18266926-6 2008 Focusing on mechanisms responsible for this synergy, we found that maneb+PQ increased the expression of three strong Bak inhibitors, Bfl-1, Bcl-xL and Mcl-1, and also induced Bax activators that included Bik and Bim. maneb+pq 67-75 BCL2 like 11 Homo sapiens 212-215 18566236-3 2008 We report that induction of HNSCC apoptosis by the proteasome inhibitor bortezomib is accompanied by up-regulation of the proapoptotic proteins Bik and Bim, natural cellular inhibitors of Bcl-X(L) and Bcl-2. Bortezomib 72-82 BCL2 like 11 Homo sapiens 152-155 18566236-5 2008 Inhibition of Bik or Bim up-regulation using small interfering RNA markedly attenuated bortezomib-induced cell death. Bortezomib 87-97 BCL2 like 11 Homo sapiens 21-24 18064628-4 2008 We found dose- and time-dependent upregulation of Bim protein, a pro-apoptotic Bcl-2 family member, with highest levels at 24-48 h for 1 microM Dex. Dexamethasone 144-147 BCL2 like 11 Homo sapiens 50-53 18493594-0 2008 Antagomir-17-5p abolishes the growth of therapy-resistant neuroblastoma through p21 and BIM. antagomir-17-5p 0-15 BCL2 like 11 Homo sapiens 88-91 18064628-7 2008 Bim mRNA was upregulated in response to 1 microM Dex; both cycloheximide and the GC receptor antagonist, RU486, prevented Dex-induction of Bim protein, indicating transcriptional regulation involving the GC receptor. Dexamethasone 49-52 BCL2 like 11 Homo sapiens 0-3 18064628-7 2008 Bim mRNA was upregulated in response to 1 microM Dex; both cycloheximide and the GC receptor antagonist, RU486, prevented Dex-induction of Bim protein, indicating transcriptional regulation involving the GC receptor. Cycloheximide 59-72 BCL2 like 11 Homo sapiens 139-142 18064628-7 2008 Bim mRNA was upregulated in response to 1 microM Dex; both cycloheximide and the GC receptor antagonist, RU486, prevented Dex-induction of Bim protein, indicating transcriptional regulation involving the GC receptor. Mifepristone 105-110 BCL2 like 11 Homo sapiens 0-3 18064628-7 2008 Bim mRNA was upregulated in response to 1 microM Dex; both cycloheximide and the GC receptor antagonist, RU486, prevented Dex-induction of Bim protein, indicating transcriptional regulation involving the GC receptor. Mifepristone 105-110 BCL2 like 11 Homo sapiens 139-142 18064628-7 2008 Bim mRNA was upregulated in response to 1 microM Dex; both cycloheximide and the GC receptor antagonist, RU486, prevented Dex-induction of Bim protein, indicating transcriptional regulation involving the GC receptor. Dexamethasone 122-125 BCL2 like 11 Homo sapiens 0-3 18064628-7 2008 Bim mRNA was upregulated in response to 1 microM Dex; both cycloheximide and the GC receptor antagonist, RU486, prevented Dex-induction of Bim protein, indicating transcriptional regulation involving the GC receptor. Dexamethasone 122-125 BCL2 like 11 Homo sapiens 139-142 18064628-8 2008 The proteasome inhibitor, MG132, potently increased Bim protein levels. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 26-31 BCL2 like 11 Homo sapiens 52-55 18064628-10 2008 Gene silencing experiments show that short interference RNA (siRNA) specific for Bim or the downstream effector Bax both reduced apoptosis induced by Dex in osteoblastic cells. Dexamethasone 150-153 BCL2 like 11 Homo sapiens 81-84 17828309-4 2008 In particular, the stabilization of BH3-only proteins BIK, NOXA and BIM, appear to be essential for effecting BAX- and BAK-dependent cell death. bakuchiol 119-122 BCL2 like 11 Homo sapiens 68-71 18200035-0 2008 Sorafenib induces apoptosis of AML cells via Bim-mediated activation of the intrinsic apoptotic pathway. Sorafenib 0-9 BCL2 like 11 Homo sapiens 45-48 18200035-4 2008 Mechanistically, treatment with sorafenib resulted in upregulation of proapoptotic Bim, accompanied by an increase in Bad, Bax and Bak protein levels and decreased Mcl-1, X-linked inhibitor of apoptosis and surviving levels, which mainly led to the activation of the intrinsic apoptotic pathway. Sorafenib 32-41 BCL2 like 11 Homo sapiens 83-86 18200035-5 2008 Silencing of Bim protein expression significantly abrogated sorafenib-induced apoptosis, suggesting a critical function of Bim in the activation of the intrinsic mitochondrial pathway induced by sorafenib. Sorafenib 60-69 BCL2 like 11 Homo sapiens 13-16 18200035-5 2008 Silencing of Bim protein expression significantly abrogated sorafenib-induced apoptosis, suggesting a critical function of Bim in the activation of the intrinsic mitochondrial pathway induced by sorafenib. Sorafenib 195-204 BCL2 like 11 Homo sapiens 13-16 18200035-5 2008 Silencing of Bim protein expression significantly abrogated sorafenib-induced apoptosis, suggesting a critical function of Bim in the activation of the intrinsic mitochondrial pathway induced by sorafenib. Sorafenib 195-204 BCL2 like 11 Homo sapiens 123-126 18200035-6 2008 Importantly, sorafenib also modulated phospho-Erk, Bim, Bax and Mcl-1 levels in samples procured from patients in an ongoing Phase I clinical trial of sorafenib in AML. Sorafenib 13-22 BCL2 like 11 Homo sapiens 51-54 18174237-2 2008 Here, we showed that lack of Bcl-2-interacting mediator of cell death (Bim)(EL) protein expression, a BH3-only member of the Bcl-2 family proteins, conferred resistance of a T-ALL cell line, Sup-T1, to etoposide-induced apoptosis. Etoposide 202-211 BCL2 like 11 Homo sapiens 29-69 18084006-4 2008 DLC1 phosphorylation on Ser(88) by p21-activated kinase 1 (Pak1), a signaling nodule, promotes mammalian cell survival by regulating its interaction with Bim and the stability of Bim. Serine 24-27 BCL2 like 11 Homo sapiens 154-157 18084006-4 2008 DLC1 phosphorylation on Ser(88) by p21-activated kinase 1 (Pak1), a signaling nodule, promotes mammalian cell survival by regulating its interaction with Bim and the stability of Bim. Serine 24-27 BCL2 like 11 Homo sapiens 179-182 18084006-5 2008 Here we discovered that phosphorylation of Ser(88), which juxtapose each other at the interface of the DLC dimer, disrupts DLC1 dimer formation and consequently impairs its interaction with Bim. Serine 43-46 BCL2 like 11 Homo sapiens 190-193 18084006-6 2008 Overexpression of a Ser(88) phosphorylation-inactive DLC1 mutant in mammary epithelium cells and in a transgenic animal model caused apoptosis and accelerated mammary gland involution, respectively, with increased Bim levels. Serine 20-23 BCL2 like 11 Homo sapiens 214-217 18063582-9 2008 Consistent with this, ERK1/2-mediated Ser(69) phosphorylation of Bim, a key signal for turnover of Bim, is suppressed by the removal of PINCH-1. Serine 38-41 BCL2 like 11 Homo sapiens 65-68 18063582-9 2008 Consistent with this, ERK1/2-mediated Ser(69) phosphorylation of Bim, a key signal for turnover of Bim, is suppressed by the removal of PINCH-1. Serine 38-41 BCL2 like 11 Homo sapiens 99-102 17652622-7 2007 Interestingly, also the single knockout of Bim or Bax, but not that of Bak or Bid, conferred partial resistance, suggesting a particular role of these mediators in the cell-death pathway activated by paclitaxel. Paclitaxel 200-210 BCL2 like 11 Homo sapiens 43-46 17914587-0 2007 Isoprenoid-independent pathway is involved in apoptosis induced by risedronate, a bisphosphonate, in which Bim plays a critical role in breast cancer cell line MCF-7. Terpenes 0-10 BCL2 like 11 Homo sapiens 107-110 17914587-0 2007 Isoprenoid-independent pathway is involved in apoptosis induced by risedronate, a bisphosphonate, in which Bim plays a critical role in breast cancer cell line MCF-7. Risedronic Acid 67-78 BCL2 like 11 Homo sapiens 107-110 17914587-0 2007 Isoprenoid-independent pathway is involved in apoptosis induced by risedronate, a bisphosphonate, in which Bim plays a critical role in breast cancer cell line MCF-7. Diphosphonates 82-96 BCL2 like 11 Homo sapiens 107-110 17914587-5 2007 These data clearly indicate that both isoprenoid-dependent and -independent pathways might be involved in the apoptosis induced by bisphosphonate, and Bim might be a critical component for the isoprenoid-independent apoptotic pathway. Terpenes 193-203 BCL2 like 11 Homo sapiens 151-154 17938269-0 2007 Malignant mesothelioma cells are rapidly sensitized to TRAIL-induced apoptosis by low-dose anisomycin via Bim. Anisomycin 91-101 BCL2 like 11 Homo sapiens 106-109 17927446-5 2007 The process requires induction of the proapoptotic BH3-only BCL2 family member BIM (i.e., BCL2-like 11, or BCL2L11); erlotinib dramatically induces BIM levels in sensitive but not in resistant cell lines, and knockdown of BIM expression by RNA interference virtually eliminates drug-induced cell killing in vitro. Erlotinib Hydrochloride 117-126 BCL2 like 11 Homo sapiens 90-102 17927446-5 2007 The process requires induction of the proapoptotic BH3-only BCL2 family member BIM (i.e., BCL2-like 11, or BCL2L11); erlotinib dramatically induces BIM levels in sensitive but not in resistant cell lines, and knockdown of BIM expression by RNA interference virtually eliminates drug-induced cell killing in vitro. Erlotinib Hydrochloride 117-126 BCL2 like 11 Homo sapiens 107-114 17927446-5 2007 The process requires induction of the proapoptotic BH3-only BCL2 family member BIM (i.e., BCL2-like 11, or BCL2L11); erlotinib dramatically induces BIM levels in sensitive but not in resistant cell lines, and knockdown of BIM expression by RNA interference virtually eliminates drug-induced cell killing in vitro. bim 79-82 BCL2 like 11 Homo sapiens 90-102 17927446-5 2007 The process requires induction of the proapoptotic BH3-only BCL2 family member BIM (i.e., BCL2-like 11, or BCL2L11); erlotinib dramatically induces BIM levels in sensitive but not in resistant cell lines, and knockdown of BIM expression by RNA interference virtually eliminates drug-induced cell killing in vitro. bim 79-82 BCL2 like 11 Homo sapiens 107-114 17913853-0 2007 Synergistic cytotoxicity between tamoxifen and the plant toxin persin in human breast cancer cells is dependent on Bim expression and mediated by modulation of ceramide metabolism. Tamoxifen 