PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 34873220-8 2021 Although TAC upregulated the Bcl-2 family proapoptotic (Bax and Bak) and anti-apoptotic (Bcl-2 and Bcl-xL) molecules in non-transgenic mice, TAC-induced upregulation of Bax and Bak was alleviated and that of Bcl-2 was enhanced in Lats2 +/- mice. tac 9-12 BCL2-like 1 Mus musculus 99-105 34873220-8 2021 Although TAC upregulated the Bcl-2 family proapoptotic (Bax and Bak) and anti-apoptotic (Bcl-2 and Bcl-xL) molecules in non-transgenic mice, TAC-induced upregulation of Bax and Bak was alleviated and that of Bcl-2 was enhanced in Lats2 +/- mice. tac 141-144 BCL2-like 1 Mus musculus 99-105 34857016-9 2021 In PDAC cells, Pladienolide-B increased apoptosis and decreased multiple tumor-related features, including cell proliferation, migration, and colony/sphere formation, altering AKT and JNK signaling, and favoring proapoptotic splicing variants (BCL-XS/BCL-XL, KRASa/KRAS, Delta133TP53/TP53). pladienolide 15-27 BCL2-like 1 Mus musculus 251-257 34791636-14 2021 iBET-151 plus paclitaxel significantly promoted cell cycle arrest and apoptosis and suppressed c-Myc, Bcl-2 and Bcl-xL expression. GSK1210151A 0-8 BCL2-like 1 Mus musculus 112-118 34791636-14 2021 iBET-151 plus paclitaxel significantly promoted cell cycle arrest and apoptosis and suppressed c-Myc, Bcl-2 and Bcl-xL expression. Paclitaxel 14-24 BCL2-like 1 Mus musculus 112-118 33517789-10 2021 Real-time RT-PCR demonstrated that matrine could significantly reduce the expression of AKT1, TP53, TNF, IL6 and ATM in mice with liver injury or lung injury (P < 0.05), and increase the expression of BCL2L1 to a certain extent (P > 0.05). matrine 35-42 BCL2-like 1 Mus musculus 201-207 33715588-5 2021 In MCF-7-xenograft tumour nude mice and immunosuppressive mice, 30 mg/kg Phy treatment inhibited tumour growth from the 8th day, and reduced Bcl-2 and Bcl-xL >50%, HO-1 and SOD-1 > 70% in tumour tissues of immunosuppressive mice. physcione 73-76 BCL2-like 1 Mus musculus 151-157 34659562-13 2021 To less extent, metformin can also downregulate the expression of another anti-apoptotic protein, BCL-xl. Metformin 16-25 BCL2-like 1 Mus musculus 98-104 34808021-3 2022 MPN-induced phenotype in the peripheral blood by conditional knockin of JAK2V617F was abrogated by conditional knockout of Bcl2l1, which presented anemia and thrombocytopenia independently of JAK2 mutation status. N-nitrosomethyl-N-propylamine 0-3 BCL2-like 1 Mus musculus 123-129 34504546-10 2021 Notably, DHMEQ inhibited the expression of NF-kappaB-dependent anti-apoptotic proteins, such as Bcl-XL, FLIP, and Bfl-1. dehydroxymethylepoxyquinomicin 9-14 BCL2-like 1 Mus musculus 96-102 34427858-0 2021 Treatment with the BCL-2/BCL-xL inhibitor senolytic drug ABT263/Navitoclax improves functional hyperemia in aged mice. navitoclax 57-63 BCL2-like 1 Mus musculus 25-31 34638536-10 2021 Western blot was performed to determine the levels of p-ERK1/2, Bcl-XL, Bax, and Hsp70 proteins upon DEX or DEX plus colostrum exposure. Dexamethasone 101-104 BCL2-like 1 Mus musculus 64-70 34638536-10 2021 Western blot was performed to determine the levels of p-ERK1/2, Bcl-XL, Bax, and Hsp70 proteins upon DEX or DEX plus colostrum exposure. Dexamethasone 108-111 BCL2-like 1 Mus musculus 64-70 34638536-12 2021 Cells, upon colostrum co-treated with DEX, exhibited higher levels of p-ERK1/2 and lower levels of Bcl-XL, Bax, and Hsp70. Dexamethasone 38-41 BCL2-like 1 Mus musculus 99-105 34659562-14 2021 Conclusion: Metformin downregulates the expression of anti-apoptotic proteins Mcl-1 and Bcl-xl by inhibiting protein production, and shows a synergistic anti-tumor effect with ABT-199 in acute myeloid leukemia. Metformin 12-21 BCL2-like 1 Mus musculus 88-94 34659562-14 2021 Conclusion: Metformin downregulates the expression of anti-apoptotic proteins Mcl-1 and Bcl-xl by inhibiting protein production, and shows a synergistic anti-tumor effect with ABT-199 in acute myeloid leukemia. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 176-179 BCL2-like 1 Mus musculus 88-94 34491906-8 2021 Consequently, SCFAs could promote the formation of DNTs, activate OX40 signal and simultaneously up-regulate the protein expression of Bcl-2, Bcl-xl and Survivin. 2,6-dinitrotoluene 51-55 BCL2-like 1 Mus musculus 142-148 34373701-10 2021 The combination of bufalin and hydroxycampothecin also increased the expression of apoptosis-related proteins Bax, p53, PDCD4 and GSK-3beta, and decreased the expression of Bcl-XL and p-AKT compared with a single drug treatment. bufalin 19-26 BCL2-like 1 Mus musculus 173-179 34376637-6 2021 We developed a mCherry-BCLXL fusion protein, which prevented BAX recruitment and activation to the mitochondria in tissue culture cells exposed to staurosporine. Staurosporine 147-160 BCL2-like 1 Mus musculus 23-28 34305900-7 2021 3HK and 3HAA, as direct and downstream products of KMO, effectively protected TEC from injury via increasing expression of Bcl-xL and TJP1. CHEMBL400689 0-3 BCL2-like 1 Mus musculus 123-129 34305900-7 2021 3HK and 3HAA, as direct and downstream products of KMO, effectively protected TEC from injury via increasing expression of Bcl-xL and TJP1. 3haa 8-12 BCL2-like 1 Mus musculus 123-129 34305900-7 2021 3HK and 3HAA, as direct and downstream products of KMO, effectively protected TEC from injury via increasing expression of Bcl-xL and TJP1. Turpentine 78-81 BCL2-like 1 Mus musculus 123-129 34277801-0 2021 Apatinib enhances the anti-tumor effect of paclitaxel via the PI3K/p65/Bcl-xl pathway in triple-negative breast cancer. apatinib 0-8 BCL2-like 1 Mus musculus 71-77 34277801-0 2021 Apatinib enhances the anti-tumor effect of paclitaxel via the PI3K/p65/Bcl-xl pathway in triple-negative breast cancer. Paclitaxel 43-53 BCL2-like 1 Mus musculus 71-77 34277801-2 2021 This study aimed to investigate the synergistic effects of apatinib and paclitaxel (PTX) on triple-negative breast cancer (TNBC) in vivo and in vitro, and to explore the molecular mechanism of the PI3K/p65/Bcl-xl pathway. apatinib 59-67 BCL2-like 1 Mus musculus 206-212 34277801-2 2021 This study aimed to investigate the synergistic effects of apatinib and paclitaxel (PTX) on triple-negative breast cancer (TNBC) in vivo and in vitro, and to explore the molecular mechanism of the PI3K/p65/Bcl-xl pathway. Paclitaxel 72-82 BCL2-like 1 Mus musculus 206-212 34277801-2 2021 This study aimed to investigate the synergistic effects of apatinib and paclitaxel (PTX) on triple-negative breast cancer (TNBC) in vivo and in vitro, and to explore the molecular mechanism of the PI3K/p65/Bcl-xl pathway. Paclitaxel 84-87 BCL2-like 1 Mus musculus 206-212 34277801-4 2021 Western blot (WB) was conducted to detect protein expression levels of PI3K, p65, and Bcl-xl after the application of apatinib and PTX. apatinib 118-126 BCL2-like 1 Mus musculus 86-92 34277801-4 2021 Western blot (WB) was conducted to detect protein expression levels of PI3K, p65, and Bcl-xl after the application of apatinib and PTX. Paclitaxel 131-134 BCL2-like 1 Mus musculus 86-92 34277801-8 2021 Apatinib could reduce the expression of p-PI3K, p65, and Bcl-xl proteins (P<0.05). apatinib 0-8 BCL2-like 1 Mus musculus 57-63 34277801-10 2021 Conclusions: Apatinib could enhance the anti-tumor effect of PTX on TNBC cells through the PI3K/p65/Bcl-xl molecular pathway, and apatinib combined with PTX might be a promising option for TNBC treatment. apatinib 13-21 BCL2-like 1 Mus musculus 100-106 34277801-10 2021 Conclusions: Apatinib could enhance the anti-tumor effect of PTX on TNBC cells through the PI3K/p65/Bcl-xl molecular pathway, and apatinib combined with PTX might be a promising option for TNBC treatment. Paclitaxel 61-64 BCL2-like 1 Mus musculus 100-106 34068575-6 2021 Early apoptosis and Bax/Bcl-xL were lower with alpha-TCP 400 muM (2.4 +- 0.4% and 0.5-fold) and ZDF 200 muM (1.8 +- 0.4% and 0.3-fold) supplementation in comparison with the control (5.3 +- 1.4% and 1.0-fold) with normal characterization and functional activity. alpha-Tocopherol 47-56 BCL2-like 1 Mus musculus 24-30 34068575-6 2021 Early apoptosis and Bax/Bcl-xL were lower with alpha-TCP 400 muM (2.4 +- 0.4% and 0.5-fold) and ZDF 200 muM (1.8 +- 0.4% and 0.3-fold) supplementation in comparison with the control (5.3 +- 1.4% and 1.0-fold) with normal characterization and functional activity. benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone 96-99 BCL2-like 1 Mus musculus 24-30 33786627-11 2021 The immunohistochemistry results demonstrated that caspase-8 and Fas expression levels were notably increased, whereas Bcl-2 and Bcl-xl expression levels were obviously decreased in matrine-treated tumors compared with PBS-treated tumors. matrine 182-189 BCL2-like 1 Mus musculus 129-135 35344814-4 2022 Metformin upregulated BAX activation with facilitation of BIM, BAD and PUMA; downregulated Bcl-2 and Bcl-xl, but did not affect Mcl-1. Metformin 0-9 BCL2-like 1 Mus musculus 101-107 33786627-6 2021 The results demonstrated that compared with the control group, matrine significantly induced ovarian cancer cell apoptosis by upregulating caspase-8 and Fas cell surface death receptor (Fas) expression levels, and downregulating Bcl-2 and Bcl-xl expression levels. matrine 63-70 BCL2-like 1 Mus musculus 239-245 34169637-6 2021 Curcumin could also inhibit the expression of cyclin D1/CDK4/6 and anti-apoptotic protein Bcl-2/Bcl-XL induced by NE, and induced cell cycle changes and increased apoptosis. Curcumin 0-8 BCL2-like 1 Mus musculus 96-102 34149855-9 2021 The expression of the Bcl-xl gene was downregulated in docetaxel + CPA2, docetaxel + Vit2 and Vit2 compared to docetaxel group. Docetaxel 55-64 BCL2-like 1 Mus musculus 22-28 34149855-9 2021 The expression of the Bcl-xl gene was downregulated in docetaxel + CPA2, docetaxel + Vit2 and Vit2 compared to docetaxel group. Docetaxel 73-82 BCL2-like 1 Mus musculus 22-28 34149855-9 2021 The expression of the Bcl-xl gene was downregulated in docetaxel + CPA2, docetaxel + Vit2 and Vit2 compared to docetaxel group. Docetaxel 111-120 BCL2-like 1 Mus musculus 22-28 34149855-10 2021 The Bax/Bcl-xl ratio significantly increased in docetaxel + CPA2, docetaxel + Vit1, docetaxel + Vit2, Vit1 and Vit2 groups compared to control, docetaxel and the docetaxel + CPA1 group. Docetaxel 48-57 BCL2-like 1 Mus musculus 8-14 34149855-10 2021 The Bax/Bcl-xl ratio significantly increased in docetaxel + CPA2, docetaxel + Vit1, docetaxel + Vit2, Vit1 and Vit2 groups compared to control, docetaxel and the docetaxel + CPA1 group. Docetaxel 66-75 BCL2-like 1 Mus musculus 8-14 34149855-10 2021 The Bax/Bcl-xl ratio significantly increased in docetaxel + CPA2, docetaxel + Vit1, docetaxel + Vit2, Vit1 and Vit2 groups compared to control, docetaxel and the docetaxel + CPA1 group. Docetaxel 84-93 BCL2-like 1 Mus musculus 8-14 34149855-10 2021 The Bax/Bcl-xl ratio significantly increased in docetaxel + CPA2, docetaxel + Vit1, docetaxel + Vit2, Vit1 and Vit2 groups compared to control, docetaxel and the docetaxel + CPA1 group. Docetaxel 144-153 BCL2-like 1 Mus musculus 8-14 34149855-10 2021 The Bax/Bcl-xl ratio significantly increased in docetaxel + CPA2, docetaxel + Vit1, docetaxel + Vit2, Vit1 and Vit2 groups compared to control, docetaxel and the docetaxel + CPA1 group. Docetaxel 162-171 BCL2-like 