33-42 BCL2 like 11 Homo sapiens 115-118 17938269-7 2007 Consistent with this, we found that anisomycin induces rapid accumulation of the BH3-only protein Bim; moreover, small interfering RNA knockdown of Bim inhibits anisomycin-induced sensitization. Anisomycin 36-46 BCL2 like 11 Homo sapiens 98-101 17938269-7 2007 Consistent with this, we found that anisomycin induces rapid accumulation of the BH3-only protein Bim; moreover, small interfering RNA knockdown of Bim inhibits anisomycin-induced sensitization. Anisomycin 161-171 BCL2 like 11 Homo sapiens 148-151 17938269-8 2007 Bim accumulation seems not to be transcriptional; instead, it is associated with Bim phosphorylation and increased stability, both consistent with the activation of c-jun NH2-terminal kinase signals by anisomycin. Anisomycin 202-212 BCL2 like 11 Homo sapiens 0-3 17938269-9 2007 Overall, our data indicate that the rapid and selective sensitization by anisomycin in mesothelioma cells is mediated by posttranslational potentiation of Bim, which primes the cells for apoptosis via the death receptor pathway. Anisomycin 73-83 BCL2 like 11 Homo sapiens 155-158 17595328-7 2007 Finally, stable knockdown of Bcl-2-interacting mediator of cell death (Bim) with short hairpin RNA in K562 cells significantly diminished sorafenib lethality, arguing strongly for a functional role of this proapoptotic Bcl-2 family member in the lethality of this agent. Sorafenib 138-147 BCL2 like 11 Homo sapiens 29-69 17503221-7 2007 Bim isoforms were differentially regulated after chemotherapeutic drug 5-Fluorouracil (5-FU) treatment. Fluorouracil 71-85 BCL2 like 11 Homo sapiens 0-3 17503221-7 2007 Bim isoforms were differentially regulated after chemotherapeutic drug 5-Fluorouracil (5-FU) treatment. Fluorouracil 87-91 BCL2 like 11 Homo sapiens 0-3 17973572-6 2007 Here we show that up-regulation of the BH3-only polypeptide BIM (also known as BCL2-like 11) correlated with gefitinib-induced apoptosis in gefitinib-sensitive EGFR-mutant lung cancer cells. Gefitinib 109-118 BCL2 like 11 Homo sapiens 79-91 17973572-6 2007 Here we show that up-regulation of the BH3-only polypeptide BIM (also known as BCL2-like 11) correlated with gefitinib-induced apoptosis in gefitinib-sensitive EGFR-mutant lung cancer cells. Gefitinib 140-149 BCL2 like 11 Homo sapiens 79-91 17973573-7 2007 Gefitinib caused a rapid increase in the level of the proapoptotic BH3-only protein BIM (also called BCL2-like 11) through both transcriptional and post-translational mechanisms. Gefitinib 0-9 BCL2 like 11 Homo sapiens 101-113 17716672-5 2007 Accordingly, we provide the evidence that Bim mediates PM-induced apoptosis via mitochondrial pathway. Promethium 55-57 BCL2 like 11 Homo sapiens 42-45 17699104-13 2007 We further found that anisomycin+CH-11 up-regulated the proapoptotic protein Bim by approximately 14-fold. Anisomycin 22-32 BCL2 like 11 Homo sapiens 77-80 17699104-13 2007 We further found that anisomycin+CH-11 up-regulated the proapoptotic protein Bim by approximately 14-fold. 4-dimethylamino-3',4'-dimethoxychalcone 33-38 BCL2 like 11 Homo sapiens 77-80 17699104-14 2007 Simultaneously inhibiting Bim expression and JNK activation additively desensitized U87 cells to anisomycin+CH-11. Anisomycin 97-107 BCL2 like 11 Homo sapiens 26-29 17699104-14 2007 Simultaneously inhibiting Bim expression and JNK activation additively desensitized U87 cells to anisomycin+CH-11. 4-dimethylamino-3',4'-dimethoxychalcone 108-113 BCL2 like 11 Homo sapiens 26-29 17699104-15 2007 These findings show that anisomycin-induced ribotoxic stress sensitizes glioblastoma cells to death receptor-induced apoptosis via a specific mechanism requiring both JNK activation and Bim induction. Anisomycin 25-35 BCL2 like 11 Homo sapiens 186-189 17432977-8 2007 Expression of Bim, which plays an important role in imatinib-induced cell-killing, was not suppressed in MYL-R. Imatinib Mesylate 52-60 BCL2 like 11 Homo sapiens 14-17 17525735-7 2007 The dissociation of Bim from Mcl-1 is specific for Bim(EL) and requires ERK1/2-dependent phosphorylation of Bim(EL) at Ser(65). Serine 119-122 BCL2 like 11 Homo sapiens 20-23 17525735-7 2007 The dissociation of Bim from Mcl-1 is specific for Bim(EL) and requires ERK1/2-dependent phosphorylation of Bim(EL) at Ser(65). Serine 119-122 BCL2 like 11 Homo sapiens 51-54 17525735-7 2007 The dissociation of Bim from Mcl-1 is specific for Bim(EL) and requires ERK1/2-dependent phosphorylation of Bim(EL) at Ser(65). Serine 119-122 BCL2 like 11 Homo sapiens 51-54 17538248-0 2007 Imatinib and nilotinib induce apoptosis of chronic myeloid leukemia cells through a Bim-dependant pathway modulated by cytokines. Imatinib Mesylate 0-8 BCL2 like 11 Homo sapiens 84-87 17538248-0 2007 Imatinib and nilotinib induce apoptosis of chronic myeloid leukemia cells through a Bim-dependant pathway modulated by cytokines. nilotinib 13-22 BCL2 like 11 Homo sapiens 84-87 17538248-6 2007 In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 h. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA. Imatinib Mesylate 70-78 BCL2 like 11 Homo sapiens 123-126 17538248-6 2007 In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 h. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA. Imatinib Mesylate 70-78 BCL2 like 11 Homo sapiens 177-180 17538248-6 2007 In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 h. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA. Imatinib Mesylate 70-78 BCL2 like 11 Homo sapiens 177-180 17538248-6 2007 In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 h. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA. nilotinib 82-91 BCL2 like 11 Homo sapiens 123-126 17538248-6 2007 In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 h. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA. nilotinib 82-91 BCL2 like 11 Homo sapiens 177-180 17538248-6 2007 In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 h. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA. nilotinib 82-91 BCL2 like 11 Homo sapiens 177-180 17538248-7 2007 However, the anti-proliferative effect of imatinib was preserved in Bim-depleted cells. Imatinib Mesylate 42-50 BCL2 like 11 Homo sapiens 68-71 17538248-8 2007 When K562 cells were cultured in a cytokine containing medium, the pro-apoptotic effect of nilotinib was decreased by 68% and this was related to a decrease in Bim-EL dephosphorylation and accumulation. nilotinib 91-100 BCL2 like 11 Homo sapiens 160-163 17538248-10 2007 In conclusion, both nilotinib and imatinib induce apoptosis through Bim accumulation independently of cell cycle arrest. nilotinib 20-29 BCL2 like 11 Homo sapiens 68-71 17538248-10 2007 In conclusion, both nilotinib and imatinib induce apoptosis through Bim accumulation independently of cell cycle arrest. Imatinib Mesylate 34-42 BCL2 like 11 Homo sapiens 68-71 17287517-2 2007 Here, we report that 17beta-estradiol (E2) selectively regulates neuronal expression of the Bcl-2 family (bcl-2, bcl-x, bcl-w, bax, bak, bad, bik, bnip3, bid, and bim). Estradiol 21-37 BCL2 like 11 Homo sapiens 163-166 17218385-6 2007 Bim knockdown by shRNA suppressed BAX and BAK conformational change and protected cells from dasatinib/PD184352 lethality. bakuchiol 42-45 BCL2 like 11 Homo sapiens 0-3 17218385-6 2007 Bim knockdown by shRNA suppressed BAX and BAK conformational change and protected cells from dasatinib/PD184352 lethality. Dasatinib 93-102 BCL2 like 11 Homo sapiens 0-3 17218385-6 2007 Bim knockdown by shRNA suppressed BAX and BAK conformational change and protected cells from dasatinib/PD184352 lethality. 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide 103-111 BCL2 like 11 Homo sapiens 0-3 17339365-11 2007 Additional experiments showed that selenium increased the transactivation activity of FOXO3A, as evidenced by a reporter gene assay, as well as by the elevated expression of Bim (a target gene of FOXO3A). Selenium 35-43 BCL2 like 11 Homo sapiens 174-177 17339365-12 2007 The functional significance of Bim was confirmed by the observation that RNA interference of Bim markedly reduced the potency of selenium/doxorubicin to induce apoptosis. Selenium 129-137 BCL2 like 11 Homo sapiens 31-34 17339365-12 2007 The functional significance of Bim was confirmed by the observation that RNA interference of Bim markedly reduced the potency of selenium/doxorubicin to induce apoptosis. Selenium 129-137 BCL2 like 11 Homo sapiens 93-96 17339365-12 2007 The functional significance of Bim was confirmed by the observation that RNA interference of Bim markedly reduced the potency of selenium/doxorubicin to induce apoptosis. Doxorubicin 138-149 BCL2 like 11 Homo sapiens 31-34 17339365-12 2007 The functional significance of Bim was confirmed by the observation that RNA interference of Bim markedly reduced the potency of selenium/doxorubicin to induce apoptosis. Doxorubicin 138-149 BCL2 like 11 Homo sapiens 93-96 17062728-3 2007 The main pathway by which Fas signaling regulates the levels of Bim expression in human T-cell blasts is the death-domain- and caspase-independent generation of discrete levels of H2O2, which results in the net increase of Foxo3a levels. ammonium ferrous sulfate 26-29 BCL2 like 11 Homo sapiens 64-67 17389404-4 2007 We compared the three-dimensional structures of the complexes formed between BH3 peptides of both Bim and Noxa, and we show that a discrete C-terminal sequence of the Noxa BH3 is necessary to instigate Mcl-1 degradation. BH 3 77-80 BCL2 like 11 Homo sapiens 98-101 17062728-3 2007 The main pathway by which Fas signaling regulates the levels of Bim expression in human T-cell blasts is the death-domain- and caspase-independent generation of discrete levels of H2O2, which results in the net increase of Foxo3a levels. Hydrogen Peroxide 180-184 BCL2 like 11 Homo sapiens 64-67 17287517-4 2007 In the presence of toxic levels of Abeta, we observe that E2 attenuates indices of neuronal apoptosis: c-Jun N-terminal kinase (JNK)-dependent downregulation of Bcl-w and upregulation