1 Mus musculus 8-14 35332309-8 2022 In an orthotopic mouse model of GBM, we demonstrate that the BCL-XL inhibitor A1331852 can penetrate the brain, with A1331852 detected in both tumour and healthy brain regions. A-1331852 78-86 BCL2-like 1 Mus musculus 61-67 35332309-8 2022 In an orthotopic mouse model of GBM, we demonstrate that the BCL-XL inhibitor A1331852 can penetrate the brain, with A1331852 detected in both tumour and healthy brain regions. A-1331852 117-125 BCL2-like 1 Mus musculus 61-67 35342408-0 2022 microRNA-106b-5p Promotes Cell Growth and Sensitizes Chemosensitivity to Sorafenib by Targeting the BTG3/Bcl-xL/p27 Signaling Pathway in Hepatocellular Carcinoma. Sorafenib 73-82 BCL2-like 1 Mus musculus 105-111 35342408-9 2022 Altogether, these data suggest that miR-106b-5p promotes cell proliferation and cell cycle and increases HCC cells" resistance to sorafenib through the BTG3/Bcl-xL/p27 signaling pathway. Sorafenib 130-139 BCL2-like 1 Mus musculus 157-163 35422916-8 2022 Meanwhile, the unbalanced expressions of Bax and Bcl-xL in renal tubules were restored by artemether. Artemether 90-100 BCL2-like 1 Mus musculus 49-55 32840726-8 2021 The expression of Bcl-xL and Xiap was increased in most conditions by having high Zn in the medium regardless of the presence of insulin or IL6. Zinc 82-84 BCL2-like 1 Mus musculus 18-24 34050131-7 2021 These pre-clinical findings provide a rationale for the future clinical evaluation for novel BH3-mimetic formulations in MPM, and indeed, other solid tumor types dependent on BCL-XL. BH 3 93-96 BCL2-like 1 Mus musculus 175-181 33911065-8 2021 Similarly, compared with that of the miR-1283 inhibited group, the expression of ATF4, CHOP, BID, BIM, and caspase-3 in the miR-1283 overexpression group was downregulated, while the expression of BCL-2 and BCL-X was upregulated (P<0.05). mir-1283 124-132 BCL2-like 1 Mus musculus 207-212 33737021-0 2021 Pyrazole (1, 2-diazole) induce apoptosis in lymphoma cells by targeting BCL-2 and BCL-XL genes and mitigate murine solid tumour development by regulating cyclin-D1 and Ki-67 expression. pyrazole 0-8 BCL2-like 1 Mus musculus 82-88 33737021-0 2021 Pyrazole (1, 2-diazole) induce apoptosis in lymphoma cells by targeting BCL-2 and BCL-XL genes and mitigate murine solid tumour development by regulating cyclin-D1 and Ki-67 expression. pyrazole 10-22 BCL2-like 1 Mus musculus 82-88 33737021-9 2021 In addition, the mRNA expression levels of anti-apoptotic genes, BCL-2 and BCL-XL were downregulated in solid tumours, corroborating the in vitro results that pyrazole encourage apoptotic cell death in DLA cells. pyrazole 159-167 BCL2-like 1 Mus musculus 75-81 33900313-6 2021 Consistently, in AGS cells, erinacine S treatment not only triggers the activation of extrinsic apoptosis pathways (TRAIL, Fas-L and caspase-8, -9, -3), but it also suppresses the expression of the anti-apoptotic molecules Bcl-2 and Bcl-XL in a time-dependent manner. erinacine S 28-39 BCL2-like 1 Mus musculus 233-239 33801158-5 2021 In addition, we present evidence that Bcl-xL fosters ATP generation by the mitochondria to fuel high energy needs by neurons, and its contribution to synaptic transmission. Adenosine Triphosphate 53-56 BCL2-like 1 Mus musculus 38-44 32931040-7 2021 Further studies revealed that krill oil induced mitochondrial-dependent apoptosis of CT-26 cells, including loss of mitochondrial membrane potential, increased cytosolic calcium levels, activation of caspase-3, and downregulation of anti-apoptotic proteins MCL-1 and BCL-XL. krill oil 30-39 BCL2-like 1 Mus musculus 267-273 33170418-2 2021 The aim of the present study is to evaluate the in vivo effect of acute and chronic lithium treatment on the expression of beta-catenin target genes, addressing its transcripts HIG2, Bcl-xL, Cyclin D1, c-myc, in cortical and hippocampal tissue from adult mice. Lithium 84-91 BCL2-like 1 Mus musculus 183-189 33406839-6 2021 DHA-PC and EPA-PC accelerate cancer cell apoptosis by decreasing NF-kappaB-mediated antiapoptotic factors Bcl-2 and Bcl-XL, thereby inhibiting tumor growth. dha-pc 0-6 BCL2-like 1 Mus musculus 116-122 33406839-6 2021 DHA-PC and EPA-PC accelerate cancer cell apoptosis by decreasing NF-kappaB-mediated antiapoptotic factors Bcl-2 and Bcl-XL, thereby inhibiting tumor growth. epa-pc 11-17 BCL2-like 1 Mus musculus 116-122 33431795-5 2021 A preclinical study using in vivo mouse model also validated that suppressing BCL-XL led to enhance high dose DHT effect to induce PCa cell death. Dihydrotestosterone 110-113 BCL2-like 1 Mus musculus 78-84 33170418-10 2021 We conclude that Wnt/beta-catenin transcriptional response (HIG2, Bcl-xL, Cyclin D1 and c-myc) is up-regulated in the mouse brain in response to acute and chronic lithium treatment at therapeutic concentrations. Lithium 163-170 BCL2-like 1 Mus musculus 66-72 33552868-7 2021 Mechanistically, BCL-XL inhibition exacerbates the dependency of TNBC cells on WEE1 function, leading to Histone H3 and phosphoS33RPA32 upregulation, RRM2 downregulation, cell cycle perturbation, mitotic catastrophe, and apoptosis. phosphos33rpa32 120-135 BCL2-like 1 Mus musculus 17-23 32863923-5 2020 In vitro, inhibiting TLR9 expression levels using chloroquine decreased the cell viability, proliferation and migration of the CRC cell line HT29, and further experiments indicated that this may occur through downregulating the expression levels of NF-kappaB, proliferating cell nuclear antigen and Bcl-xl. Chloroquine 50-61 BCL2-like 1 Mus musculus 299-305 32913503-10 2020 Immunohistochemical staining demonstrated that SPR064 and paclitaxel significantly reduced the expression of Ki-67 and BCL-xL in the endometrial tumors of both obese and lean mice. spr064 47-53 BCL2-like 1 Mus musculus 119-125 32843706-6 2020 To determine if depletion of senescent-like neuronal cells may effectively mitigate CIPN, we used a pharmacological "senolytic" agent, ABT263, which inhibits the anti-apoptotic proteins BCL-2 and BCL-xL and selectively kills senescent cells. navitoclax 135-141 BCL2-like 1 Mus musculus 196-202 32824972-6 2020 The observed effects were associated with strong hypoxia-inducible factor 1-alpha (HIF-1alpha) induction and B-cell lymphoma-extra-large anti-apoptotic protein (Bcl-xL)-mediated anti-apoptotic response in normoxic DOX-treated TEV donor cells, being also tightly connected to the DOX-TEV-mediated HIF-1alpha induction, as well as Bcl-xL levels increasing in recipient cells. Doxorubicin 214-217 BCL2-like 1 Mus musculus 161-167 32824972-6 2020 The observed effects were associated with strong hypoxia-inducible factor 1-alpha (HIF-1alpha) induction and B-cell lymphoma-extra-large anti-apoptotic protein (Bcl-xL)-mediated anti-apoptotic response in normoxic DOX-treated TEV donor cells, being also tightly connected to the DOX-TEV-mediated HIF-1alpha induction, as well as Bcl-xL levels increasing in recipient cells. Doxorubicin 279-282 BCL2-like 1 Mus musculus 161-167 32913503-10 2020 Immunohistochemical staining demonstrated that SPR064 and paclitaxel significantly reduced the expression of Ki-67 and BCL-xL in the endometrial tumors of both obese and lean mice. Paclitaxel 58-68 BCL2-like 1 Mus musculus 119-125 32677976-6 2020 RESULTS: The results showed that DT2216 selectively killed various Bcl-xL-dependent TCL cells including MyLa cells in vitro. DT2216 33-39 BCL2-like 1 Mus musculus 67-73 32677976-8 2020 Furthermore, DT2216 combined with ABT199 (a selective Bcl-2 inhibitor) synergistically reduced disease burden and improved survival in a TCL PDX mouse model dependent on both Bcl-2 and Bcl-xL. DT2216 13-19 BCL2-like 1 Mus musculus 185-191 32677976-8 2020 Furthermore, DT2216 combined with ABT199 (a selective Bcl-2 inhibitor) synergistically reduced disease burden and improved survival in a TCL PDX mouse model dependent on both Bcl-2 and Bcl-xL. venetoclax 34-40 BCL2-like 1 Mus musculus 185-191 31708095-7 2020 Using a mouse xenograft model, we found that Proscillaridin A treatment significantly inhibited tumor growth and lung metastasis in vivo and decreased the expression levels of Bcl-xl and MMP2. Proscillaridin 45-61 BCL2-like 1 Mus musculus 176-182 32952128-5 2020 Also, CuSO4 induced apoptosis, which was accompanied by decreasing Bcl-2, Bcl-xL mRNA expression levels and protein expression levels, and increasing Bax, Bak, cleaved-caspase-3, cleaved-caspase-9 mRNA, and protein expression levels, and Bax/Bcl-2 ratio. Copper Sulfate 6-11 BCL2-like 1 Mus musculus 74-80 33073261-5 2020 It also exhibited synergy with ibrutinib, selinexor, venetoclax and A-1331852 (a novel BCL-XL inhibitor). A-1331852 68-77 BCL2-like 1 Mus musculus 87-93 32706077-8 2020 Also, rapamycin treatment increased the expressions of bcl-2, bcl-xL, HSP70, and HSP90. Sirolimus 6-15 BCL2-like 1 Mus musculus 62-68 32361189-10 2020 Moreover, the decreased expression of Bcl-xl and Bcl-2 and the increased expression of Bax protein were also blocked by hydrogen treatment. Hydrogen 120-128 BCL2-like 1 Mus musculus 38-44 32580291-7 2020 Its combination with ABT-737, which inhibits Bcl-2, Bcl-xl, and Bcl-w, led to an induction of the intrinsic apoptotic pathway and to a synergistic cytotoxicity in prostate cancer cells and 3D spheroids. ABT-737 21-28 BCL2-like 1 Mus musculus 52-58 32353736-0 2020 miR-548e Sponged by ZFAS1 Regulates Metastasis and Cisplatin Resistance of OC by Targeting CXCR4 and let-7a/BCL-XL/S Signaling Axis. mir-548e 0-8 BCL2-like 1 Mus musculus 108-116 32353736-0 2020 miR-548e Sponged by ZFAS1 Regulates Metastasis and Cisplatin Resistance of OC by Targeting CXCR4 and let-7a/BCL-XL/S Signaling Axis. Cisplatin 51-60 BCL2-like 1 Mus musculus 108-116 32353736-6 2020 Cisplatin resistance induced by ZFAS1 and CXCR4 overexpression in OC cells was mediated by their suppression on let-7a and elevation of BCL-XL/S expression. Cisplatin 0-9 BCL2-like 1 Mus musculus 136-144 32189339-0 2020 Correction of Bcl-x splicing improves responses to imatinib in chronic myeloid leukaemia cells and mouse models. Imatinib Mesylate 51-59 BCL2-like 1 Mus musculus 14-19 32189339-4 2020 The aberrant Bcl-x splicing in CML cells was effectively restored using vivo-Morpholino Antisense Oligomer (vMO). vivo-morpholino 72-87 BCL2-like 1 Mus musculus 13-18 32071300-9 2020 Moreover, BP-1-102 dramatically reduced the expression of JAK2, p-STAT3, p-NF-kappaB, and Bcl-xL but maintained the expression of LC3B and Beclin in AAA tissues. BP-1-102 10-18 BCL2-like 1 Mus musculus 90-96 31809801-5 2020 Moreover, VERU-111 treatment induced apoptosis and modulated the expression of Bid, Bcl-xl, Survivin, Bax, Bcl2 and cleavage in PARP. R 111 10-18 BCL2-like 1 Mus musculus 84-90 31286669-6 2019 Mechanistically, cisplatin injection induced the increased apoptosis and regulated the corresponding protein expression of BCL-2, BCL-XL, BAX, cleaved caspase 3 and caspase 12 in the injured kidney tissues. Cisplatin 17-26 BCL2-like 1 Mus musculus 130-136 31546406-5 2019 Mechanistic studies revealed that the complexes induced the excessive production of cellular reactive oxygen species (ROS) leading to apoptosis through up regulation of p53 and downregulation of Bcl-xL, which might be the plausible mechanisms underlying their anti-cancer properties. Reactive Oxygen Species 93-116 BCL2-like 1 Mus musculus 195-201 31546406-5 2019 Mechanistic studies revealed that the complexes induced the excessive production of cellular reactive oxygen species (ROS) leading to apoptosis through up regulation of p53 and downregulation of Bcl-xL, which might be the plausible mechanisms underlying their anti-cancer properties. Reactive Oxygen Species 118-121 BCL2-like 1 Mus musculus 195-201 32123852-9 2019 Additionally, treatment of senescent fibroblasts with aspirin or celecoxib, a COX2 specific inhibitor, reduced cell viability and decreased the levels of Bcl-xL protein. Aspirin 54-61 BCL2-like 1 Mus musculus 154-160 32123852-9 2019 Additionally, treatment of senescent fibroblasts with aspirin or celecoxib, a COX2 specific inhibitor, reduced cell viability and decreased the levels of Bcl-xL protein. Celecoxib 65-74 BCL2-like 1 Mus musculus 154-160 31499069-5 2019 KEY FINDINGS: We conclude that XQ-1H preserved the motor functions, limited apoptosis, and concomitantly promoted neurogenesis-related protein expression by Wnt signaling-dependently compromising GSK3beta/Caspase-3 activity and enhancing the expression of Wnt1/beta-catenin/Neuro D1/Cyclin D1 and Bcl-xL. xq-1h 31-36 BCL2-like 1 Mus musculus 297-303 31243598-2 2019 In vitro and in vivo analysis showed that aspirin induced compromised Bcl-XL level and subsequent ATP depletion. Aspirin 42-49 BCL2-like 1 Mus musculus 70-76 31243598-8 2019 Collectively, aspirin inhibits tumors growth in mice and induces oncosis in which the compromised Bcl-XL and intracellular ATP depletion play a dominant role, which provides insights into the therapeutic strategy of aspirin in oncology. Aspirin 14-21 BCL2-like 1 Mus musculus 98-104 31243598-8 2019 Collectively, aspirin inhibits tumors growth in mice and induces oncosis in which the compromised Bcl-XL and intracellular ATP depletion play a dominant role, which provides insights into the therapeutic strategy of aspirin in oncology. Aspirin 216-223 BCL2-like 1 Mus musculus 98-104 31252023-0 2019 CDK2 and Bcl-xL inhibitory mechanisms by docking simulations and anti-tumor activity from piperine enriched supercritical extract. piperine 90-98 BCL2-like 1 Mus musculus 9-15 31252023-5 2019 Other predicted interaction showed piperine inside the hydrophobic groove of Bcl-xL. piperine 35-43 BCL2-like 1 Mus musculus 77-83 31150651-7 2019 Albiflorin inhibited the mitochondrial pathway of apoptosis by increasing the levels of Bcl-2 and Bcl-xl and decreasing the levels of Bax, caspase-3 and cytochrome c in both the hippocampus and the cortex and by reducing the number of apoptotic cells in the anterior parietal cortex of the APP/PS1 mice. albiflorin 0-10 BCL2-like 1 Mus musculus 98-104 31078568-8 2019 SRI110 co-treatment reversed the cisplatin-induced changes in the expression levels of Bcl2l1, Ccnd1, Jak2, Jak3, and Src and significantly attenuated the changes in the expression levels of Cdkn1a, Egfr, Fas, Il6st, Jak1, Stat3, and Tyk2. sri110 0-6 BCL2-like 1 Mus musculus 87-93 31078568-8 2019 SRI110 co-treatment reversed the cisplatin-induced changes in the expression levels of Bcl2l1, Ccnd1, Jak2, Jak3, and Src and significantly attenuated the changes in the expression levels of Cdkn1a, Egfr, Fas, Il6st, Jak1, Stat3, and Tyk2. Cisplatin 33-42 BCL2-like 1 Mus musculus 87-93 30804792-13 2018 Taxol up-regulated the protein levels of P-H2A, PARP, Chk1, p53, and p21 and down-regulated Bcl-Xl and Mcl-1, and RAP reversed the expression of all these proteins. Paclitaxel 0-5 BCL2-like 1 Mus musculus 92-98 30874970-6 2019 This SCT-induced transcriptional regulation of Bcl-2 and Bcl-xL was dependent on the cyclic AMP (cAMP) response element-binding protein (CREB), which is a key survival factor at the convergence of multiple signaling cascades. Cyclic AMP 85-95 BCL2-like 1 Mus musculus 57-63 30874970-6 2019 This SCT-induced transcriptional regulation of Bcl-2 and Bcl-xL was dependent on the cyclic AMP (cAMP) response element-binding protein (CREB), which is a key survival factor at the convergence of multiple signaling cascades. Cyclic AMP 97-101 BCL2-like 1 Mus musculus 57-63 30213181-8 2019 5-Fluorouracil treatment also accelerated the expression of the pro-apoptotic protein BAX and decelerated the expression of the anti-apoptotic protein Bcl-xL on melanoma cell line. Fluorouracil 0-14 BCL2-like 1 Mus musculus 151-157 30676695-8 2019 In addition, isoflurane induced increase in Bcl-xL phosphorylation, cytochrome c release, and caspase-3 activation that resulted in neuronal cell death. Isoflurane 13-23 BCL2-like 1 Mus musculus 44-50 31182913-5 2019 Additionally, nitroxoline downregulated the expressions of phospho-PI3 kinase, phospho-Akt (Thr308), phospho-Akt (Ser473), phospho-GSK-3beta, Bcl-2, and Bcl-xL. nitroxoline 14-25 BCL2-like 1 Mus musculus 153-159 30841431-6 2019 This was through the phosphorylation of 3"-5"-cyclic adenosine monophosphate response element-binding protein (CREB) in beta-cells, hence activating CREB downstream anti-apoptotic genes, Bcl-2 and Bcl-xL. 3"-5"-cyclic adenosine monophosphate 40-76 BCL2-like 1 Mus musculus 197-203 30452878-6 2019 Mechanistically, upon exposure to PA, endogenous SK2 was shuttled from the nucleus to the cytoplasm, where it interacted with B-cell lymphoma-extra-large (Bcl-xL), leading to mitochondrial apoptotic pathway activation and cell death. Protactinium 34-36 BCL2-like 1 Mus musculus 155-161 31096772-9 2019 Fisetin inhibited anti-apoptotic protein Bcl-2 and Bcl-xL and increased pro-apoptotic protein Bax and Bak. fisetin 0-7 BCL2-like 1 Mus musculus 51-57 29855540-4 2019 Administration of ABT-737, a Bcl-xL inhibitor, upregulated DNase II activity in murine hepatocyte cell line BNL CL.2 cells and induced apoptosis. ABT-737 18-25 BCL2-like 1 Mus musculus 29-35 30506375-8 2019 Mechanistic studies revealed that sitosterol-treatment reduced the expression of PI3K/Akt, promoted the activation of Bad, decreased Bcl-xl, and enhanced cyto-c release, leading to caspase-9 and caspase-3 activation, PARP cleavage, and apoptosis. gamma-sitosterol 34-44 BCL2-like 1 Mus musculus 133-139 30529602-6 2019 Beneficial effects of hydrogen sulfide were mediated by upregulation of anti-apoptotic Bcl-XL and abolished by nitric oxide synthase 2 deficiency. Hydrogen Sulfide 22-38 BCL2-like 1 Mus musculus 87-93 30847145-7 2019 RT-PCR results showed that expression of Bcl-x and PARP gene was intensively increased, whereas expression of p53 gene was decreased in the mouse liver tissues treated with carmoisine. azo rubin S 173-183 BCL2-like 1 Mus musculus 41-46 30651087-8 2019 Coincident with these metabolic changes, MOMIPP selectively activates the JNK1/2 stress kinase pathway, resulting in phosphorylation of c-Jun, Bcl-2 and Bcl-xL. 3-(5-methoxy-2-methyl-1H-indol-3-yl)-1-(4-pyridinyl)-2-propen-1-one 41-47 BCL2-like 1 Mus musculus 153-159 30393195-12 2019 At that time, cocaine treatment decreased Bcl-2 and Bcl-xL levels, and increased Bax, cytosolic cytochrome c, and cleaved caspase-3 levels. Cocaine 14-21 BCL2-like 1 Mus musculus 52-58 29218248-5 2017 Mechanistically, our data from the proteomics, Western blot and flow cytometry analyses demonstrated that propafenone caused mitochondrial dysfunction as indicated by a decreased mitochondrial membrane potential and reduced expression of Bcl-xL and Bcl-2. Propafenone 106-117 BCL2-like 1 Mus musculus 238-244 30074260-6 2018 Quantitative polymerase chain reaction revealed that melatonin significantly upregulated the transcription of catalase, superoxide dismutase 2, glutathione peroxidase, and the antiapoptotic factors Bcl-2 and Bcl-x while downregulated the transcription of pro-apoptotic genes p53 and Bax. Melatonin 53-62 BCL2-like 1 Mus musculus 208-213 30107910-5 2018 While the ubiquinol treatment significantly decreased active Bax protein expression in the ischemic retina, phosphorylation of Bad at serine 112 and Bcl-xL protein expression were preserved in the ubiquinol-treated ischemic retina at 12 h. Consistently, the ubiquinol treatment prevented apoptotic cell death by blocking caspase-3 cleavage. ubiquinol 197-206 BCL2-like 1 Mus musculus 149-155 30107910-5 2018 While the ubiquinol treatment significantly decreased active Bax protein expression in the ischemic retina, phosphorylation of Bad at serine 112 and Bcl-xL protein expression were preserved in the ubiquinol-treated ischemic retina at 12 h. Consistently, the ubiquinol treatment prevented apoptotic cell death by blocking caspase-3 cleavage. ubiquinol 197-206 BCL2-like 1 Mus musculus 149-155 30107910-6 2018 These results suggest that the ubiquinol enhances RGC survival by modulating the Bax/Bad/Bcl-xL-mediated apoptotic pathway in the ischemic retina. ubiquinol 31-40 BCL2-like 1 Mus musculus 89-95 30017199-9 2018 Following ABT-199 treatment in NPC cells, upregulation of Mcl-1 and Bcl-xL can lead to drug resistance, while concomitant Noxa overexpression partially neutralized the Mcl-1-caused resistance. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 10-13 BCL2-like 1 Mus musculus 68-74 28777484-0 2018 5-Azacytidine specifically inhibits the NIH-3T3 PCD process induced by TNF-alpha and cycloheximide via affecting BCL-XL. Azacitidine 0-13 BCL2-like 1 Mus musculus 113-119 28777484-0 2018 5-Azacytidine specifically inhibits the NIH-3T3 PCD process induced by TNF-alpha and cycloheximide via affecting BCL-XL. Cycloheximide 85-98 BCL2-like 1 Mus musculus 113-119 29312803-4 2017 Co-treatment of sorafenib and VPA synergistically inhibited HCC cell viability, induced cell apoptosis, along with the up-regulation of p21, Bax, cleaved caspase9, cleaved caspase3, cleaved PARP and down-regulation of Bcl-xL, suggesting this combination activated intrinsic apoptotic pathway. Sorafenib 16-25 BCL2-like 1 Mus musculus 218-224 30227325-8 2018 Moreover, 15-HETE increases viability and impaired mitochondrial depolarization, and promotes the expression of Bcl-2 and Bcl-xL in PASMCs without serum. 