of Bim, mitochondrial release of cytochrome c and Smac, and cell death. UNII-042A8N37WH 35-40 BCL2 like 11 Homo sapiens 187-190 17287517-7 2007 These results suggest that E2 may reduce Abeta-induced neuronal apoptosis at least in part by two complementary pathways: (1) ER-dependent, JNK-independent upregulation of Bcl-w and downregulation of Bim under basal conditions, and (2) ER-dependent inhibition of Abeta-induced JNK activation and subsequent JNK-dependent downregulation of Bcl-w and upregulation of Bim, resulting in mitochondrial release of cytochrome c and Smac and eventual cell death. UNII-042A8N37WH 41-46 BCL2 like 11 Homo sapiens 200-203 17287517-7 2007 These results suggest that E2 may reduce Abeta-induced neuronal apoptosis at least in part by two complementary pathways: (1) ER-dependent, JNK-independent upregulation of Bcl-w and downregulation of Bim under basal conditions, and (2) ER-dependent inhibition of Abeta-induced JNK activation and subsequent JNK-dependent downregulation of Bcl-w and upregulation of Bim, resulting in mitochondrial release of cytochrome c and Smac and eventual cell death. UNII-042A8N37WH 41-46 BCL2 like 11 Homo sapiens 365-368 16778834-0 2007 Downregulation of Bim by brain-derived neurotrophic factor activation of TrkB protects neuroblastoma cells from paclitaxel but not etoposide or cisplatin-induced cell death. Paclitaxel 112-122 BCL2 like 11 Homo sapiens 18-21 16778834-4 2007 Bim was involved in paclitaxel but not etoposide or cisplatin-induced cell death in NB cells. Paclitaxel 20-30 BCL2 like 11 Homo sapiens 0-3 16645638-4 2007 When Bim binds and inactivates prosurvival proteins, most residues remain disordered, only the BH3 element becomes structured, and the short alpha-helical molecular recognition element can be considered to behave as a "bead on a string". BH 3 95-98 BCL2 like 11 Homo sapiens 5-8 17283153-7 2007 Combination treatment with DNA-damaging agents was extremely synergistic with ABT-737 and was associated with the down-regulation of Mcl-1 and the up-regulation of Noxa, Puma, and Bim in H196 cells. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 78-81 BCL2 like 11 Homo sapiens 180-183 17203211-0 2007 Arsenic trioxide induces apoptosis via the mitochondrial pathway by upregulating the expression of Bax and Bim in human B cells. Arsenic Trioxide 0-16 BCL2 like 11 Homo sapiens 107-110 17203211-4 2007 As2O3-induced apoptosis is associated with reduced mitochondrial transmembrane potential (delta psi), enhanced generation of intracellular reactive oxygen species (ROS), release of cytochrome c and apoptosis-inducing factor (AIF) from mitochondria into cytoplasm, activation of caspases, and upregulation of Bax and Bim expression. Arsenic Trioxide 0-5 BCL2 like 11 Homo sapiens 316-319 16443928-7 2006 Treatment of cells with a MEK inhibitor (U0126) or proteasome inhibitor (epoxomicin) also up-regulated Bim accumulation and rendered cells more sensitive to anoikis. U 0126 41-46 BCL2 like 11 Homo sapiens 103-106 17075901-4 2007 Staurosporine-induced the release of Mcl-1 from mitochondria that formed a complex with Bim. Staurosporine 0-13 BCL2 like 11 Homo sapiens 88-91 16446371-10 2006 PS-341 activated the BH3-only proteins Bik and Bim and down-regulated Bcl-2 and Bcl-xL mRNA and protein expression. Bortezomib 0-6 BCL2 like 11 Homo sapiens 47-50 17233818-7 2007 Reducing Bim levels by short hairpin RNA targeting inhibited imatinib and mitoxantrone-induced cell death. Imatinib Mesylate 61-69 BCL2 like 11 Homo sapiens 9-12 17233818-7 2007 Reducing Bim levels by short hairpin RNA targeting inhibited imatinib and mitoxantrone-induced cell death. Mitoxantrone 74-86 BCL2 like 11 Homo sapiens 9-12 17233818-9 2007 Together our data indicate that disrupting beta1 integrin-mediated regulation of Bim degradation may increase the efficacy of drugs, including imatinib, used to treat haematopoietic malignancies. Imatinib Mesylate 143-151 BCL2 like 11 Homo sapiens 81-84 17051334-0 2006 Bim plays a crucial role in synergistic induction of apoptosis by the histone deacetylase inhibitor SBHA and TRAIL in melanoma cells. suberoyl bis-hydroxamic acid 100-104 BCL2 like 11 Homo sapiens 0-3 17051334-7 2006 Inhibition of Bim by siRNA attenuated conformational changes of Bax, mitochondrial apoptotic events, and activation of caspase-3, leading to marked inhibition of the synergy between SBHA and TRAIL. suberoyl bis-hydroxamic acid 182-186 BCL2 like 11 Homo sapiens 14-17 17051334-8 2006 Thus, Bim plays an essential role in synergistic induction of apoptosis by SBHA and TRAIL in melanoma. suberoyl bis-hydroxamic acid 75-79 BCL2 like 11 Homo sapiens 6-9 16596265-6 2006 Moreover, the levels of both c-Jun and JunB, two components of the AP-1 complex, and those of FasL and Bim, two transcriptional targets of AP-1, also increased during anandamide treatment. anandamide 167-177 BCL2 like 11 Homo sapiens 103-106 16443928-7 2006 Treatment of cells with a MEK inhibitor (U0126) or proteasome inhibitor (epoxomicin) also up-regulated Bim accumulation and rendered cells more sensitive to anoikis. epoxomicin 73-83 BCL2 like 11 Homo sapiens 103-106 16431916-5 2006 Ubiquitinated proteins are degraded by the proteasome, and inhibition of the proteasome with MG132 (a proteasome inhibitor) prevented Bim degradation and blocked rapid ischemic tolerance. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 93-98 BCL2 like 11 Homo sapiens 134-137 16431916-6 2006 Inhibition of p42/p44 mitogen-activated protein kinase activation by U0126 reduced Bim ubiquitination and Bim degradation and blocked rapid ischemic tolerance. U 0126 69-74 BCL2 like 11 Homo sapiens 83-86 16431916-6 2006 Inhibition of p42/p44 mitogen-activated protein kinase activation by U0126 reduced Bim ubiquitination and Bim degradation and blocked rapid ischemic tolerance. U 0126 69-74 BCL2 like 11 Homo sapiens 106-109 16431916-7 2006 Finally, inhibition of Bim expression using antisense oligonucleotides also reduced cell death following ischemic challenge. Oligonucleotides 54-70 BCL2 like 11 Homo sapiens 23-26 16091744-0 2005 Melphalan-induced apoptosis in multiple myeloma cells is associated with a cleavage of Mcl-1 and Bim and a decrease in the Mcl-1/Bim complex. Melphalan 0-9 BCL2 like 11 Homo sapiens 97-100 16183168-2 2005 In the present study, we reported that carbachol, a muscarinic cholinergic receptor agonist, regulated Bim in human SH-SY5Y neuroblastoma cells. Carbachol 39-48 BCL2 like 11 Homo sapiens 103-106 16309671-3 2006 New protein synthesis was required before Dex-induced mitochondrial changes, and the kinetics of the apoptotic events correlated with the upregulation of the Bim protein. Dexamethasone 42-45 BCL2 like 11 Homo sapiens 158-161 16333030-12 2005 Blockade of Bax, Bim, and p53 mRNA expression by siRNA reduced estradiol-induced apoptosis relative to control by 76% [95% confidence interval (CI) = 73% to 79%, P < .001], 85% [95% CI = 90% to 80%, P < .001], and 40% [95% CI = 45% to 35%, P < .001], respectively, whereas blockade of FasL by siRNA had no effect. Estradiol 63-72 BCL2 like 11 Homo sapiens 17-20 16183168-3 2005 Carbachol rapidly induced an upward gel mobility shift of Bim, which was abolished by protein phosphatase treatment, indicating an increased Bim phosphorylation by carbachol. Carbachol 0-9 BCL2 like 11 Homo sapiens 58-61 16183168-3 2005 Carbachol rapidly induced an upward gel mobility shift of Bim, which was abolished by protein phosphatase treatment, indicating an increased Bim phosphorylation by carbachol. Carbachol 0-9 BCL2 like 11 Homo sapiens 141-144 16183168-3 2005 Carbachol rapidly induced an upward gel mobility shift of Bim, which was abolished by protein phosphatase treatment, indicating an increased Bim phosphorylation by carbachol. Carbachol 164-173 BCL2 like 11 Homo sapiens 58-61 16183168-3 2005 Carbachol rapidly induced an upward gel mobility shift of Bim, which was abolished by protein phosphatase treatment, indicating an increased Bim phosphorylation by carbachol. Carbachol 164-173 BCL2 like 11 Homo sapiens 141-144 16183168-4 2005 The effect of carbachol was mimicked by the protein kinase C activator 12-myristate 13-acetate (PMA) and was blocked by the protein kinase C inhibitor rottlerin, suggesting that activation of protein kinase C was required for carbachol-induced phosphorylation of Bim. Carbachol 14-23 BCL2 like 11 Homo sapiens 263-266 16183168-4 2005 The effect of carbachol was mimicked by the protein kinase C activator 12-myristate 13-acetate (PMA) and was blocked by the protein kinase C inhibitor rottlerin, suggesting that activation of protein kinase C was required for carbachol-induced phosphorylation of Bim. rottlerin 151-160 BCL2 like 11 Homo sapiens 263-266 16183168-4 2005 The effect of carbachol was mimicked by the protein kinase C activator 12-myristate 13-acetate (PMA) and was blocked by the protein kinase C inhibitor rottlerin, suggesting that activation of protein kinase C was required for carbachol-induced phosphorylation of Bim. Carbachol 226-235 BCL2 like 11 Homo sapiens 263-266 16183168-5 2005 Prolonged treatment with carbachol and PMA significantly decreased Bim protein levels in total cell lysates and mitrochondria. Carbachol 25-34 BCL2 like 11 Homo sapiens 67-70 16183168-6 2005 Carbachol and PMA had no effect in the transcriptional regulation of Bim, whereas the reduction of Bim by both carbachol and PMA was reversed by the proteosome inhibitors, suggesting that carbachol and PMA facilitated the proteosome-dependent Bim degradation. Carbachol 111-120 BCL2 like 11 Homo sapiens 99-102 16183168-6 2005 Carbachol and PMA had no effect in the transcriptional regulation of Bim, whereas the reduction of Bim by both carbachol and PMA was reversed by the proteosome inhibitors, suggesting that carbachol and PMA facilitated the proteosome-dependent Bim degradation. Carbachol 111-120 BCL2 like 11 Homo sapiens 99-102 16183168-6 2005 Carbachol and PMA had no effect in the transcriptional regulation of Bim, whereas the reduction of Bim by both carbachol and PMA was reversed by the proteosome inhibitors, suggesting that carbachol and PMA facilitated the proteosome-dependent Bim degradation. Tetradecanoylphorbol Acetate 125-128 BCL2 like 11 Homo sapiens 99-102 16183168-6 2005 Carbachol and PMA had no effect in the transcriptional regulation of Bim, whereas the reduction of Bim by both carbachol and PMA was reversed by the proteosome inhibitors, suggesting that carbachol and PMA facilitated the proteosome-dependent Bim degradation. Tetradecanoylphorbol Acetate 125-128 BCL2 like 11 Homo sapiens 99-102 16183168-6 2005 Carbachol and PMA had no effect in the transcriptional regulation of Bim, whereas the reduction of Bim by both carbachol and PMA was reversed by the proteosome inhibitors, suggesting that carbachol and PMA facilitated the proteosome-dependent Bim degradation. Carbachol 188-197 BCL2 like 11 Homo sapiens 99-102 16183168-6 2005 Carbachol and PMA had no effect in the transcriptional regulation of Bim, whereas the reduction of Bim by both carbachol and PMA was reversed by the proteosome inhibitors, suggesting that carbachol and PMA facilitated the proteosome-dependent Bim degradation. Carbachol 188-197 BCL2 like 11 Homo sapiens 99-102 16183168-6 2005 Carbachol and PMA had no effect in the transcriptional regulation of Bim, whereas the reduction of Bim by both carbachol and PMA was reversed by the proteosome inhibitors, suggesting that carbachol and PMA facilitated the proteosome-dependent Bim degradation. Tetradecanoylphorbol Acetate 125-128 BCL2 like 11 Homo sapiens 99-102 16183168-6 2005 Carbachol and PMA had no effect in the transcriptional regulation of Bim, whereas the reduction of Bim by both carbachol and PMA was reversed by the proteosome inhibitors, suggesting that carbachol and PMA facilitated the proteosome-dependent Bim degradation. Tetradecanoylphorbol Acetate 125-128 BCL2 like 11 Homo sapiens 99-102 16091744-0 2005 Melphalan-induced apoptosis in multiple myeloma cells is associated with a cleavage of Mcl-1 and Bim and a decrease in the Mcl-1/Bim complex. Melphalan 0-9 BCL2 like 11 Homo sapiens 129-132 16091744-6 2005 In this study, we demonstrate that melphalan disrupts the Mcl-1/Bim complex whereas the Bcl-2/Bim complex is not modified. Melphalan 35-44 BCL2 like 11 Homo sapiens 64-67 16091744-8 2005 Thus, we can hypothesize that the cleaved 26 kDa proapoptotic Mcl-1 and the 19 and 12 kDa of Bim, generated during melphalan treatment could contribute to the amplification loop of apoptosis. Melphalan 115-124 BCL2 like 11 Homo sapiens 93-96 16230407-8 2005 To show functional significance of "Bim reexpression," a Bim-specific small interfering RNA was applied and found to rescue BCR/ABL-transformed leukemic cells from imatinib-induced cell death. Imatinib Mesylate 164-172 BCL2 like 11 Homo sapiens 36-39 16230407-8 2005 To show functional significance of "Bim reexpression," a Bim-specific small interfering RNA was applied and found to rescue BCR/ABL-transformed leukemic cells from imatinib-induced cell death. Imatinib Mesylate 164-172 BCL2 like 11 Homo sapiens 57-60 16230407-4 2005 The BCR/ABL inhibitors imatinib and AMN107 were found to promote expression of Bim in CML cells. Imatinib Mesylate 23-31 BCL2 like 11 Homo sapiens 79-82 16230407-9 2005 In summary, our data identify BCR/ABL as a Bim suppressor in CML cells and suggest that reexpression of Bim by novel tyrosine kinase inhibitors, proteasome inhibition, or by targeting signaling pathways downstream of BCR/ABL may be an attractive therapeutic approach in imatinib-resistant CML. Imatinib Mesylate 270-278 BCL2 like 11 Homo sapiens 104-107 16230407-6 2005 The BCR/ABL-induced decrease in expression of Bim was found to be a posttranscriptional event that depended on signaling through the mitogen-activated protein kinase pathway and was abrogated by the proteasome inhibitor MG132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 220-225 BCL2 like 11 Homo sapiens 46-49 15855272-7 2005 Bim phosphorylation was inhibited by PD98059 and LY294002 treatment, suggesting the involvement of mitogen-activated protein kinase kinase/mitogen-activated protein kinase (MEK/MAPK) and phosphatidylinositol 3 (PI3)-kinase pathways in this process. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 37-44 BCL2 like 11 Homo sapiens 0-3 15855272-7 2005 Bim phosphorylation was inhibited by PD98059 and LY294002 treatment, suggesting the involvement of mitogen-activated protein kinase kinase/mitogen-activated protein kinase (MEK/MAPK) and phosphatidylinositol 3 (PI3)-kinase pathways in this process. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 49-57 BCL2 like 11 Homo sapiens 0-3 15855272-7 2005 Bim phosphorylation was inhibited by PD98059 and LY294002 treatment, suggesting the involvement of mitogen-activated protein kinase kinase/mitogen-activated protein kinase (MEK/MAPK) and phosphatidylinositol 3 (PI3)-kinase pathways in this process. Phosphatidylinositols 187-207 BCL2 like 11 Homo sapiens 0-3 15824087-9 2005 In addition, atorvastatin reduced the expression of the proapoptotic forkhead-regulated protein Bim in a PI3K-dependent manner. Atorvastatin 13-25 BCL2 like 11 Homo sapiens 96-99 15870701-6 2005 Furthermore, we observed Bax activation and Bim induction only in p53-deficient cells after PTX-2 treatment. pectenotoxin 2 92-97 BCL2 like 11 Homo sapiens 44-47 15870701-7 2005 RNA interference of either Bim or Bax resulted in the inhibition of caspases and apoptosis induced by PTX-2. pectenotoxin 2 102-107 BCL2 like 11 Homo sapiens 27-30 15944736-7 2005 TAp63alpha upregulates expression of proapoptotic Bcl-2 family members like Bax and BCL2L11 and the expression of RAD9, DAP3 and APAF1. tap63alpha 0-10 BCL2 like 11 Homo sapiens 84-91 15953346-2 2005 Removal of depolarizing potassium triggers CGN apoptosis that requires induction of Bim, a BH3-only Bcl-2 family member. Potassium 24-33 BCL2 like 11 Homo sapiens 84-87 15728578-3 2005 ERK1/2-dependent phosphorylation correlates with the presence of a domain unique to the Bim(EL) splice variant that includes the major ERK1/2 phosphorylation site Ser(65). Serine 163-166 BCL2 like 11 Homo sapiens 88-91 15661735-8 2005 Finally, we demonstrate that HN prevents BimEL-induced oligomerization of Bak using isolated mitochondria. bakuchiol 74-77 BCL2 like 11 Homo sapiens 41-46 15708859-8 2005 Moreover, Smad7 was found to be important for the basal expression of Bim, a pro-apoptotic Bcl-2 family member, and for 2-ME-induced expression of Bim. 2-Methoxyestradiol 120-124 BCL2 like 11 Homo sapiens 147-150 15766661-2 2005 Here we demonstrate that the proapoptotic BH3-only protein BIM is a tumor suppressor in epithelial solid tumors and also is a determinant in paclitaxel sensitivity in vivo. Paclitaxel 141-151 BCL2 like 11 Homo sapiens 59-62 15721302-6 2005 Whereas PD98059 treatment alone led to marked activation of the pro-apoptotic Bim and Bad proteins and significantly increased anoikis, these effects were clearly reversed by PMA. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 8-15 BCL2 like 11 Homo sapiens 78-81 15843898-0 2005 Zinc pyrithione induces apoptosis and increases expression of Bim. pyrithione zinc 0-15 BCL2 like 11 Homo sapiens 62-65 15843898-6 2005 This increase in Bim isoform expression was dependent on transcription being blocked by treatment with actinomycin D. Dactinomycin 103-116 BCL2 like 11 Homo sapiens 17-20 15766661-3 2005 Furthermore, the H-ras/mitogen-activated protein kinase (MAPK) pathway conferred resistance to paclitaxel that was dependent on functional inactivation of BIM. Paclitaxel 95-105 BCL2 like 11 Homo sapiens 155-158 15766661-4 2005 Whereas paclitaxel induced BIM accumulation and BIM-dependent apoptosis in vitro and in tumors in vivo, the H-ras/MAPK pathway suppressed this BIM induction by phosphorylating BIM and targeting BIM for degradation in proteasomes. Paclitaxel 8-18 BCL2 like 11 Homo sapiens 27-30 15766661-4 2005 Whereas paclitaxel induced BIM accumulation and BIM-dependent apoptosis in vitro and in tumors in vivo, the H-ras/MAPK pathway suppressed this BIM induction by phosphorylating BIM and targeting BIM for degradation in proteasomes. Paclitaxel 8-18 BCL2 like 11 Homo sapiens 48-51 15766661-4 2005 Whereas paclitaxel induced BIM accumulation and BIM-dependent apoptosis in vitro and in tumors in vivo, the H-ras/MAPK pathway suppressed this BIM induction by phosphorylating BIM and targeting BIM for degradation in proteasomes. Paclitaxel 8-18 BCL2 like 11 Homo sapiens 48-51 15766661-4 2005 Whereas paclitaxel induced BIM accumulation and BIM-dependent apoptosis in vitro and in tumors in vivo, the H-ras/MAPK pathway suppressed this BIM induction by phosphorylating BIM and targeting BIM for degradation in proteasomes. Paclitaxel 8-18 BCL2 like 11 Homo sapiens 48-51 15766661-4 2005 Whereas paclitaxel induced BIM accumulation and BIM-dependent apoptosis in vitro and in tumors in vivo, the H-ras/MAPK pathway suppressed this BIM induction by phosphorylating BIM and targeting BIM for degradation in proteasomes. Paclitaxel 8-18 BCL2 like 11 Homo sapiens 48-51 15766661-5 2005 The proteasome inhibitor Velcade (P-341, Bortezomib) restored BIM induction, abrogated H-ras-dependent paclitaxel resistance, and promoted BIM-dependent tumor regression, suggesting the potential benefits of combinatorial chemotherapy of Velcade and paclitaxel. Bortezomib 25-32 BCL2 like 11 Homo sapiens 62-65 15766661-5 2005 The proteasome inhibitor Velcade (P-341, Bortezomib) restored BIM induction, abrogated H-ras-dependent paclitaxel resistance, and promoted BIM-dependent tumor regression, suggesting the potential benefits of combinatorial chemotherapy of Velcade and paclitaxel. Bortezomib 25-32 BCL2 like 11 Homo sapiens 139-142 15766661-5 2005 The proteasome inhibitor Velcade (P-341, Bortezomib) restored BIM induction, abrogated H-ras-dependent paclitaxel resistance, and promoted BIM-dependent tumor regression, suggesting the potential benefits of combinatorial chemotherapy of Velcade and paclitaxel. Bortezomib 34-39 BCL2 like 11 Homo sapiens 62-65 15767553-0 2005 The proteasome inhibitor bortezomib sensitizes cells to killing by death receptor ligand TRAIL via BH3-only proteins Bik and Bim. Bortezomib 25-35 BCL2 like 11 Homo sapiens 125-128 15766661-5 2005 The proteasome inhibitor Velcade (P-341, Bortezomib) restored BIM induction, abrogated H-ras-dependent paclitaxel resistance, and promoted BIM-dependent tumor regression, suggesting the potential benefits of combinatorial chemotherapy of Velcade and paclitaxel. Bortezomib 34-39 BCL2 like 11 Homo sapiens 139-142 15766661-5 2005 The proteasome inhibitor Velcade (P-341, Bortezomib) restored BIM induction, abrogated H-ras-dependent paclitaxel resistance, and promoted BIM-dependent tumor regression, suggesting the potential benefits of combinatorial chemotherapy of Velcade and paclitaxel. Bortezomib 41-51 BCL2 like 11 Homo sapiens 62-65 15766661-5 2005 The proteasome inhibitor Velcade (P-341, Bortezomib) restored BIM induction, abrogated H-ras-dependent paclitaxel resistance, and promoted BIM-dependent tumor regression, suggesting the potential benefits of combinatorial chemotherapy of Velcade and paclitaxel. Bortezomib 41-51 BCL2 like 11 Homo sapiens 139-142 15711598-0 2005 Apoptosis of non-small-cell lung cancer cell lines after paclitaxel treatment involves the BH3-only proapoptotic protein Bim. Paclitaxel 57-67 BCL2 like 11 Homo sapiens 121-124 15711598-2 2005 Susceptibility to killing by paclitaxel correlated with expression of the BH3-only protein, Bim, but not with other members of Bcl-2 family. Paclitaxel 29-39 BCL2 like 11 Homo sapiens 92-95 15711598-3 2005 NSCLC cell lines with the highest level of Bim expression are most susceptible to apoptosis induction after paclitaxel treatment. Paclitaxel 108-118 BCL2 like 11 Homo sapiens 43-46 15711598-4 2005 Forced expression of Bim increased paclitaxel-mediated killing of cells expressing an undetectable level of Bim. Paclitaxel 35-45 BCL2 like 11 Homo sapiens 21-24 15711598-4 2005 Forced expression of Bim increased paclitaxel-mediated killing of cells expressing an undetectable level of Bim. Paclitaxel 35-45 BCL2 like 11 Homo sapiens 108-111 15711598-5 2005 Conversely, knock down of Bim, but not Bcl-2 expression, decreased the susceptibility of tumor cells to paclitaxel-mediated killing. Paclitaxel 104-114 BCL2 like 11 Homo sapiens 26-29 15711598-8 2005 These results established Bim as a critical molecular link between the microtubule poison, paclitaxel, and apoptosis. Paclitaxel 91-101 BCL2 like 11 Homo sapiens 26-29 15767553-6 2005 Similarly, the synergy between bortezomib and TRAIL in killing human prostate cancer cells was impaired in cells in which both Bik and Bim were down-regulated by RNA interference. Bortezomib 31-41 BCL2 like 11 Homo sapiens 135-138 15767553-8 2005 These results implicate BH3-only proteins, in particular both Bik and Bim, as important mediators of the antitumor action of bortezomib and establish their role in its enhancement of TRAIL-induced apoptosis. Bortezomib 125-135 BCL2 like 11 Homo sapiens 70-73 15226421-5 2004 In addition, the expression levels of Bim are uniformly low in cell lines established from patients in the blast crisis phase of CML, and imatinib induced Bim in these cells. Imatinib Mesylate 138-146 BCL2 like 11 Homo sapiens 38-41 15520191-11 2004 Ceramide-mediated changes in localization of JNK were consistent with the observed changes in phosphorylation status of c-Jun and Bim. Ceramides 0-8 BCL2 like 11 Homo sapiens 130-133 15520191-12 2004 Furthermore, ceramide promoted Bim translocation to the mitochondria. Ceramides 13-21 BCL2 like 11 Homo sapiens 31-34 15520191-14 2004 These results suggest that JNK may participate in ceramide-induced apoptosis in A549 cells by a mechanism involving Bim. Ceramides 50-58 BCL2 like 11 Homo sapiens 116-119 15470142-3 2004 Here, we report that JNK catalyzed the phosphorylation of the BH3-only protein Bcl-2 interacting mediator of cell death (BimEL) at serine 65, both in vitro and in vivo. Serine 131-137 BCL2 like 11 Homo sapiens 79-119 15319368-7 2004 High glucose increases expression of the pro-apoptotic Bcl protein Bim (a transcriptional target of FKHR). Glucose 5-12 BCL2 like 11 Homo sapiens 67-70 15520191-10 2004 On the other hand, ceramide promoted phosphorylation of Bim and induced translocation of active JNK from the nucleus to the cytoplasm and mitochondrial fraction. Ceramides 19-27 BCL2 like 11 Homo sapiens 56-59 15226421-5 2004 In addition, the expression levels of Bim are uniformly low in cell lines established from patients in the blast crisis phase of CML, and imatinib induced Bim in these cells. Imatinib Mesylate 138-146 BCL2 like 11 Homo sapiens 155-158 14996839-8 2004 8-CPT-cAMP also induced Bim expression and enhanced dexamethasone-promoted apoptosis in human T-cell leukemia CEM-C7-14 (glucocorticoid-sensitive) and CEM-C1-15 (glucocorticoid-resistant) cells; increased Bim expression in 8-CPT-cAMP-treated CEM-C1-15 cells correlated with conversion of the cells from resistance to sensitivity to glucocorticoid-promoted apoptosis. 8-cpt 0-5 BCL2 like 11 Homo sapiens 205-208 15069698-6 2004 FK228 increased expression of proapoptotic BH3-only Bim proteins, and gene transfer-mediated overexpression of Bimalpha radiosensitized DLD1 cells. romidepsin 0-5 BCL2 like 11 Homo sapiens 52-55 15069698-7 2004 These data suggest that the FK228-mediated increase of Bim expression may at least partially contribute to its augmentation of radiation-induced apoptosis. romidepsin 28-33 BCL2 like 11 Homo sapiens 55-58 14970329-7 2004 Immunosuppressive drugs known to prevent T cell deletion in vivo, such as cyclosporin A or FK506, blocked Bim up-regulation and rescued T cells from death receptor-independent AICD, whereas rapamycin, which allows the development of stable immunological tolerance, did not exhibit these activities. Cyclosporine 74-87 BCL2 like 11 Homo sapiens 106-109 15078986-8 2004 In addition, SBHA induced relocation of the protein Bim to mitochondria and its association with Bcl-2. suberic bishydroxamate 13-17 BCL2 like 11 Homo sapiens 52-55 15078986-11 2004 The protein Bim may be a key initiator of apoptosis in cells treated with SBHA. suberic bishydroxamate 74-78 BCL2 like 11 Homo sapiens 12-15 15030401-0 2004 Lovastatin-induced up-regulation of the BH3-only protein, Bim, and cell death in glioblastoma cells. Lovastatin 0-10 BCL2 like 11 Homo sapiens 58-61 15030401-4 2004 Lovastatin-induced death occurs in correlation with significantly increased levels of the BH3-only protein, Bim. Lovastatin 0-10 BCL2 like 11 Homo sapiens 108-111 15030401-7 2004 Changes in levels of Bim, as well as increase phosphorylation of Erk1/2, c-jun, and p38 are all prevented by co-incubation of lovastatin and the isoprenylation metabolite, geranylgeranyl pyrophosphate. Lovastatin 126-136 BCL2 like 11 Homo sapiens 21-24 15030401-7 2004 Changes in levels of Bim, as well as increase phosphorylation of Erk1/2, c-jun, and p38 are all prevented by co-incubation of lovastatin and the isoprenylation metabolite, geranylgeranyl pyrophosphate. geranylgeranyl pyrophosphate 172-200 BCL2 like 11 Homo sapiens 21-24 15030401-9 2004 Further elucidation of the mechanisms of lovastatin-induced up-regulation of Bim and apoptosis in glioblastoma cells are important in determining a potential role for lovastatin as a chemotherapy agent. Lovastatin 41-51 BCL2 like 11 Homo sapiens 77-80 14681225-5 2004 By using the peptidylprolyl isomerase, Pin1, as a probe for proline-directed phosphorylation, we show that ERK1/2-dependent phosphorylation of Bim(EL) occurs at (S/T)P motifs. Proline 60-67 BCL2 like 11 Homo sapiens 143-150 14970329-7 2004 Immunosuppressive drugs known to prevent T cell deletion in vivo, such as cyclosporin A or FK506, blocked Bim up-regulation and rescued T cells from death receptor-independent AICD, whereas rapamycin, which allows the development of stable immunological tolerance, did not exhibit these activities. Tacrolimus 91-96 BCL2 like 11 Homo sapiens 106-109 14527951-0 2003 FoxO3a transcriptional regulation of Bim controls apoptosis in paclitaxel-treated breast cancer cell lines. Paclitaxel 63-73 BCL2 like 11 Homo sapiens 37-40 14527951-3 2003 Western blotting revealed that in a panel of nine breast cancer cell lines expression of FoxO1a and FoxO3a correlated with the expression of the pro-apoptotic FoxO target Bim, which was associated with paclitaxel-induced apoptosis. Paclitaxel 202-212 BCL2 like 11 Homo sapiens 171-174 14527951-4 2003 In MCF-7 cells, which were paclitaxel-sensitive, the already high basal levels of FoxO3a and Bim protein increased dramatically after drug treatment, as did Bim mRNA, which correlated with apoptosis induction. Paclitaxel 27-37 BCL2 like 11 Homo sapiens 93-96 14527951-4 2003 In MCF-7 cells, which were paclitaxel-sensitive, the already high basal levels of FoxO3a and Bim protein increased dramatically after drug treatment, as did Bim mRNA, which correlated with apoptosis induction. Paclitaxel 27-37 BCL2 like 11 Homo sapiens 157-160 14527951-7 2003 Gene silencing experiments showed that small interference RNA (siRNA) specific for FoxO3a reduced the levels of FoxO3a and Bim protein as well as inhibited apoptosis in paclitaxel-treated MCF-7 cells. Paclitaxel 169-179 BCL2 like 11 Homo sapiens 123-126 14527951-8 2003 Furthermore, siRNA specific for Bim reduced the levels of Bim protein and inhibited apoptosis in paclitaxel-treated MCF-7 cells. Paclitaxel 97-107 BCL2 like 11 Homo sapiens 32-35 14527951-9 2003 This is the first demonstration that up-regulation of FoxO3a by paclitaxel can result in increased levels of Bim mRNA and protein, which can be a direct cause of apoptosis in breast cancer cells. Paclitaxel 64-74 BCL2 like 11 Homo sapiens 109-112 10946267-5 2000 The early phase was inhibited by the protein kinase C inhibitor bisindolylmaleimide I (BIM), whereas the late phase was not blocked by BIM, protein tyrosine kinase inhibitor genistein, or the mitogen-activated protein kinase/extracellular signal-related kinase inhibitor PD98059. bisindolylmaleimide I 64-85 BCL2 like 11 Homo sapiens 87-90 12427831-7 2002 Bim knockdown using an antisense oligonucleotide strategy suppressed Abeta(25-35)-induced Smac release and resulted in attenuation of CEC death. Oligonucleotides 33-48 BCL2 like 11 Homo sapiens 0-3 12427831-8 2002 Furthermore, AP-1 inhibition, with curcumin or c-fos antisense oligonucleotide, reduced bim expression. Curcumin 35-43 BCL2 like 11 Homo sapiens 88-91 12427831-8 2002 Furthermore, AP-1 inhibition, with curcumin or c-fos antisense oligonucleotide, reduced bim expression. Oligonucleotides 63-78 BCL2 like 11 Homo sapiens 88-91 12934079-4 2003 Similar to neurons undergoing trophic factor deprivation-induced apoptosis, ara-C-exposed neurons became hypometabolic before death and upregulated c-myb, c-fos, and Bim. Cytarabine 76-81 BCL2 like 11 Homo sapiens 166-169 12749905-3 2003 We show here that Bim is serine phosphorylated in lymphocytes, predominantly on the EL form. Serine 25-31 BCL2 like 11 Homo sapiens 18-21 9430630-2 1998 An expression screen for proteins that bind to Bcl-2 yielded a small novel protein, denoted Bim, whose only similarity to any known protein is the short (nine amino acid) BH3 motif shared by most Bcl-2 homologues. BH 3 171-174 BCL2 like 11 Homo sapiens 92-95 34826170-0 2022 Melatonin induces apoptotic cell death through Bim stabilization by Sp1-mediated OTUD1 upregulation. Melatonin 0-9 BCL2 like 11 Homo sapiens 47-50 31273056-0 2019 MicroRNA-222 promotes drug resistance to doxorubicin in breast cancer via regulation of miR-222/bim pathway. Doxorubicin 41-52 BCL2 like 11 Homo sapiens 96-99 31273056-7 2019 Conversely, in MCF-7 cells transfected with miR-222 mimics, up-regulation of miR-222 was associated with decreased Bim level accompanied by less apoptosis and higher IC50 Moreover, miR-222 inhibitors reversed DOX resistance via miR-222-Bim-caspase pathway. Doxorubicin 209-212 BCL2 like 11 Homo sapiens 115-118 31273056-8 2019 Collectively, these data first elucidated that miR-222 could function as an oncogene and was able to reduce the sensitivity of breast cancer cells to DOX through miR-222-Bim-caspase pathway, which provided a potential target to increase DOX sensitivity in clinical breast cancer treatment. Doxorubicin 150-153 BCL2 like 11 Homo sapiens 170-173 31273056-8 2019 Collectively, these data first elucidated that miR-222 could function as an oncogene and was able to reduce the sensitivity of breast cancer cells to DOX through miR-222-Bim-caspase pathway, which provided a potential target to increase DOX sensitivity in clinical breast cancer treatment. Doxorubicin 237-240 BCL2 like 11 Homo sapiens 170-173 34826170-2 2022 Previously, we showed that melatonin induced the expression of Bim, a pro-apoptotic Bcl-2 protein, at both the transcriptional and post-translational levels. Melatonin 27-36 BCL2 like 11 Homo sapiens 63-66 34826170-3 2022 In the present study, we investigated the molecular mechanisms underlying the melatonin-mediated Bim upregulation through post-translational regulation. Melatonin 78-87 BCL2 like 11 Homo sapiens 97-100 34826170-5 2022 OTUD1 knockdown inhibited melatonin-induced Bim upregulation and apoptosis in cancer cells. Melatonin 26-35 BCL2 like 11 Homo sapiens 44-47 34826170-7 2022 Melatonin-induced OTUD1 upregulation caused deubiquitnation at the lysine 3 residue of Bim, resulting in its stabilization. Melatonin 0-9 BCL2 like 11 Homo sapiens 87-90 34826170-7 2022 Melatonin-induced OTUD1 upregulation caused deubiquitnation at the lysine 3 residue of Bim, resulting in its stabilization. Lysine 67-73 BCL2 like 11 Homo sapiens 87-90 34826170-8 2022 In addition, melatonin-induced activation of Sp1 was found to be involved in OTUD1 upregulation at the transcriptional level, and pharmacological inhibition and genetic ablation of Sp1 (siRNA) interrupted melatonin-induced OTUD1-mediated Bim upregulation. Melatonin 13-22 BCL2 like 11 Homo sapiens 238-241 34826170-8 2022 In addition, melatonin-induced activation of Sp1 was found to be involved in OTUD1 upregulation at the transcriptional level, and pharmacological inhibition and genetic ablation of Sp1 (siRNA) interrupted melatonin-induced OTUD1-mediated Bim upregulation. Melatonin 205-214 BCL2 like 11 Homo sapiens 238-241 34826170-11 2022 Thus, our results demonstrated that melatonin induced apoptosis by stabilizing Bim via Sp1-mediated OTUD1 upregulation. Melatonin 36-45 BCL2 like 11 Homo sapiens 79-82 34910385-8 2021 Pralatrexate and alcohol had synergistic effects on the cell death mediators of Bim, caspase3 and PARP. 10-propargyl-10-deazaaminopterin 0-12 BCL2 like 11 Homo sapiens 80-83 34910385-8 2021 Pralatrexate and alcohol had synergistic effects on the cell death mediators of Bim, caspase3 and PARP. Alcohols 17-24 BCL2 like 11 Homo sapiens 80-83 34753395-10 2021 Increased Bim expression indicated that apcin promotes the apoptosis of glioma cells. apcin 40-45 BCL2 like 11 Homo sapiens 10-13 34882068-10 2021 Immunoblot analyses of MKN-45 and KATO-III cells revealed that dovitinib decreased phospho-FGFR, phospho-AKT, phospho-ERK, phospho-p70S6K, phospho-4EBP1, Bcl-2 and increased cleaved PARP-1, cleaved-caspase-3, p27, Bax, Bim, with an additive effect from combination therapy. 4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one 63-72 BCL2 like 11 Homo sapiens 219-222 34160887-8 2021 The upregulation of BIM is the event responsible for the sensitization of OC cells to cisplatin. Cisplatin 86-95 BCL2 like 11 Homo sapiens 20-23 34478517-7 2021 These manifestations depend on the BH3-profile of parental cells which guide the enhanced formation of Bcl-2:BIM and/or dynamic (i.e. treatment-induced) formation of Bcl-xL:BIM and Bcl-xL:BAK complexes. BH 3 35-38 BCL2 like 11 Homo sapiens 109-112 34635799-6 2021 Both genetic and pharmacological inhibition of SREBP1 sensitized osimertinib-resistant cells and tumors to osimertinib primarily through enhancing Bim-dependent induction of apoptosis, whereas enforced expression of ectopic SREBP1 in sensitive EGFR-mutant NSCLC cells compromised osimertinib"s cell-killing effects. osimertinib 107-118 BCL2 like 11 Homo sapiens 147-150 34811352-6 2021 Live-cell fluorescence resonance energy transfer (FRET) analysis showed that Met unlocked the binding of Mcl-1 to Bak, and enhanced the binding of Bim to Bak and subsequent Bak homo-oligomerization. bakuchiol 154-157 BCL2 like 11 Homo sapiens 147-150 34811352-6 2021 Live-cell fluorescence resonance energy transfer (FRET) analysis showed that Met unlocked the binding of Mcl-1 to Bak, and enhanced the binding of Bim to Bak and subsequent Bak homo-oligomerization. bakuchiol 173-176 BCL2 like 11 Homo sapiens 147-150 34811352-9 2021 In summary, our data demonstrate for the first time that Met promotes ROS-dependent apoptosis by regulating the Mcl-1-Bim-Bak axis. Reactive Oxygen Species 70-73 BCL2 like 11 Homo sapiens 118-121 34811352-9 2021 In summary, our data demonstrate for the first time that Met promotes ROS-dependent apoptosis by regulating the Mcl-1-Bim-Bak axis. bakuchiol 122-125 BCL2 like 11 Homo sapiens 118-121 34759291-8 2021 Mechanistic insights indicate that a combination of AZD5363 and AZD8055 activated FOXO3a to induce Bim-associated apoptosis in p53 mutated HCC cells, whereas cells retaining functional p53 enhanced Bax. capivasertib 52-59 BCL2 like 11 Homo sapiens 99-102 34759291-8 2021 Mechanistic insights indicate that a combination of AZD5363 and AZD8055 activated FOXO3a to induce Bim-associated apoptosis in p53 mutated HCC cells, whereas cells retaining functional p53 enhanced Bax. (5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol 64-71 BCL2 like 11 Homo sapiens 99-102 34606419-6 2021 Moreover, we found that forskolin induced mitochondrion-dependent apoptosis which was accompanied by the increase of pro-apoptotic proteins Bax, Bad, Bim and Bid, the decrease of anti-apoptotic proteins Bcl-2 and Bcl-xl, the changes of the mitochondrial membrane potential (MMP) and increase of cleaved caspase-9, cleaved caspase-3 and cleaved PARP. Colforsin 24-33 BCL2 like 11 Homo sapiens 150-153 34245854-0 2021 Inhibition of MEK5/ERK5 signaling overcomes acquired resistance to the third generation EGFR inhibitor, osimertinib, via enhancing Bim-dependent apoptosis. osimertinib 104-115 BCL2 like 11 Homo sapiens 131-134 34834209-1 2021 The present study demonstrated that 2"-hydroxycinnamaldehyde (2"-HCA) induced apoptosis in human promyelocytic leukemia HL-60 cells through the activation of mitochondrial pathways including (1) translocation of Bim and Bax from the cytosol to mitochondria, (2) downregulation of Bcl-2 protein expression, (3) cytochrome c release into the cytosol, (4) loss of mitochondrial membrane potential (DeltaPsim), and (5) caspase activation. 2"-hydroxycinnamaldehyde 36-60 BCL2 like 11 Homo sapiens 212-215 34834209-1 2021 The present study demonstrated that 2"-hydroxycinnamaldehyde (2"-HCA) induced apoptosis in human promyelocytic leukemia HL-60 cells through the activation of mitochondrial pathways including (1) translocation of Bim and Bax from the cytosol to mitochondria, (2) downregulation of Bcl-2 protein expression, (3) cytochrome c release into the cytosol, (4) loss of mitochondrial membrane potential (DeltaPsim), and (5) caspase activation. 2"-hca 62-68 BCL2 like 11 Homo sapiens 212-215 34741230-6 2022 This indicates that TAK-580 enhances KPT-330-induced cytotoxicity and apoptosis primarily via the FOXO3a-Bim axis. tak-580 20-27 BCL2 like 11 Homo sapiens 105-108 34741230-6 2022 This indicates that TAK-580 enhances KPT-330-induced cytotoxicity and apoptosis primarily via the FOXO3a-Bim axis. selinexor 37-44 BCL2 like 11 Homo sapiens 105-108 34707185-7 2021 Indeed, the Mcl-1-specific inhibitor S63845 restored apoptosis by disrupting the interaction of Mcl-1 with Bim and Bak and significantly increased AraC toxicity in CD157-high but not in CD157-low AML cells. S63845 37-43 BCL2 like 11 Homo sapiens 107-110 34478517-7 2021 These manifestations depend on the BH3-profile of parental cells which guide the enhanced formation of Bcl-2:BIM and/or dynamic (i.e. treatment-induced) formation of Bcl-xL:BIM and Bcl-xL:BAK complexes. BH 3 35-38 BCL2 like 11 Homo sapiens 173-176 34257718-13 2021 miR-9a-5p mimic reversed the increase in cell apoptosis induced by CSE by inhibiting BCL2L11 expression in HPMECs. mir-9a-5p 0-9 BCL2 like 11 Homo sapiens 85-92 34608124-6 2021 Bim knockdown did not affect the doxorubicin-induced apoptosis in U2OS, suggested that a BH3-only protein other than Bim might participate in apoptosis induced by doxorubicin. Doxorubicin 163-174 BCL2 like 11 Homo sapiens 117-120 34339756-11 2021 Gene and protein detection showed that DG-8d or DG-8d combined with LY294002 could down-regulate signaling molecules of Bcl-2, PI3k, p-Akt, p-FoxO3a and up-regulate signaling molecules of Bax snd Bim. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 68-76 BCL2 like 11 Homo sapiens 196-199 34903991-6 2021 The result indicated that zebularine and TSA changed the expression level of the Bax, Bak, Bim Bcl-2, Bcl-xL, Mcl-1, DR4, DR5, FAS, FAS-L, TRAIL, DNA methyltransferase 1, 3a, and 3b, histone deacetylase inhibitors 1, 2, and 3 by which induced cell apoptosis and inhibit cell growth in all three cell lines. pyrimidin-2-one beta-ribofuranoside 26-36 BCL2 like 11 Homo sapiens 91-94 34366664-9 2021 By loading the encoding mRNA from the suicide gene Bim, a locally administered mBim/DMP-039 complex strongly inhibited growth in two colon cancer models. dmp-039 84-91 BCL2 like 11 Homo sapiens 51-54 34327135-6 2021 Mechanistically, PD98059 was able to potently suppress GCDA-stimulated nuclear aggregation of ERK1/2 and p-ERK1/2, upregulate pro-survival protein Mcl-1 and downregulate pro-apoptotic protein Bim. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 17-24 BCL2 like 11 Homo sapiens 192-195 34327135-6 2021 Mechanistically, PD98059 was able to potently suppress GCDA-stimulated nuclear aggregation of ERK1/2 and p-ERK1/2, upregulate pro-survival protein Mcl-1 and downregulate pro-apoptotic protein Bim. Glycochenodeoxycholic Acid 55-59 BCL2 like 11 Homo sapiens 192-195 34903991-6 2021 The result indicated that zebularine and TSA changed the expression level of the Bax, Bak, Bim Bcl-2, Bcl-xL, Mcl-1, DR4, DR5, FAS, FAS-L, TRAIL, DNA methyltransferase 1, 3a, and 3b, histone deacetylase inhibitors 1, 2, and 3 by which induced cell apoptosis and inhibit cell growth in all three cell lines. trichostatin A 41-44 BCL2 like 11 Homo sapiens 91-94 34203351-6 2021 Compared to single-agent neratinib, everolimus, or trametinib, both everolimus plus neratinib and trametinib plus neratinib significantly suppressed proliferation marker Ki67 and enhanced antitumor efficacy by activating the apoptosis pathway shown by increased Bim and cleaved-PARP expression. neratinib 25-34 BCL2 like 11 Homo sapiens 262-265 34279763-4 2021 METHODS AND RESULTS: According to our MTT assay results, Resveratrol (RSV), Nutlin3a and Suramin was found to be more effective in HCT-116 p53+/+ cells and these differences were evaluated together with the effect of 5-FU on the SIRT5, FOXO3a and Bim protein expressions in HCT-116 p53 +/+ and HCT-116 p53 -/- cells. Fluorouracil 217-221 BCL2 like 11 Homo sapiens 247-250 34203351-6 2021 Compared to single-agent neratinib, everolimus, or trametinib, both everolimus plus neratinib and trametinib plus neratinib significantly suppressed proliferation marker Ki67 and enhanced antitumor efficacy by activating the apoptosis pathway shown by increased Bim and cleaved-PARP expression. Everolimus 36-46 BCL2 like 11 Homo sapiens 262-265 34203351-6 2021 Compared to single-agent neratinib, everolimus, or trametinib, both everolimus plus neratinib and trametinib plus neratinib significantly suppressed proliferation marker Ki67 and enhanced antitumor efficacy by activating the apoptosis pathway shown by increased Bim and cleaved-PARP expression. trametinib 51-61 BCL2 like 11 Homo sapiens 262-265 34203351-6 2021 Compared to single-agent neratinib, everolimus, or trametinib, both everolimus plus neratinib and trametinib plus neratinib significantly suppressed proliferation marker Ki67 and enhanced antitumor efficacy by activating the apoptosis pathway shown by increased Bim and cleaved-PARP expression. Everolimus 68-78 BCL2 like 11 Homo sapiens 262-265 34203351-6 2021 Compared to single-agent neratinib, everolimus, or trametinib, both everolimus plus neratinib and trametinib plus neratinib significantly suppressed proliferation marker Ki67 and enhanced antitumor efficacy by activating the apoptosis pathway shown by increased Bim and cleaved-PARP expression. neratinib 84-93 BCL2 like 11 Homo sapiens 262-265 34203351-6 2021 Compared to single-agent neratinib, everolimus, or trametinib, both everolimus plus neratinib and trametinib plus neratinib significantly suppressed proliferation marker Ki67 and enhanced antitumor efficacy by activating the apoptosis pathway shown by increased Bim and cleaved-PARP expression. trametinib 98-108 BCL2 like 11 Homo sapiens 262-265 34203351-6 2021 Compared to single-agent neratinib, everolimus, or trametinib, both everolimus plus neratinib and trametinib plus neratinib significantly suppressed proliferation marker Ki67 and enhanced antitumor efficacy by activating the apoptosis pathway shown by increased Bim and cleaved-PARP expression. neratinib 114-123 BCL2 like 11 Homo sapiens 262-265 34105393-7 2021 This protein induced mitochondrial translocation of phosphatidylinositol-3,4,5-trisphosphate (PIP3) via its N-term, resulting in the stimulation of the protein kinase B (Akt)/forkhead box O3a (FOXO3a) pathway, which inhibited HR-induced mitochondrial accumulation of a mitochondrial target of FOXO3a, Bim, also known as a pro-apoptotic protein. phosphatidylinositol 3,4,5-triphosphate 52-92 BCL2 like 11 Homo sapiens 301-304 34060394-5 2022 Moreover, this agent induced ROS-mediated apoptosis by altering the expression of Bax, Bim, Caspase3, Bcl2, and XIAP. ros 29-32 BCL2 like 11 Homo sapiens 87-90 34121978-6 2021 Here, we evaluated the effect of miR-30c-2-3p on controlling XBP1-CHOP-BIM and its apoptotic effects on ovarian cancer cell lines during ERS. mir-30c-2-3p 33-45 BCL2 like 11 Homo sapiens 71-74 34077012-9 2021 FTI-277 and GGTI-287 decreased the concentration of phosphorylated ERK1/2 and mTOR via membrane localization of Ras and enhanced Bim expression. FTI 277 0-7 BCL2 like 11 Homo sapiens 129-132 34077012-9 2021 FTI-277 and GGTI-287 decreased the concentration of phosphorylated ERK1/2 and mTOR via membrane localization of Ras and enhanced Bim expression. GGTI 287 12-20 BCL2 like 11 Homo sapiens 129-132 34105393-7 2021 This protein induced mitochondrial translocation of phosphatidylinositol-3,4,5-trisphosphate (PIP3) via its N-term, resulting in the stimulation of the protein kinase B (Akt)/forkhead box O3a (FOXO3a) pathway, which inhibited HR-induced mitochondrial accumulation of a mitochondrial target of FOXO3a, Bim, also known as a pro-apoptotic protein. PIP3 94-98 BCL2 like 11 Homo sapiens 301-304 35625692-4 2022 Flow cytometry analysis revealed that metformin combined with FuOx induced late apoptosis (p < 0.05) by mediating mitochondria-related Mcl-1 and Bim protein expression. Metformin 38-47 BCL2 like 11 Homo sapiens 145-148 35609325-0 2022 BAY-885, a mitogen-activated protein kinase kinase 5 inhibitor, induces apoptosis by regulating the endoplasmic reticulum stress/Mcl-1/Bim pathway in breast cancer cells. BAY885 0-7 BCL2 like 11 Homo sapiens 135-138 35609325-7 2022 Moreover, the BAY-885-mediated downregulation of myeloid cell leukemia-1 (Mcl-1) and upregulation of Bim were dependent on ERK5 inhibition. BAY885 14-21 BCL2 like 11 Homo sapiens 101-104 35609325-8 2022 Furthermore, BAY-885 triggered activation of endoplasmic reticulum (ER) stress, which further led to the upregulation of Bim and downregulation of Mcl-1. BAY885 13-20 BCL2 like 11 Homo sapiens 121-124 35609325-10 2022 These findings suggested that BAY-885 induced apoptosis in BC cells via ER stress/Mcl-1/Bim axis, suggesting that BAY-885 may serve as a therapeutic agent for BC. BAY885 30-37 BCL2 like 11 Homo sapiens 88-91 35609325-10 2022 These findings suggested that BAY-885 induced apoptosis in BC cells via ER stress/Mcl-1/Bim axis, suggesting that BAY-885 may serve as a therapeutic agent for BC. BAY885 114-121 BCL2 like 11 Homo sapiens 88-91 35443722-0 2022 Artesunate improves venetoclax plus cytarabine AML cell targeting by regulating the Noxa/Bim/Mcl-1/p-Chk1 axis. Artesunate 0-10 BCL2 like 11 Homo sapiens 89-92 35346662-0 2022 Hydroquinone destabilizes BIM mRNA through upregulation of p62 in chronic myeloid leukemia cells. hydroquinone 0-12 BCL2 like 11 Homo sapiens 26-29 35346662-5 2022 Increased p62 expression in K562 cells reduced BIM mRNA stability and protein expression, which conferred resistance against the BH3 mimetics ABT-199 (BCL2 inhibitor) and A-1210477 (MCL1 inhibitor). 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 142-146 BCL2 like 11 Homo sapiens 47-50 35346662-5 2022 Increased p62 expression in K562 cells reduced BIM mRNA stability and protein expression, which conferred resistance against the BH3 mimetics ABT-199 (BCL2 inhibitor) and A-1210477 (MCL1 inhibitor). A-1210477 171-180 BCL2 like 11 Homo sapiens 47-50 35459209-7 2022 Meanwhile, we found that the combination of lorlatinib and CQ, an inhibitor of autophagy, inhibited autophagy and promoted apoptosis both in vitro and in vivo, which sensitized cells to lorlatinib through the dephosphorylation of Foxo3a and promoted nuclear translocation, then activation of Foxo3a/Bim axis. lorlatinib 44-54 BCL2 like 11 Homo sapiens 299-302 35459209-7 2022 Meanwhile, we found that the combination of lorlatinib and CQ, an inhibitor of autophagy, inhibited autophagy and promoted apoptosis both in vitro and in vivo, which sensitized cells to lorlatinib through the dephosphorylation of Foxo3a and promoted nuclear translocation, then activation of Foxo3a/Bim axis. Chloroquine 59-61 BCL2 like 11 Homo sapiens 299-302 35459209-7 2022 Meanwhile, we found that the combination of lorlatinib and CQ, an inhibitor of autophagy, inhibited autophagy and promoted apoptosis both in vitro and in vivo, which sensitized cells to lorlatinib through the dephosphorylation of Foxo3a and promoted nuclear translocation, then activation of Foxo3a/Bim axis. lorlatinib 186-196 BCL2 like 11 Homo sapiens 299-302 35443722-9 2022 Artesunate serves as a bridge for venetoclax and cytarabine combination by Noxa and Bim-mediated apoptosis and Mcl-1 reduction. venetoclax 34-44 BCL2 like 11 Homo sapiens 84-87 35443722-9 2022 Artesunate serves as a bridge for venetoclax and cytarabine combination by Noxa and Bim-mediated apoptosis and Mcl-1 reduction. Cytarabine 49-59 BCL2 like 11 Homo sapiens 84-87 35443722-10 2022 We provide a new triple combination for AML treatment by targeting the Noxa/Mcl-1/Bim axis to reverse Mcl-1/p-Chk1 resistance of cytarabine therapy. Cytarabine 129-139 BCL2 like 11 Homo sapiens 82-85 35443722-0 2022 Artesunate improves venetoclax plus cytarabine AML cell targeting by regulating the Noxa/Bim/Mcl-1/p-Chk1 axis. Cytarabine 36-46 BCL2 like 11 Homo sapiens 89-92 35443722-3 2022 Cytarabine induces S phase arrest-mediated DNA damage with activation of DNA replication checkpoint kinase 1 (Chk1) through phosphorylation, while venetoclax induces B cell lymphoma 2 (Bcl-2)-interacting mediator of cell death (Bim)-mediated apoptotic DNA damage. Cytarabine 0-10 BCL2 like 11 Homo sapiens 228-231 35443722-6 2022 Artesunate, an antimalaria drug, induces Noxa to replace Bim from Mcl-1 and induces synergistic apoptosis with venetoclax accompanied with Mcl-1 reduction. Artesunate 0-10 BCL2 like 11 Homo sapiens 57-60 35443722-9 2022 Artesunate serves as a bridge for venetoclax and cytarabine combination by Noxa and Bim-mediated apoptosis and Mcl-1 reduction. Artesunate 0-10 BCL2 like 11 Homo sapiens 84-87 35455398-5 2022 Specifically, dehydrocrenatidine significantly increased the expression of extrinsic pathway components (FAS, DR5, FADD, and TRADD) as well as intrinsic pathway components (Bax and Bim L/S) in liver cancer cells. dehydrocrenatidine 14-32 BCL2 like 11 Homo sapiens 181-184 35409154-6 2022 A mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK-ERK) pathway seems to be a particularly attractive target, as its activation leads to steroid resistance via a phosphorylating Bcl-2-interacting mediator of cell death (BIM), which is crucial in the steroid-induced cell death. Steroids 165-172 BCL2 like 11 Homo sapiens 206-246 35409154-6 2022 A mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK-ERK) pathway seems to be a particularly attractive target, as its activation leads to steroid resistance via a phosphorylating Bcl-2-interacting mediator of cell death (BIM), which is crucial in the steroid-induced cell death. Steroids 278-285 BCL2 like 11 Homo sapiens 206-246 35170373-0 2022 Role of long noncoding RNA KCNQ1 overlapping transcript 1/microRNA-124-3p/BCL-2-like 11 axis in hydrogen peroxide (H2O2)-stimulated human lens epithelial cells. Hydrogen Peroxide 96-113 BCL2 like 11 Homo sapiens 74-87 35530161-0 2022 Targeting PFKL with penfluridol inhibits glycolysis and suppresses esophageal cancer tumorigenesis in an AMPK/FOXO3a/BIM-dependent manner. Penfluridol 20-31 BCL2 like 11 Homo sapiens 117-120 35530161-7 2022 Mechanistically, direct binding of penfluridol and PFKL inhibits glucose consumption, lactate and ATP production, leads to nuclear translocation of FOXO3a and subsequent transcriptional activation of BIM in an AMPK-dependent manner. Penfluridol 35-46 BCL2 like 11 Homo sapiens 200-203 35170373-0 2022 Role of long noncoding RNA KCNQ1 overlapping transcript 1/microRNA-124-3p/BCL-2-like 11 axis in hydrogen peroxide (H2O2)-stimulated human lens epithelial cells. Hydrogen Peroxide 115-119 BCL2 like 11 Homo sapiens 74-87 35205731-7 2022 Mechanistically, dexamethasone induces a pro-apoptotic BCL2-interacting mediator of cell death (BIM) expression and apoptosis in ALL cells but enhances pro-survival B-cell lymphoma extra-large (BCLXL) expression in cardiomyocytes and clinical recovery with the reversion of cardiac atrophy. Dexamethasone 17-30 BCL2 like 11 Homo sapiens 55-94 35063650-8 2022 Moreover, knockout of Bim or Bax not only remarkably inhibited AC-induced apoptosis, but also markedly inhibited AC-triggered downregulation of SLC711 and GPX4, accumulation of lipid ROS, and damage to the plasma membrane. Reactive Oxygen Species 183-186 BCL2 like 11 Homo sapiens 22-25 35063650-9 2022 This suggests that Bim and Bax act upstream of SLC7A11 and GPX4 to mediate AC-induced ferroptosis. Actinium 75-77 BCL2 like 11 Homo sapiens 19-22 35063650-10 2022 Collectively, AC induces ferroptosis and apoptosis, in which the Bim- and Bax-mediated mitochondrial pathways play a dominant role. Actinium 14-16 BCL2 like 11 Homo sapiens 65-68 35189130-6 2022 By destabilizing the alpha-helix of BIM with a covalently linked azobenzene photoswitch, the dynamical response of the whole complex upon an ultrafast photo-perturbation was characterized. azobenzene 65-75 BCL2 like 11 Homo sapiens 36-39 35136485-9 2022 GZ17-6.02 and axitinib increased the expression of BAK, BIM, Beclin1 and ATG5, effects blocked by knock down of eIF2alpha. gz17-6 0-6 BCL2 like 11 Homo sapiens 56-59 35136485-9 2022 GZ17-6.02 and axitinib increased the expression of BAK, BIM, Beclin1 and ATG5, effects blocked by knock down of eIF2alpha. Axitinib 14-22 BCL2 like 11 Homo sapiens 56-59 34999051-7 2022 Moreover, we identified BIM protein as a mediator of ML324-induced apoptosis using CRISPR/Cas9 knockout analysis. ML324 53-58 BCL2 like 11 Homo sapiens 24-27 34999051-8 2022 We showed that the loss of Bim suppressed ML324-induced apoptosis by flow cytometry analysis, colony formation assay, and caspase-3 activation assay. ML324 42-47 BCL2 like 11 Homo sapiens 27-30 34999051-11 2022 Physical binding of KDM4E to Bim and CHOP promoters decreased the response to ML324. ML324 78-83 BCL2 like 11 Homo sapiens 29-32 35260176-8 2022 Mechanistically, sotorasib treatment led to stabilization of BIM and co-treatment with DT2216 inhibited sotorasib-induced BCL-XL/BIM interaction leading to enhanced apoptosis in KRASG12C tumor cell lines. AMG-510 17-26 BCL2 like 11 Homo sapiens 61-64 35260176-8 2022 Mechanistically, sotorasib treatment led to stabilization of BIM and co-treatment with DT2216 inhibited sotorasib-induced BCL-XL/BIM interaction leading to enhanced apoptosis in KRASG12C tumor cell lines. AMG-510 17-26 BCL2 like 11 Homo sapiens 129-132 35260176-8 2022 Mechanistically, sotorasib treatment led to stabilization of BIM and co-treatment with DT2216 inhibited sotorasib-induced BCL-XL/BIM interaction leading to enhanced apoptosis in KRASG12C tumor cell lines. DT2216 87-93 BCL2 like 11 Homo sapiens 61-64 35260176-8 2022 Mechanistically, sotorasib treatment led to stabilization of BIM and co-treatment with DT2216 inhibited sotorasib-induced BCL-XL/BIM interaction leading to enhanced apoptosis in KRASG12C tumor cell lines. DT2216 87-93 BCL2 like 11 Homo sapiens 129-132 35260176-8 2022 Mechanistically, sotorasib treatment led to stabilization of BIM and co-treatment with DT2216 inhibited sotorasib-induced BCL-XL/BIM interaction leading to enhanced apoptosis in KRASG12C tumor cell lines. AMG-510 104-113 BCL2 like 11 Homo sapiens 129-132 35151247-9 2022 To verify the mechanism of cell death induced by artemisinin in A-253 cells, we found an increased level of Bax, Bim, Bad, Bak and reduced level of antiapoptotic protein Bcl-2, Bcl-XL with concomitant release of mitochondrial resident protein cytochrome c into the cytoplasm. artemisinin 49-60 BCL2 like 11 Homo sapiens 113-116 35225486-11 2022 A significant negative correlation was evident between plasma miR-92a and serum Bim both in adenoma and CRC groups (P<0.001 for both). mir-92a 62-69 BCL2 like 11 Homo sapiens 80-83 34999051-0 2022 Inhibition of histone demethylase KDM4 by ML324 induces apoptosis through the unfolded protein response and Bim upregulation in hepatocellular carcinoma cells. kdm4 34-38 BCL2 like 11 Homo sapiens 108-111 34999051-0 2022 Inhibition of histone demethylase KDM4 by ML324 induces apoptosis through the unfolded protein response and Bim upregulation in hepatocellular carcinoma cells. ML324 42-47 BCL2 like 11 Homo sapiens 108-111 35417658-8 2022 We found that the expression level of FOXO3, Bax, and Bim increased, whereas Bcl-2, caspase-3, and caspase-7 decreased by remdesivir in SKOV3 cells. remdesivir 122-132 BCL2 like 11 Homo sapiens 54-57 35253767-8 2022 The analysis revealed an exceptionally high usage of CpC dinucleotide in all the envisaged 31 isoforms of Bim. cpc dinucleotide 53-69 BCL2 like 11 Homo sapiens 106-109 35253767-11 2022 CONCLUSION: An exceptionally high usage of CpC dinucleotide in all the envisaged 31 isoforms of Bim indicates a high order selectional force to fine tune Bim gene expression. cpc dinucleotide 43-59 BCL2 like 11 Homo sapiens 96-99 35253767-11 2022 CONCLUSION: An exceptionally high usage of CpC dinucleotide in all the envisaged 31 isoforms of Bim indicates a high order selectional force to fine tune Bim gene expression. cpc dinucleotide 43-59 BCL2 like 11 Homo sapiens 154-157 34979841-4 2021 Notably, peroxynitrite-evoked nitration of SIRT2 destroyed its enzymatic activity and the capability to deacetylate FOXO3a, and enhanced expression of Bim and caspase3, facilitating renal cell apoptosis in renal ischaemia/reperfusion and SIN-1(peroxynitrite donor) treatment in vitro, and these effects were reversed by FeTMPyP, a peroxynitrite decomposition scavenger. Peroxynitrous Acid 9-22 BCL2 like 11 Homo sapiens 151-154