15-Hete 10-17 BCL2-like 1 Mus musculus 122-128 30227325-8 2018 Moreover, 15-HETE increases viability and impaired mitochondrial depolarization, and promotes the expression of Bcl-2 and Bcl-xL in PASMCs without serum. pasmcs 132-138 BCL2-like 1 Mus musculus 122-128 30416757-8 2018 Baf-A1 co-treatment with TMZ significantly decrease Mcl-1 expression compared to TMZ while increase Bax expression in C2C12 cells (Bcl2 and Bcl-XL do not significantly change in Baf-A1/TMZ co-treatment). Temozolomide 25-28 BCL2-like 1 Mus musculus 140-146 30098330-8 2018 Furthermore, SIRT5 overexpression reversed the decreasing trend of anti-apoptotic factors BCL-2 and BCL-XL expression under High-PA-G condition. Protactinium 129-131 BCL2-like 1 Mus musculus 100-106 29928387-13 2018 Additionally, naringin reduced the expression of B-cell lymphoma (Bcl)-2, Bcl-extra large (Bcl-xL), cyclin D1, c-Myc and survivin, while it increased the expression of caspase-3 and caspase-7. naringin 14-22 BCL2-like 1 Mus musculus 91-97 29751524-10 2018 beta-asarone also suppressed the hnRNP A2/B1 expression, enhanced the expression of cleaved-caspase 3 and p27 and the ratio of Bcl-xS/Bcl-xL, and reduced the expression of CDK2 in U251 xenografts. asarone 0-12 BCL2-like 1 Mus musculus 134-140 29534229-17 2018 Cy increased the expression of BAX (P < 0.01) and decreased the expression of BCLX-L compared to control ovaries (P < 0.01). Cyclophosphamide 0-2 BCL2-like 1 Mus musculus 81-87 29534229-18 2018 The ovarian BCLX-L:BAX ratio was also lower in Cy-treated mice (P < 0.05). Cyclophosphamide 47-49 BCL2-like 1 Mus musculus 12-18 29207077-6 2018 Furthermore, reduced expression of B-cell lymphoma-extra large (Bcl-xL) and Bcl-2 were observed in arbutin- and acetylated arbutin-treated cells. Arbutin 99-106 BCL2-like 1 Mus musculus 35-62 29207077-6 2018 Furthermore, reduced expression of B-cell lymphoma-extra large (Bcl-xL) and Bcl-2 were observed in arbutin- and acetylated arbutin-treated cells. Arbutin 99-106 BCL2-like 1 Mus musculus 64-70 29207077-6 2018 Furthermore, reduced expression of B-cell lymphoma-extra large (Bcl-xL) and Bcl-2 were observed in arbutin- and acetylated arbutin-treated cells. Arbutin 123-130 BCL2-like 1 Mus musculus 35-62 29207077-6 2018 Furthermore, reduced expression of B-cell lymphoma-extra large (Bcl-xL) and Bcl-2 were observed in arbutin- and acetylated arbutin-treated cells. Arbutin 123-130 BCL2-like 1 Mus musculus 64-70 28802066-12 2018 Treatment with the Bcl-xL-specific inhibitor, A-1331852, reduces liver fibrosis, possibly by a dual effect on activated fibroblasts and senescent cholangiocytes. A-1331852 46-55 BCL2-like 1 Mus musculus 19-25 29237758-6 2017 Therapeutic blockade of BCL-XL with ABT-263 (navitoclax) effectively treats established fibrosis in a mouse model of scleroderma dermal fibrosis by inducing myofibroblast apoptosis. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 36-39 BCL2-like 1 Mus musculus 24-30 29312803-4 2017 Co-treatment of sorafenib and VPA synergistically inhibited HCC cell viability, induced cell apoptosis, along with the up-regulation of p21, Bax, cleaved caspase9, cleaved caspase3, cleaved PARP and down-regulation of Bcl-xL, suggesting this combination activated intrinsic apoptotic pathway. Valproic Acid 30-33 BCL2-like 1 Mus musculus 218-224 29383091-4 2017 Moreover, splenocytes from sodium fluoride-treated mice showed high expression of pro-apoptotic proteins, including Bim, Bax, Bak, caspase-3 and poly ADP-ribose polymerase, and low expression of the anti-apoptotic proteins BcL-2 and BcL-xL. Sodium Fluoride 27-42 BCL2-like 1 Mus musculus 233-239 28645939-5 2017 The combination reduced tumor proliferation, NF-kappaB signaling, and expression of BCL-xL and MCL-1 more potently than single-agent therapy.Conclusions: The combination of acalabrutinib and ACP-319 was superior to single-agent treatment in a murine CLL model, warranting further investigation of this combination in clinical studies. acalabrutinib 173-186 BCL2-like 1 Mus musculus 84-90 28807815-0 2017 Bcl-xL knockout attenuates mitochondrial respiration and causes oxidative stress that is compensated by pentose phosphate pathway activity. Pentosephosphates 104-121 BCL2-like 1 Mus musculus 0-6 28839001-6 2017 Dasatinib also increased the rate of apoptosis in T790M-positive cells induced by T790M-selective EGFR-TKIs, as determined by the Annexin-V binding assay; this was associated with downregulation of the antiapoptotic Bcl-2 family member Bcl-xL, a finding that was confirmed in mice bearing T790M-positive xenografts. Dasatinib 0-9 BCL2-like 1 Mus musculus 236-242 27401946-5 2017 However, capsaicin pre-treatment significantly suppressed the spermatogenic cell death, oxidative stress (levels of MDA, PHGPx immunoreactivity, and Hsp72, PHGPx, and MnSOD mRNA) and apoptosis (levels of TUNEL-positive cells, and Bcl-xL and Bax mRNA) in testes by HS. Capsaicin 9-18 BCL2-like 1 Mus musculus 230-236 28533436-0 2017 Metformin Synergizes with BCL-XL/BCL-2 Inhibitor ABT-263 to Induce Apoptosis Specifically in p53-Defective Cancer Cells. Metformin 0-9 BCL2-like 1 Mus musculus 26-32 28533436-1 2017 p53 deficiency, a frequent event in multiple kinds of malignancies, decreases the sensitivity of diverse targeted chemotherapeutics including the BCL-XL/BCL-2 inhibitor ABT-263. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 169-172 BCL2-like 1 Mus musculus 146-152 28533436-6 2017 Mechanistic studies revealed that metformin sensitized ABT-263 via attenuating mTORC1-mediated cap-dependent translation of MCL-1 and survivin and weakening internal ribosome entry site (IRES)-dependent translation of XIAP Meanwhile, ABT-263 sensitized metformin through disrupting the BCL-XL/BIM complex. Metformin 34-43 BCL2-like 1 Mus musculus 286-292 28533436-6 2017 Mechanistic studies revealed that metformin sensitized ABT-263 via attenuating mTORC1-mediated cap-dependent translation of MCL-1 and survivin and weakening internal ribosome entry site (IRES)-dependent translation of XIAP Meanwhile, ABT-263 sensitized metformin through disrupting the BCL-XL/BIM complex. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 55-58 BCL2-like 1 Mus musculus 286-292 28668383-10 2017 Furthermore, it"s found that expression of cytochrome C, as well as the restoration of Bcl-2/Bax and Bcl-xl/Bax ratio in the presence of Berberine, led to a decline in the apoptotic rate. Berberine 137-146 BCL2-like 1 Mus musculus 101-107 27086916-6 2017 In contrast, the combination of SC-2001 with ABT-737 (a BCL-2/BCL-XL/BCL-W inhibitor) significantly decreases ALDH+ cells, disrupts primary spheres, and inhibits the self-renewability of MICs. ABT-737 45-52 BCL2-like 1 Mus musculus 62-68 28526407-10 2017 BCL2L1 expression was lower, while Caspase-3 expression was significantly elevated in the sirtinol-treated group. sirtinol 90-98 BCL2-like 1 Mus musculus 0-6 28682312-6 2017 Using an in vivo mouse model of tamoxifen-inducible Bclx gene deletion and in vitro assays with a BCL-XL-selective inhibitor, we interrogated each stage of erythrocyte differentiation for BCL-XL dependency. Tamoxifen 32-41 BCL2-like 1 Mus musculus 52-56 28582759-10 2017 Moreover, alpha-mangostin promoted the apoptosis of skin tumor dose-dependently by up-regulating of Bax, cleaved caspase-3, cleaved PARP and Bad, and down-regulating of Bcl-2 and Bcl-xl. mangostin 10-25 BCL2-like 1 Mus musculus 179-185 28363658-7 2017 Further investigations revealed that CAs increased the levels of tumor infiltrating CD8+ T lymphocytes, blocked tumor cell cycle in S phase, down-regulated anti-apoptotic protein Bcl-xL and Mcl-1 expression, and led to the activation of caspase 3. Calcium 37-40 BCL2-like 1 Mus musculus 179-185 26948951-10 2017 Radiation-induced gastrointestinal DNA strand breaks, lipid peroxidation, and expression of proapoptotic-p53, Bax, and antiapoptotic-Bcl-xL proteins were reversed in melatonin pretreated mice. Melatonin 166-175 BCL2-like 1 Mus musculus 133-139 28301380-9 2017 NXQ also suppressed prosurvival proteins Bcl-xL and Mcl-1. 2-[5-fluoranyl-2-[[3-[methyl(oxidanyl)-$l^{3}-sulfanyl]phenyl]methylcarbamoyl]phenoxy]ethanoic acid 0-3 BCL2-like 1 Mus musculus 41-47 28129627-0 2017 Camel whey protein improves oxidative stress and histopathological alterations in lymphoid organs through Bcl-XL/Bax expression in a streptozotocin-induced type 1 diabetic mouse model. Streptozocin 133-147 BCL2-like 1 Mus musculus 106-112 28948203-1 2017 BACKGROUND & AIMS: Bcl-xL, an anti-apoptotic Bcl-2 family protein, is overexpressed in 90% of pancreatic ductal adenocarcinoma (PDAC) cases. Adenosine Monophosphate 12-15 BCL2-like 1 Mus musculus 23-29 28948203-16 2017 Anti-Bcl-xL treatments may have the potency to suppress the progression from PanINs to PDAC. pdac 87-91 BCL2-like 1 Mus musculus 5-11 28618955-6 2017 Western blotting analysis showed that Oridonin treatment rapidly and distinctly increased the levels of all three forms of Bim and also markedly reduced the levels of Bcl-2 and Bcl-xl in osteosarcoma cells. oridonin 38-46 BCL2-like 1 Mus musculus 177-183 28481901-5 2017 Analysis of the mechanisms of these events indicated that beta-lapachone regulated the expression of Bcl-2, Bcl-xL, and Bax, resulting in the activation of caspase-3, -8, -9, and poly-ADP-ribose polymerase (PARP). beta-lapachone 58-72 BCL2-like 1 Mus musculus 108-114 28294314-3 2017 In vitro, doxycycline-controlled c-myc/bcl-xL-overexpressing CD19+ CD93+ c-kikt+ IgM- pre-BI cells differentiate to and survive as CD19+ CD93+ c-kit- IgM+ immature B1 cells. Doxycycline 10-21 BCL2-like 1 Mus musculus 39-45 28319809-9 2017 ABT-737 displaced BCL-xL from mitochondria and induced oligomerization of BAK. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 0-3 BCL2-like 1 Mus musculus 18-24 27385439-7 2016 FAIM2 protects from Fas by direct interaction with Fas receptor, as well as by modulating calcium release at the endoplasmic reticulum through interaction with Bcl-xL. Calcium 90-97 BCL2-like 1 Mus musculus 160-166 29035884-10 2017 Pretreatment with quercetin also inhibited osteoblast apoptosis, significantly restored the down-regulated expression of Bcl-2 and Bcl-XL and decreased the upregulated expression of caspase-3, Bax, and cytochrome c in MC3T3-E1 cells induced by LPS. Quercetin 18-27 BCL2-like 1 Mus musculus 131-137 28086800-10 2017 Expectedly, GW4064 induced phosphorylation of Akt, expression of the anti-apoptotic molecules (Bcl-xL and Bcl-2), and reduced harmful hepatic molecules (Fas ligand and Fas). GW 4064 12-18 BCL2-like 1 Mus musculus 95-101 27729467-6 2016 Through this mechanism, ORP4L sustains antiapoptotic Bcl-XL expression through Ca2+-mediated c-AMP responsive element binding protein transcriptional regulation and thus protects macrophages from apoptosis. c-amp 93-98 BCL2-like 1 Mus musculus 53-59 27729467-7 2016 Excessive stimulation with the oxysterol 25-hydroxycholesterol disassembles the ORP4L/Galphaq/11/PLCbeta3 complexes, resulting in reduced PLCbeta3 activity, IP3 production, and Ca2+ release, as well as decreased Bcl-XL expression and increased apoptosis. Oxysterols 31-40 BCL2-like 1 Mus musculus 212-218 27729467-7 2016 Excessive stimulation with the oxysterol 25-hydroxycholesterol disassembles the ORP4L/Galphaq/11/PLCbeta3 complexes, resulting in reduced PLCbeta3 activity, IP3 production, and Ca2+ release, as well as decreased Bcl-XL expression and increased apoptosis. 25-hydroxycholesterol 41-62 BCL2-like 1 Mus musculus 212-218 27241100-8 2016 Inhibition of NF-kappaB activation with the specific NF-kappaB inhibitor, PDTC (pyrrolidine dithiocarbamate), reversed Bcl-xL down-regulation and Bax up-regulation, and led to a significant increase in LIGHT- and IFN-gamma-treated cell viability. pyrrolidine dithiocarbamic acid 80-107 BCL2-like 1 Mus musculus 119-125 27070098-3 2016 We recently demonstrated that Bcl-2 and Bcl-xL, in addition to promoting survival, suppress beta-cell glucose metabolism and insulin secretion. Glucose 102-109 BCL2-like 1 Mus musculus 40-46 28929662-14 2016 Therefore, astragaloside could increase the contents of Akt, PI3K, BCL-xl, bad, mTOR (P<0.01), decrease the concentrations of FoxO, PTEN (P<0.05). astragaloside 11-24 BCL2-like 1 Mus musculus 67-73 27580845-6 2016 Treatment with CsA and FK506 also inhibited PAN-induced podocytes apoptosis, which was associated with the induction of Bcl-xL and inhibition of Bax, cleaved caspase 3, and cleaved PARP expression. Cyclosporine 15-18 BCL2-like 1 Mus musculus 120-126 27580845-6 2016 Treatment with CsA and FK506 also inhibited PAN-induced podocytes apoptosis, which was associated with the induction of Bcl-xL and inhibition of Bax, cleaved caspase 3, and cleaved PARP expression. Tacrolimus 23-28 BCL2-like 1 Mus musculus 120-126 27560714-3 2016 By combining inducible knockout mouse models with the BH3-mimetic compound ABT-737, which inhibits BCL-2, BCL-XL and BCL-W, we found that dependency on MCL-1, BCL-XL or BCL-2 expression changes during B-cell development. BH 3 54-57 BCL2-like 1 Mus musculus 106-112 27560714-3 2016 By combining inducible knockout mouse models with the BH3-mimetic compound ABT-737, which inhibits BCL-2, BCL-XL and BCL-W, we found that dependency on MCL-1, BCL-XL or BCL-2 expression changes during B-cell development. BH 3 54-57 BCL2-like 1 Mus musculus 159-165 27560714-3 2016 By combining inducible knockout mouse models with the BH3-mimetic compound ABT-737, which inhibits BCL-2, BCL-XL and BCL-W, we found that dependency on MCL-1, BCL-XL or BCL-2 expression changes during B-cell development. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 75-78 BCL2-like 1 Mus musculus 106-112 27560714-3 2016 By combining inducible knockout mouse models with the BH3-mimetic compound ABT-737, which inhibits BCL-2, BCL-XL and BCL-W, we found that dependency on MCL-1, BCL-XL or BCL-2 expression changes during B-cell development. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 75-78 BCL2-like 1 Mus musculus 159-165 27747134-10 2016 While saline and microbead injection increased Bcl-xl and Socs3 mRNA in both WT and IL-6-/- mice, IL-6-/- deficiency led to smaller increases for both Bcl-xl and Socs3. Sodium Chloride 6-12 BCL2-like 1 Mus musculus 47-53 26563498-7 2016 MPPE, selegiline, or pifithrin-mu significantly attenuated mitochondrial p53/Bcl-xL interaction, impaired mitochondrial transmembrane potential, cytosolic cytochrome c release, and cleaved caspase-3 in wild-type mice. Selegiline 6-16 BCL2-like 1 Mus musculus 77-83 26563498-7 2016 MPPE, selegiline, or pifithrin-mu significantly attenuated mitochondrial p53/Bcl-xL interaction, impaired mitochondrial transmembrane potential, cytosolic cytochrome c release, and cleaved caspase-3 in wild-type mice. pifithrin 21-30 BCL2-like 1 Mus musculus 77-83 25895139-11 2016 At the same time, TMT-induced inhibition of phosphoinositol 3-kinase (PI3K)/Akt signaling was evident, thereby decreasing phospho-Bad, expression of Bcl-xL and Bcl-2, and the interaction between phospho-Bad and 14-3-3 protein, and increasing Bax expression and caspase-3 cleavage were observed. trimethyltin 18-21 BCL2-like 1 Mus musculus 149-155 26522133-5 2016 EGF induces Bcl-XL expression through activation of a unique bcl-X promoter, the P1; being not only the PI3K/AKT signaling pathway but also the increase in cAMP levels and the concomitant PKA/CREB activation necessary for both bcl-XL upregulation and apoptosis avoidance. Cyclic AMP 156-160 BCL2-like 1 Mus musculus 12-18 27224523-8 2016 Melatonin supplement also increased antiapoptotic gene Bcl-xl expression in the thawed sperm. Melatonin 0-9 BCL2-like 1 Mus musculus 55-61 27239851-0 2016 [Influence of chronic alcohol treatment on the expression of the Bdnf, Bax, Bcl-xL, and CASP3 genes in the mouse brain: Role of the C1473G polymorphism in the gene encoding tryptophan hydroxylase 2]. Alcohols 22-29 BCL2-like 1 Mus musculus 76-82 27239851-3 2016 The influence of chronic ethanol consumption on the expression of the Bdnf, Bax, Bcl-xL, and CASP3 genes was studied in the brain structures of B6-1473C (C/C) and B6-1473G (G/G) mice that had been obtained on the base of the C57BL/6 strain. Ethanol 25-32 BCL2-like 1 Mus musculus 81-87 27239851-7 2016 At the same time, chronic ethanol administration reduced the level of the antiapoptotic Bcl-xL mRNA in the midbrain of B6-1473C mice. Ethanol 26-33 BCL2-like 1 Mus musculus 88-94 27572165-5 2016 Consequently, a single dose of a BCL-XL-targeted BH3-mimetic therapy, or myeloid cell-restricted deletion of BCL-XL, limits Legionella replication and prevents lethal lung infections in mice. BH 3 49-52 BCL2-like 1 Mus musculus 33-39 26099903-7 2016 We found that FTY720 administration after TBI improved neurobehavioral function, alleviated brain edema, accompanied by modulation of apoptotic indicators such as Bcl-2, Bcl-xL, Bax, and cytochrome c. In experiment 2, ICR mice were also divided into four groups: sham group, TBI + vehicle group, TBI + FTY720 group, and TBI + FTY720 + inhibitors group. Fingolimod Hydrochloride 14-20 BCL2-like 1 Mus musculus 170-176 26825069-5 2016 Therefore a series of mixed polyphenol-heterocyclic molecules, were rationally designed by molecular docking as Bax/Bcl-xL inhibitors. Polyphenols 28-38 BCL2-like 1 Mus musculus 116-122 26850368-4 2016 Treatment with cocaine resulted in significant decreases in expression of Bcl-2 and Bcl-xl in the kidney of non-TG mice, which resulted in significant increases in Bax and cleaved-caspase 3. Cocaine 15-22 BCL2-like 1 Mus musculus 84-90 27009084-7 2016 NVP-Bez235 combined with lenalidomide remarkably increased apoptosis through intrinsic pathway by upregulating Bim, Bax and downregulating Bcl-xL. dactolisib 4-10 BCL2-like 1 Mus musculus 139-145 27009084-7 2016 NVP-Bez235 combined with lenalidomide remarkably increased apoptosis through intrinsic pathway by upregulating Bim, Bax and downregulating Bcl-xL. Lenalidomide 25-37 BCL2-like 1 Mus musculus 139-145 26675347-4 2016 Of interest, in the MCL cell lines with lower half-maximal inhibitory concentration (0.1-0.5 muM), pevonedistat induced G1-phase cell cycle arrest, downregulation of Bcl-xL levels, decreased nuclear factor (NF)-kappaB activity, and apoptosis. pevonedistat 99-111 BCL2-like 1 Mus musculus 166-172 26675347-8 2016 Our data suggest that pevonedistat has significant activity in MCL preclinical models, possibly related to effects on NF-kappaB activity, Bcl-xL downregulation, and G1 cell cycle arrest. pevonedistat 22-34 BCL2-like 1 Mus musculus 138-144 26667450-4 2016 In vitro, piperlongumine inhibited the proliferation of pancreatic cancer cell lines, potentiated the apoptotic effects of gemcitabine, inhibited the constitutive and inducible activation of NF-kappaB, and suppressed the NF-kappaB-regulated expression of c-Myc, cyclin D1, Bcl-2, Bcl-xL, Survivin, XIAP, VEGF, and matrix metalloproteinase-9 (MMP-9). piperlonguminine 10-24 BCL2-like 1 Mus musculus 280-286 25942381-8 2016 TGTA and TGTB significantly increased tumor cell apoptosis on lymphoma bearing mice, primarily through down-regulation of BCL2 and BCL-XL and up-regulation of BID. TGTA 0-4 BCL2-like 1 Mus musculus 131-137 25942381-8 2016 TGTA and TGTB significantly increased tumor cell apoptosis on lymphoma bearing mice, primarily through down-regulation of BCL2 and BCL-XL and up-regulation of BID. tgtb 9-13 BCL2-like 1 Mus musculus 131-137 26593251-6 2016 We also showed that inhibition of PDK1 with DAP increased the cleavage of pro-apoptotic proteins (PARP and Caspase 3) and decreased the expression of the anti-apoptotic proteins (BCL-xL and BCL-2) and autophagy regulators (ULK1, Beclin-1 and Atg). 2,2-dichloroacetophenone 44-47 BCL2-like 1 Mus musculus 179-185 26593251-8 2016 Furthermore, we demonstrated that PDK1 interacted with ULK1, BCL-xL and E3 ligase CBL-b in AML cells, and DPA treatment could inhibit the interactions. dpa 106-109 BCL2-like 1 Mus musculus 61-67 26522133-5 2016 EGF induces Bcl-XL expression through activation of a unique bcl-X promoter, the P1; being not only the PI3K/AKT signaling pathway but also the increase in cAMP levels and the concomitant PKA/CREB activation necessary for both bcl-XL upregulation and apoptosis avoidance. Cyclic AMP 156-160 BCL2-like 1 Mus musculus 61-66 27579149-9 2016 The melatonin-treated REMSD group also showed the highest expression of Bcl-2 and Bcl-xL as compared to the rest of the groups. Melatonin 4-13 BCL2-like 1 Mus musculus 82-88 26421001-7 2015 Jacaric acid also triggered apoptosis as reflected by induction of DNA fragmentation, phosphatidylserine externalization, mitochondrial membrane depolarization, up-regulation of pro-apoptotic Bax protein and down-regulation of anti-apoptotic Bcl-2 and Bcl-xL proteins. jacaric acid 0-12 BCL2-like 1 Mus musculus 252-258 26397133-9 2015 Lung tumors harvested from mice exposed to rapamycin showed a significant decrease in p-mTOR, p-S6K1, PCNA and Bcl-xL as compared with controls in the early and late stage intervention studies. Sirolimus 43-52 BCL2-like 1 Mus musculus 111-117 26657143-4 2016 To test this idea, we screened a collection of compounds and identified ABT263 (a specific inhibitor of the anti-apoptotic proteins BCL-2 and BCL-xL) as a potent senolytic drug. navitoclax 72-78 BCL2-like 1 Mus musculus 142-148 26343046-9 2015 RESULTS: Fenofibrate precondition can significantly alleviate the renal dysfunction, the pathological change, up-regulate the expression of p-PPAR-alpha, Bcl-2, Bcl-xl, Caspase3 and down-regulate the expression of p-JAK2, p-STAT3, p53, p21, CytC and Bax induced by renal IR injury. Fenofibrate 9-20 BCL2-like 1 Mus musculus 161-167 26254443-7 2015 BA treatment also induced apoptosis of the in vitro isolated, ibrutinib-resistant MCL cells, which overexpress CDK6, BCL2, Bcl-xL, XIAP, and AKT, but lack ibrutinib resistance-conferring BTK mutation. Barium 0-2 BCL2-like 1 Mus musculus 123-129 26038117-4 2015 In cultured hepatocytes, the administration of ABT-737, a Bcl-xL/-2/-w inhibitor, led to production of reactive oxygen species (ROS) as well as activation of caspases. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 47-50 BCL2-like 1 Mus musculus 58-64 26212257-5 2015 Resveratrol+curcumin combination caused apoptosis by increasing Bax/Bcl-xL ratio, Cytochrome C release, cleaved product of PARP and caspase 3 in cells. Resveratrol 0-11 BCL2-like 1 Mus musculus 68-74 26212257-5 2015 Resveratrol+curcumin combination caused apoptosis by increasing Bax/Bcl-xL ratio, Cytochrome C release, cleaved product of PARP and caspase 3 in cells. Curcumin 12-20 BCL2-like 1 Mus musculus 68-74 25684945-14 2015 After treating B7-H3 overexpressing cells with the Jak2-specific inhibitor AG490, the phosphorylation of Jak2 and STAT3, and the expression of Bcl-2 and Bcl-xl, decreased accordingly (P < 0.05). alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide 75-80 BCL2-like 1 Mus musculus 153-159 26205951-11 2015 This reduced apoptotic proteins by melatonin pre-treatment was associated with the increase of anti-apoptotic-Bcl-x and DNA repair-PCNA proteins in irradiated mice. Melatonin 35-44 BCL2-like 1 Mus musculus 110-115 26151119-9 2015 Results showed that procyanidin B2 significantly inhibited CCl4-induced hepatocyte apoptosis, markedly suppressed the upregulation of Bax expression and restored the downregulation of Bcl-xL expression. procyanidin B2 20-34 BCL2-like 1 Mus musculus 184-190 25862283-0 2015 Bcl-xL stimulates Bax relocation to mitochondria and primes cells to ABT-737. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 69-72 BCL2-like 1 Mus musculus 0-6 25862283-6 2015 Interestingly, cells overexpressing Bcl-xL were more sensitive to apoptosis upon treatment with the BH3-mimetic ABT-737, suggesting that despite its role in Bax inhibition, Bcl-xL also primes mitochondria to permeabilization and cytochrome c release. BH 3 100-103 BCL2-like 1 Mus musculus 36-42 25862283-6 2015 Interestingly, cells overexpressing Bcl-xL were more sensitive to apoptosis upon treatment with the BH3-mimetic ABT-737, suggesting that despite its role in Bax inhibition, Bcl-xL also primes mitochondria to permeabilization and cytochrome c release. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 112-115 BCL2-like 1 Mus musculus 36-42 25862283-6 2015 Interestingly, cells overexpressing Bcl-xL were more sensitive to apoptosis upon treatment with the BH3-mimetic ABT-737, suggesting that despite its role in Bax inhibition, Bcl-xL also primes mitochondria to permeabilization and cytochrome c release. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 112-115 BCL2-like 1 Mus musculus 173-179 25629551-4 2015 In contrast, blockade of GSK3beta by lithium or 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8) mitigated the expression of podocytopathic mediators, ameliorated podocyte injury, but barely affected Bcl-xL expression or sensitized apoptosis. Lithium 37-44 BCL2-like 1 Mus musculus 210-216 25629551-4 2015 In contrast, blockade of GSK3beta by lithium or 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8) mitigated the expression of podocytopathic mediators, ameliorated podocyte injury, but barely affected Bcl-xL expression or sensitized apoptosis. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 99-105 BCL2-like 1 Mus musculus 210-216 25629551-6 2015 In vivo, lithium or TDZD-8 therapy improved podocyte injury and proteinuria in mice treated with LPS or ADR, concomitant with the suppression of podocytopathic mediators, but retained Bcl-xL in glomerulus. Lithium 9-16 BCL2-like 1 Mus musculus 184-190 25629551-6 2015 In vivo, lithium or TDZD-8 therapy improved podocyte injury and proteinuria in mice treated with LPS or ADR, concomitant with the suppression of podocytopathic mediators, but retained Bcl-xL in glomerulus. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 20-26 BCL2-like 1 Mus musculus 184-190 25737433-7 2015 CFZ and z-VAD-fmk treatments resulted in higher levels of caspase-3 and BAX and lower level of BCL-XL in gastrocnemius muscles and altered the level of proteins in the renin-angiotensin system. carfilzomib 0-3 BCL2-like 1 Mus musculus 95-101 25737433-7 2015 CFZ and z-VAD-fmk treatments resulted in higher levels of caspase-3 and BAX and lower level of BCL-XL in gastrocnemius muscles and altered the level of proteins in the renin-angiotensin system. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 8-17 BCL2-like 1 Mus musculus 95-101 25747583-8 2015 Most importantly, SD-208 given orally for 24 days significantly abrogated the growth of PC3 subcutaneous tumor xenografts in nude mice, which was accompanied by reduced proliferation and increased apoptosis and decreased expression of PKD biomarkers including survivin and Bcl-xL. SD-208 18-24 BCL2-like 1 Mus musculus 273-279 25629551-2 2015 In vitro, lipopolysaccharide (LPS) or adriamycin (ADR) elicited podocyte injury and cytoskeletal disruption, associated with NFkappaB activation and induced expression of NFkappaB target molecules, including pro-survival Bcl-xL and podocytopathic mediators like MCP-1, cathepsin L, and B7-1. Doxorubicin 38-48 BCL2-like 1 Mus musculus 221-227 25643926-9 2015 Resveratrol treatment also resulted in decreased expression of iNOS, Bcl-2, and Bcl-xL in macrophages, which was linked with induction of apoptosis in macrophages. Resveratrol 0-11 BCL2-like 1 Mus musculus 80-86 25880088-1 2015 Navitoclax (ABT-263), an inhibitor of the pro-survival BCL-2 family proteins BCL-2, BCL-XL and BCL-W, has shown clinical efficacy in certain BCL-2-dependent haematological cancers, but causes dose-limiting thrombocytopaenia. navitoclax 0-10 BCL2-like 1 Mus musculus 84-90 25880088-1 2015 Navitoclax (ABT-263), an inhibitor of the pro-survival BCL-2 family proteins BCL-2, BCL-XL and BCL-W, has shown clinical efficacy in certain BCL-2-dependent haematological cancers, but causes dose-limiting thrombocytopaenia. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 12-15 BCL2-like 1 Mus musculus 84-90 25880088-2 2015 The latter effect is caused by Navitoclax directly inducing the apoptotic death of platelets, which are dependent on BCL-XL for survival. navitoclax 31-41 BCL2-like 1 Mus musculus 117-123 25880088-7 2015 Additionally, we made use of BH3 mimetics that selectively inhibit BCL-2 or BCL-XL. BH 3 29-32 BCL2-like 1 Mus musculus 76-82 25143196-8 2015 Molecular docking results indicated that calycosin could be embedded into the binding pocket of FXR, thereby increasing the expressions of STAT3 tyrosine phosphorylation and its target genes, Bcl-xl and SOCS3. 7,3'-dihydroxy-4'-methoxyisoflavone 41-50 BCL2-like 1 Mus musculus 192-198 25010671-8 2014 Aged septic Mttp-IKO mice exhibited increased gut epithelial apoptosis, increased jejunal Bax/Bcl-2 and Bax/Bcl-XL ratios yet simultaneously demonstrated increased crypt proliferation and villus length. O(4)-methylthymidine triphosphate 12-16 BCL2-like 1 Mus musculus 108-114 25876659-1 2015 We previously demonstrated that c-Jun N-terminal kinase (JNK) phosphorylates serine 62 of Bcl-xL to induce the degradation of Bcl-xL and apoptosis in WEHI-231 cells upon BCR crosslinking. Serine 77-83 BCL2-like 1 Mus musculus 90-96 25876659-1 2015 We previously demonstrated that c-Jun N-terminal kinase (JNK) phosphorylates serine 62 of Bcl-xL to induce the degradation of Bcl-xL and apoptosis in WEHI-231 cells upon BCR crosslinking. Serine 77-83 BCL2-like 1 Mus musculus 126-132 25833080-7 2015 RIPC activated cardioprotective signaling pathways and the anti-apoptotic Bcl-xL pathway in the heart, and reduced infarct size. ripc 0-4 BCL2-like 1 Mus musculus 74-80 26265154-10 2015 STZ-induced hyperglycemia resulted in downregulation of antiapoptotic proteins Bcl-2 by 66% and Bcl-XL by 51%, and upregulation of the pro-apoptotic Bad (69%) with an increase in the ratio of cytosolic/mitochondrial cytochrome c by 81% in hepatic tissue. Streptozocin 0-3 BCL2-like 1 Mus musculus 96-102 25386077-7 2014 In addition, NAC treatment significantly reduced caspase-3 activity and apoptosis after reperfusion, which correlated with the protein expression of Bcl-2 and Bcl-xl. Acetylcysteine 13-16 BCL2-like 1 Mus musculus 159-165 25187386-7 2014 Cirp(-/-) mice given dextran sodium sulfate exhibited decreased susceptibility to colonic inflammation through decreased expression of TNFalpha, IL23, Bcl-2, and Bcl-xL in colonic lamina propria cells compared with similarly treated wild-type (WT) mice. dextran sodium sulfate 21-43 BCL2-like 1 Mus musculus 162-168 25336920-6 2014 Moreover, pretreatment with R-LA stimulated the activation of PI3K-Akt through mTORC1 and mTORC2 components (mTOR, rictor and raptor) and production of antiinflammatory cytokine, IL-10 which led to the inactivation of glycogen synthase kinase-3beta (GSK-3beta) and reduction of both Bax/Bcl2 and Bax/Bcl-xL ratios, accompanied by inhibition of the cleaved caspase-3. Thioctic Acid 28-32 BCL2-like 1 Mus musculus 300-306 25016096-0 2014 Activation of p38 MAPK-regulated Bcl-xL signaling increases survival against zoledronic acid-induced apoptosis in osteoclast precursors. Zoledronic Acid 77-92 BCL2-like 1 Mus musculus 33-39 25084483-10 2014 Rutin significantly reversed ethanol-increased Bax, cytochrome c expression and caspase 3 activity, and decreased Bcl-2 and Bcl-xL protein expression in HT22 cells. Ethanol 29-36 BCL2-like 1 Mus musculus 124-130 25232677-0 2014 Radiosensitization by a novel Bcl-2 and Bcl-XL inhibitor S44563 in small-cell lung cancer. S44563 57-63 BCL2-like 1 Mus musculus 40-46 25232677-3 2014 In the current study, we investigated whether using the Bcl-2/Bcl-XL inhibitor S44563 can enhance radiosensitivity of SCLC cells in vitro and in vivo. S44563 79-85 BCL2-like 1 Mus musculus 62-68 24910348-3 2014 BCL-X(L), but not HAX-1 protected against cytokine withdrawal-induced apoptosis while HAX-1 and BCL-X(L) significantly reduced thapsigargin-triggered (calcium-dependent) apoptosis. Thapsigargin 127-139 BCL2-like 1 Mus musculus 96-104 24910348-3 2014 BCL-X(L), but not HAX-1 protected against cytokine withdrawal-induced apoptosis while HAX-1 and BCL-X(L) significantly reduced thapsigargin-triggered (calcium-dependent) apoptosis. Calcium 151-158 BCL2-like 1 Mus musculus 96-104 25023286-5 2014 However, these changes were countered by Bcl-xL induction, which is necessary to protect differentiating cells both from ER stress-induced death by tunicamycin and from the death signals inherent in differentiation. Tunicamycin 148-159 BCL2-like 1 Mus musculus 41-47 25023286-6 2014 Consistent with differentiating cells becoming dependent on Bcl-xL for survival, the addition of ABT-737 resulted in apoptosis in differentiating cells through the inhibition of sequestration of Bim. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 97-100 BCL2-like 1 Mus musculus 60-66 25046541-11 2014 On the other hand, tipifarnib upregulated antiapoptotic protein, Bcl-xL, in the liver after GalN/LPS challenge. tipifarnib 19-29 BCL2-like 1 Mus musculus 65-71 25046541-11 2014 On the other hand, tipifarnib upregulated antiapoptotic protein, Bcl-xL, in the liver after GalN/LPS challenge. Galactosamine 92-96 BCL2-like 1 Mus musculus 65-71 25368242-2 2014 BH-3 mimetics ABT-737 and ABT-263 are synthetic small-molecule inhibitors of anti-apoptotic proteins B-cell lymphoma-2 (Bcl2) and Bcl-xL, which play a critical role in survival of chondrosarcoma cells. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 14-17 BCL2-like 1 Mus musculus 130-136 25368242-2 2014 BH-3 mimetics ABT-737 and ABT-263 are synthetic small-molecule inhibitors of anti-apoptotic proteins B-cell lymphoma-2 (Bcl2) and Bcl-xL, which play a critical role in survival of chondrosarcoma cells. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 26-29 BCL2-like 1 Mus musculus 130-136 25208888-5 2014 HDACI upregulated Bim and, when combined with ABT-737, which released Bim from Bcl-2/Bcl-xL, potently killed bortezomib-resistant cells. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 46-49 BCL2-like 1 Mus musculus 85-91 25208888-5 2014 HDACI upregulated Bim and, when combined with ABT-737, which released Bim from Bcl-2/Bcl-xL, potently killed bortezomib-resistant cells. Bortezomib 109-119 BCL2-like 1 Mus musculus 85-91 25344863-6 2014 In Taxol-resistant cells, down-regulation of bcl-xL expression by the DNAzyme reversed the chemo-resistant phenotype of the cancer cells. Paclitaxel 3-8 BCL2-like 1 Mus musculus 45-51 24808369-6 2014 Our data suggest that PP6 activity is regulated to control apoptosis by modulating Ser(62) phosphorylation of Bcl-xL, which results in its polyubiquitination and degradation. Serine 83-86 BCL2-like 1 Mus musculus 110-116 24915963-13 2014 Exosomes also inhibited the APAP- and H2O2-induced hepatocytes apoptosis through upregulation of Bcl-xL protein expression. Hydrogen Peroxide 38-42 BCL2-like 1 Mus musculus 97-103 24923427-8 2014 Protein expression of ERalpha, COX-2, Cyclin A, and Bcl-xL were reduced in celecoxib-treated tumor samples, whereas only Bcl-xL expression was suppressed in those treated with aspirin. Celecoxib 75-84 BCL2-like 1 Mus musculus 52-58 24923427-8 2014 Protein expression of ERalpha, COX-2, Cyclin A, and Bcl-xL were reduced in celecoxib-treated tumor samples, whereas only Bcl-xL expression was suppressed in those treated with aspirin. Aspirin 176-183 BCL2-like 1 Mus musculus 121-127 24419931-0 2014 Melatonin modulates the expression of BCL-xl and improve the development of vitrified embryos obtained by IVF in mice. Melatonin 0-9 BCL2-like 1 Mus musculus 38-44 24639356-4 2014 We found that mutation of the PYAP motif unmasks a critical role for the proximal tyrosine motif in regulating T cell proliferation and expression of Bcl-xL but not cytokine secretion. Tyrosine 82-90 BCL2-like 1 Mus musculus 150-156 24603818-5 2014 SAHA-induced apoptosis of IPF myofibroblasts, an effect that was mediated, at least in part, by upregulation of the pro-apoptotic gene Bak and downregulation of the anti-apoptotic gene Bcl-xL. Vorinostat 0-4 BCL2-like 1 Mus musculus 185-191 24474649-5 2014 METHODS AND RESULTS: Using both human and humanized mouse models, we report that hyperglycemia-induced aldose reductase activation and subsequent reactive oxygen species production lead to increased p53 phosphorylation (Ser15), which promotes mitochondrial dysfunction, damage, and rupture by sequestration of the antiapoptotic protein Bcl-xL. Reactive Oxygen Species 146-169 BCL2-like 1 Mus musculus 336-342 24395569-2 2014 Intravenous delivery of a chemically modified cyclic STAT3 decoy oligonucleotide with improved serum and thermal stability demonstrated antitumor efficacy in conjunction with downmodulation of STAT3 target gene expression such as cyclin D1 and Bcl-X(L) in a mouse model of head and neck squamous cell carcinoma. Oligonucleotides 65-80 BCL2-like 1 Mus musculus 244-252 24676213-7 2014 The changes were accompanied with down-regulation of Bax and p53, and up-regulation of Bcl-2 and Bcl-xL by Astragaloside IV treatment. astragaloside A 107-123 BCL2-like 1 Mus musculus 97-103 24098377-10 2013 TQ also inhibited the protein expression of anti-apoptotic genes, such as XIAP, survivin, Bcl-xL and Bcl-2, in breast cancer cells and breast tumor xenograft. thymoquinone 0-2 BCL2-like 1 Mus musculus 90-96 24632563-2 2014 Clinical trials of navitoclax (ABT-263, which targets BCL-2, BCL-XL and BCL-W) have shown great promise, but encountered dose-limiting thrombocytopenia. navitoclax 19-29 BCL2-like 1 Mus musculus 61-67 24632563-2 2014 Clinical trials of navitoclax (ABT-263, which targets BCL-2, BCL-XL and BCL-W) have shown great promise, but encountered dose-limiting thrombocytopenia. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 31-34 BCL2-like 1 Mus musculus 61-67 24231956-8 2014 DETT inhibited NFkappaB transcription activity and downregulated NFkappaB-targeted genes, including Bcl-2, Bcl-XL, and XIAP as measured by their protein expression. dett 0-4 BCL2-like 1 Mus musculus 107-113 24212079-16 2014 Apoptosis induction of THHta was mediated by activation of caspase-3, PARP and inhibiting of Bcl-2, Bcl-xL and XIAP. thhta 23-28 BCL2-like 1 Mus musculus 100-106 24120472-9 2013 Placental tissue isolated from pregnant mice at E17.5 showed that the expressions of Cdk2 and 4, Cyclin D1 and Bcl-xL were reduced in zeranol-treatment groups. Zeranol 134-141 BCL2-like 1 Mus musculus 111-117 23548786-0 2013 Alterations in eicosanoid levels during U937 bcl-xL tumour growth suppression and recovery in NU/NU mice in vivo-Involvement of phospholipase A2. Eicosanoids 15-25 BCL2-like 1 Mus musculus 45-51 24227720-6 2013 Disruption of Bax:Bcl-xL binding by BH3-mimetic ABT 737 caused rapid apoptosis of cerebellar progenitors and primary murine medulloblastoma cells. BH 3 36-39 BCL2-like 1 Mus musculus 18-24 24227720-6 2013 Disruption of Bax:Bcl-xL binding by BH3-mimetic ABT 737 caused rapid apoptosis of cerebellar progenitors and primary murine medulloblastoma cells. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 48-51 BCL2-like 1 Mus musculus 18-24 23962725-9 2013 This was supported by the finding that gene expression of the anti-apoptotic genes Bcl-2 and Bcl-xL was higher in jaw cells than long bone cells, suggesting that the jaw cells might be more resistant to BP-induced apoptosis. Diphosphonates 203-205 BCL2-like 1 Mus musculus 93-99 23986435-10 2013 Finally, the hepatocyte apoptosis caused by ABT-737, which is a Bcl-xL/Bcl-2/Bcl-w inhibitor, was completely prevented in Bim/Bid double knock-out mice. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 44-47 BCL2-like 1 Mus musculus 64-70 24086701-7 2013 In vitro, silvestrol increased apoptosis and caspase 3/7 activity accompanied by loss of mitochondrial membrane potential and decreased expression of Mcl-1 and Bcl-xL. silvestrol 10-20 BCL2-like 1 Mus musculus 160-166 23997041-5 2013 However, simultaneous supplementation with quercetin (75 mg/kg) attenuated the toxicity induced by PNP through renewal of the antioxidant enzyme"s status, alleviating apoptosis by regulating the expressions of Bax and Bcl-xl, XBP-1 and HO-1mRNAs, and the regulation of caspase-3 activity. Quercetin 43-52 BCL2-like 1 Mus musculus 218-224 23857515-6 2013 Fucoxanthinol induced G1 cell cycle arrest by reducing the expression of cyclin-dependent kinase 4, cyclin-dependent kinase 6 and cyclin E and apoptosis by reducing the expression of survivin, XIAP, Bcl-2 and Bcl-xL. fucoxanthinol 0-13 BCL2-like 1 Mus musculus 209-215 24066113-4 2013 In the present study, we showed low glucose to induce a decrease of BCL2 and BCL-XL anti-apoptotic proteins expression, leading to an increase of free pro-apoptotic BAX. Glucose 36-43 BCL2-like 1 Mus musculus 77-83 24268771-3 2013 Combining the Bcl-2/Bcl-xL inhibitor ABT-737 with JAK2 inhibitors mediated prolonged disease regressions and cures in mice bearing primary human and mouse JAK2 mutant tumors. ABT-737 37-44 BCL2-like 1 Mus musculus 20-26 21786383-6 2013 Western blot analysis demonstrated that propofol promoted Fas, cytochrome c, caspase-9 and -3 active form and Bax levels, but inhibited Bcl-xl protein level which led to cell apoptosis. Propofol 40-48 BCL2-like 1 Mus musculus 136-142 23832122-6 2013 In particular, TH-302 can abrogate the accumulation of antiapoptotic Mcl-1 induced by bortezomib, and decreases the expression of the prosurvival proteins Bcl-2 and Bcl-xL. TH 302 15-21 BCL2-like 1 Mus musculus 165-171 23870437-15 2013 In contrast, only DC2.4 cells transduced with LVs encoding Bcl-XL and M11L were protected from effects of staurosporine (STS) treatment. Staurosporine 106-119 BCL2-like 1 Mus musculus 59-65 23870437-15 2013 In contrast, only DC2.4 cells transduced with LVs encoding Bcl-XL and M11L were protected from effects of staurosporine (STS) treatment. Staurosporine 121-124 BCL2-like 1 Mus musculus 59-65 23767404-0 2013 Discovery of potent and selective benzothiazole hydrazone inhibitors of Bcl-XL. benzothiazole hydrazone 34-57 BCL2-like 1 Mus musculus 72-78 23720737-2 2013 Inositol 1,4,5-trisphosphate-generating agonist evoked cytosolic Ca(2+) transients that produced a larger [Ca(2+)]mito uptake in WT cells compared with Bcl-xL-KO. Inositol 1,4,5-Trisphosphate 0-28 BCL2-like 1 Mus musculus 152-158 23080342-5 2013 Gln withdrawal-induced apoptosis was blocked by the overexpression of the anti-apoptotic protein Bcl-xL or by the caspase inhibitor Z-VAD-fmk. Glutamine 0-3 BCL2-like 1 Mus musculus 97-103 23430060-7 2013 GP7 or etoposide induced sub-G(1) peak, apoptotic DNA fragmentation, activations of caspase-3, -8, -9, and DNA fragmentation factor, downregulation of Bcl-2 and Bcl-xL, upregulation of Bax and Bak, and cytochrome-c release from mitochondria in both mouse and human OS cells. Etoposide 7-16 BCL2-like 1 Mus musculus 161-167 23674500-6 2013 Mechanistically, parthenolide increases the level of cellular ROS and causes oxidation of thioredoxin (TrX) in prostate cancer cells, leading to a TrX-dependent increase in a reduced state of KEAP1, which in turn leads to KEAP1-mediated PGAM5 and Bcl-xL (BCL2L1) degradation. parthenolide 17-29 BCL2-like 1 Mus musculus 247-253 23674500-6 2013 Mechanistically, parthenolide increases the level of cellular ROS and causes oxidation of thioredoxin (TrX) in prostate cancer cells, leading to a TrX-dependent increase in a reduced state of KEAP1, which in turn leads to KEAP1-mediated PGAM5 and Bcl-xL (BCL2L1) degradation. parthenolide 17-29 BCL2-like 1 Mus musculus 255-261 23788043-8 2013 Overexpression of Bcl-xL counteracts LC3-II increase, contributing to the hypothesis that the protective role of Bcl-xL observed in some SMA models may be mediated by its role in autophagy inhibition. lc3-ii 37-43 BCL2-like 1 Mus musculus 18-24 23643741-11 2013 Triptolide significantly induced SOCS3 protein and reduced STAT3 target anti-apoptotic genes Bcl-2 and Bcl-xl in LPMCs. triptolide 0-10 BCL2-like 1 Mus musculus 103-109 23643741-11 2013 Triptolide significantly induced SOCS3 protein and reduced STAT3 target anti-apoptotic genes Bcl-2 and Bcl-xl in LPMCs. lpmcs 113-118 BCL2-like 1 Mus musculus 103-109 23522402-6 2013 Duloxetine also increased Bcl-2, Bcl-xL, FGF-2, and NT-3 expression in the cerebral cortex, and FGF-2 expression in the hippocampus. Duloxetine Hydrochloride 0-10 BCL2-like 1 Mus musculus 33-39 23522402-8 2013 Mirtazapine decreased Bcl-xL and Bax expression in the hippocampus, and Bad and p53 expression in both the hippocampus and cerebral cortex. Mirtazapine 0-11 BCL2-like 1 Mus musculus 22-28 23528870-7 2013 Down-regulation of Bax and up-regulation of Bcl-xl protein expressions were observed in liver tissues of the dieckol administered groups. dieckol 109-116 BCL2-like 1 Mus musculus 44-50 23435943-4 2013 We observed an increase in levels of antiapoptotic Bcl-2, Bcl-XL mRNA and a decrease in levels of proapoptotic Bax mRNA following reynosin treatment of hepatocytes. reynosin 130-138 BCL2-like 1 Mus musculus 58-64 23399686-6 2013 In addition, we found SB203580 significantly decreased P-p38 MAPK levels, and inhibited HPC-induced mitochondria translocation of Bcl-xL in the brain of HPC and MCAO treated mice. SB 203580 22-30 BCL2-like 1 Mus musculus 130-136 23386286-9 2013 In addition, rosuvastatin administration decreased the pro-apoptotic proteins Bim and Bax, and increased the anti-apoptotic proteins Bcl-xL and Bcl-2. Rosuvastatin Calcium 13-25 BCL2-like 1 Mus musculus 133-139 23384965-7 2013 DMTU reduced the expression levels of TNF-alpha, Bax and c-fos and increased the expression levels of IL-6, Bcl-xL and Nrf2 in WT mice. 1,3-dimethylthiourea 0-4 BCL2-like 1 Mus musculus 108-114 23302291-8 2013 delta-Tocotrienol treatment inhibited mutant Kras-driven pathways such as MEK/ERK, PI3K/AKT and NF-kB/p65, as well as Bcl-xL and induced p27. tocotrienol, delta 0-17 BCL2-like 1 Mus musculus 118-124 23275004-3 2013 Treatment of mouse Hepa-1 cells with the antioxidant tert-butylhydroquinone led to the induction of Bcl-xL gene expression. 2-tert-butylhydroquinone 53-75 BCL2-like 1 Mus musculus 100-106 23275004-8 2013 SiRNA inhibition of both Nrf2 and Bcl-xL increased the susceptibility of cancer cells to etoposide-mediated cell death and reduced cell survival. Etoposide 89-98 BCL2-like 1 Mus musculus 34-40 23279742-12 2013 Largazole also induced HSCs to undergo apoptosis in vivo, which was correlated with downregulation of bcl-2 and bcl-xL. largazole 0-9 BCL2-like 1 Mus musculus 112-118 23341542-3 2013 Promising BH3 mimetic ABT-737 and the related orally available compound ABT-263 (navitoclax) bind avidly to antiapoptotic Bcl-2, Bcl-xL, and Bcl-w. BH 3 10-13 BCL2-like 1 Mus musculus 129-135 23341542-3 2013 Promising BH3 mimetic ABT-737 and the related orally available compound ABT-263 (navitoclax) bind avidly to antiapoptotic Bcl-2, Bcl-xL, and Bcl-w. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 22-25 BCL2-like 1 Mus musculus 129-135 23341542-3 2013 Promising BH3 mimetic ABT-737 and the related orally available compound ABT-263 (navitoclax) bind avidly to antiapoptotic Bcl-2, Bcl-xL, and Bcl-w. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 72-75 BCL2-like 1 Mus musculus 129-135 23211818-7 2013 RESULTS: The antiapoptotic molecule Bcl-X(L) significantly increased 6 hours after DEX injection. Dexamethasone 83-86 BCL2-like 1 Mus musculus 36-44 22933114-0 2013 Bcl-2 and Bcl-xL suppress glucose signaling in pancreatic beta-cells. Glucose 26-33 BCL2-like 1 Mus musculus 10-16 23245996-4 2013 ABT-263 (navitoclax), a chemical inhibitor that blocks the ability of BCL-XL to bind and inhibit pro-apoptotic proteins, in combination with a MEK inhibitor led to dramatic apoptosis in many KRAS mutant cell lines from different tissue types. navitoclax 0-7 BCL2-like 1 Mus musculus 70-76 23245996-4 2013 ABT-263 (navitoclax), a chemical inhibitor that blocks the ability of BCL-XL to bind and inhibit pro-apoptotic proteins, in combination with a MEK inhibitor led to dramatic apoptosis in many KRAS mutant cell lines from different tissue types. navitoclax 9-19 BCL2-like 1 Mus musculus 70-76 22814621-4 2013 Indeed, we report here that treatment of preleukaemic Emu-myc transgenic mice with the Bcl-2 homology (BH)3 mimetic drug ABT-737, which inhibits Bcl-x(L), as well as Bcl-2 and Bcl-w, augmented apoptosis of preneoplastic B-lymphoid cells, reduced their numbers and greatly prolonged lymphoma-free survival. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 121-124 BCL2-like 1 Mus musculus 145-153 22933114-2 2013 In this study, we demonstrate that chemical and genetic loss-of-function of antiapoptotic Bcl-2 and Bcl-x(L) significantly augments glucose-dependent metabolic and Ca(2+) signals in primary pancreatic beta-cells. Glucose 132-139 BCL2-like 1 Mus musculus 100-105 22933114-3 2013 Antagonism of Bcl-2/Bcl-x(L) by two distinct small-molecule compounds rapidly hyperpolarized beta-cell mitochondria, increased cytosolic Ca(2+), and stimulated insulin release via the ATP-dependent pathway in beta-cell under substimulatory glucose conditions. Adenosine Triphosphate 184-187 BCL2-like 1 Mus musculus 20-28 23228706-4 2013 Fucoxanthin-induced apoptosis was accompanied with the down-regulation of the protein levels of Bcl-xL, an inhibitor of apoptosis proteins (IAPs), resulting in a sequential activation of caspase-9, caspase-3, and PARP. fucoxanthin 0-11 BCL2-like 1 Mus musculus 96-102 22933114-3 2013 Antagonism of Bcl-2/Bcl-x(L) by two distinct small-molecule compounds rapidly hyperpolarized beta-cell mitochondria, increased cytosolic Ca(2+), and stimulated insulin release via the ATP-dependent pathway in beta-cell under substimulatory glucose conditions. Glucose 240-247 BCL2-like 1 Mus musculus 20-28 22933114-6 2013 Inducible deletion of Bcl-x(L) in adult mouse beta-cells also increased glucose-stimulated NAD(P)H and Ca(2+) responses and resulted in an improvement of in vivo glucose tolerance in the conditional Bcl-x(L) knockout animals. Glucose 72-79 BCL2-like 1 Mus musculus 22-30 22933114-6 2013 Inducible deletion of Bcl-x(L) in adult mouse beta-cells also increased glucose-stimulated NAD(P)H and Ca(2+) responses and resulted in an improvement of in vivo glucose tolerance in the conditional Bcl-x(L) knockout animals. Glucose 72-79 BCL2-like 1 Mus musculus 22-27 22933114-6 2013 Inducible deletion of Bcl-x(L) in adult mouse beta-cells also increased glucose-stimulated NAD(P)H and Ca(2+) responses and resulted in an improvement of in vivo glucose tolerance in the conditional Bcl-x(L) knockout animals. nad(p)h 91-98 BCL2-like 1 Mus musculus 22-30 22933114-6 2013 Inducible deletion of Bcl-x(L) in adult mouse beta-cells also increased glucose-stimulated NAD(P)H and Ca(2+) responses and resulted in an improvement of in vivo glucose tolerance in the conditional Bcl-x(L) knockout animals. nad(p)h 91-98 BCL2-like 1 Mus musculus 22-27 22933114-6 2013 Inducible deletion of Bcl-x(L) in adult mouse beta-cells also increased glucose-stimulated NAD(P)H and Ca(2+) responses and resulted in an improvement of in vivo glucose tolerance in the conditional Bcl-x(L) knockout animals. Glucose 162-169 BCL2-like 1 Mus musculus 22-30 22933114-6 2013 Inducible deletion of Bcl-x(L) in adult mouse beta-cells also increased glucose-stimulated NAD(P)H and Ca(2+) responses and resulted in an improvement of in vivo glucose tolerance in the conditional Bcl-x(L) knockout animals. Glucose 162-169 BCL2-like 1 Mus musculus 22-27 23117934-5 2013 The expression level of proapoptotic molecules such as p53, Bax, and Bak in the small intestine was downregulated and that of antiapoptotic molecules such as Bcl-2 and Bcl-X(S/L) was augmented in the PG-treated group. Phloroglucinol 200-202 BCL2-like 1 Mus musculus 168-173 22893064-3 2012 The priming action of aspirin on tumor cells was found to be dependent on an altered constitution of tumor microenvironment with respect to decline of acidosis and modulation in the expression of cell cycle and survival regulatory molecules like cyclin B1, cyclin D, bcl-2, bcl-xL, p53, and cytokines: IL-4, IL-10, IFN- gamma & VEGF. Aspirin 22-29 BCL2-like 1 Mus musculus 274-280 23117934-6 2013 On histological observation of the small intestine, PG inhibited the immunoreactivity of p53, Bax, and Bak and increased that of Bcl-2 and Bcl-X(S/L). Phloroglucinol 52-54 BCL2-like 1 Mus musculus 139-144 23255902-11 2013 In addition, EGCG downregulated the expression of Bcl-xl and upregulated the expression of Bax mRNA and protein. epigallocatechin gallate 13-17 BCL2-like 1 Mus musculus 50-56 23382877-8 2013 Furthermore, we also found that (i) increased expression of caspase-3 protein and decreased expression of Bcl-2, Bcl-XL and survivin proteins, (ii) the increased glutamate release in the hippocampus. Glutamic Acid 162-171 BCL2-like 1 Mus musculus 113-119 23000595-4 2012 The current work tested the hypothesis that MXC induces morphological atresia at early time points (24 and 48 h) by altering pro-apoptotic (Bax, Bok, Casp3, and caspase activity) and anti-apoptotic (Bcl2 and Bcl-xL) factors in the follicles. Methoxychlor 44-47 BCL2-like 1 Mus musculus 208-214 22988253-2 2012 Here, we report that when compared with their precursors, mature mitochondria-rich osteoclasts have lower levels of intracellular ATP, which is associated with receptor activator of nuclear factor kappa-B ligand (RANKL)-induced Bcl-x(L) down-regulation. Adenosine Triphosphate 130-133 BCL2-like 1 Mus musculus 228-236 22790873-5 2012 ABT-737, a Bcl-xL/Bcl-2/Bcl-w inhibitor, only caused thrombocytopenia in adult wild-type mice, but further induced massive mature megakaryocyte apoptosis in the Mcl-1 knockout mice, leading to severe hemorrhagic anemia. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 0-3 BCL2-like 1 Mus musculus 11-17 22902832-6 2012 Furthermore, the protective effect of fusaruside was attributable to a novel regulatory mechanism through down-regulating STAT1 activation and T-bet expression in liver CD4(+) T cells and up-regulating STAT3 activation and Bcl-X(L) expression in hepatocytes. fusaruside 38-48 BCL2-like 1 Mus musculus 223-231 22868912-11 2012 E2 and E2+ tamoxifen-treated cells showed upregulation of apoptotic genes caspase 1, 3, 9, P53 and Bcl-xl but the tamoxifen- and paclitaxel-treated cells did not upregulate the apoptotic genes. Tamoxifen 11-20 BCL2-like 1 Mus musculus 99-105 23047228-1 2012 The synthesis of quinoline derivatives, designed to interact with Bcl-x(L), and to inhibit its interaction with pro-apoptotic partners, is described and their biological effects investigated. quinoline 17-26 BCL2-like 1 Mus musculus 66-71 22374700-5 2012 However, treatment with ABT-737, a BH3 mimetic compound that inhibits the prosurvival proteins Bcl-2, Bcl-x(L), and Bcl-w resulted in the complete ablation of megakaryocytes and platelets. ABT-737 24-31 BCL2-like 1 Mus musculus 102-107 22952216-8 2012 Concomitant targeting of Mcl-1 by sorafenib and of Bcl-2/Bcl-xL by the antagonist ABT737 improves the efficacy of sorafenib in multiple myeloma cell lines and CD138(+)-enriched primary cells in the presence of bone marrow stromal cells. Sorafenib 114-123 BCL2-like 1 Mus musculus 57-63 22959464-7 2012 We also observed that PFOS induced p53-dependent apoptosis through the cooperation between the Bcl-xl down regulation without changing the Bcl-2 and Bax expression. perfluorooctane sulfonic acid 22-26 BCL2-like 1 Mus musculus 95-101 22968190-6 2012 This was also supported by the fact that melanin could prevent apoptosis in splenic tissue by decreasing BAX/Bcl-XL ratio, and increasing the expressions of the proliferation markers (PCNA and Cyclin D1), compared to the radiation control group. Melanins 41-48 BCL2-like 1 Mus musculus 109-115 23185674-10 2012 The zinc-citrate compound increased the expression of p21(waf1) and p53 and reduced the expression of Bcl-2 and Bcl-xL proteins but induced expression of Bax protein. Zinc citrate 4-16 BCL2-like 1 Mus musculus 112-118 22374700-5 2012 However, treatment with ABT-737, a BH3 mimetic compound that inhibits the prosurvival proteins Bcl-2, Bcl-x(L), and Bcl-w resulted in the complete ablation of megakaryocytes and platelets. BH 3 35-38 BCL2-like 1 Mus musculus 102-107 22617452-6 2012 Chemical inhibition of FGFR, NFkB, and PI3K activity by PD173074, pyrrolidine dithiocarbamate, and LY294002 respectively abrogated the FGF-2-mediated induction of Bcl2-A1 and Bcl-xL expression. pyrrolidine dithiocarbamic acid 66-93 BCL2-like 1 Mus musculus 175-181 22326437-11 2012 The anti-apoptotic effects of asTF overexpression were mediated via alpha(V)beta(3)/Akt/NFkappaB signaling and were dependent on Bcl-x(L) expression in HL-1 cells. astf 30-34 BCL2-like 1 Mus musculus 129-137 22318920-8 2012 This retained expression of Bcl-xL is inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 102-110 BCL2-like 1 Mus musculus 28-34 22461695-5 2012 Decitabine also upregulates BNIP3 and Bik expression, whereas vorinostat decreased Bcl-x(L) expression. Vorinostat 62-72 BCL2-like 1 Mus musculus 83-91 22510411-6 2012 Further, ABT-737, which can inhibit Bcl-X(L) function, sensitized NOD macrophages to apoptosis induced by diverse apoptotic stimuli, thus restoring sensitivity to cell death. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 9-12 BCL2-like 1 Mus musculus 36-44 22351692-9 2012 As compared with vehicle control, gamma-tocotrienol also suppressed the NF-kappaB activation and the expression of cyclin D1, COX-2, intercellular adhesion molecule-1 (ICAM-1), MMP-9, survivin, Bcl-xL, and XIAP. plastochromanol 8 34-51 BCL2-like 1 Mus musculus 194-200 22441020-10 2012 ADH accentuated or unmasked alcohol-induced downregulation of Bcl-2, Bcl-xL and MiR-30a. adh 0-3 BCL2-like 1 Mus musculus 69-75 22441020-10 2012 ADH accentuated or unmasked alcohol-induced downregulation of Bcl-2, Bcl-xL and MiR-30a. Alcohols 28-35 BCL2-like 1 Mus musculus 69-75 21997189-0 2012 Pharmacological blockade of Bcl-2, Bcl-x(L) and Bcl-w by the BH3 mimetic ABT-737 has only minor impact on tumour development in p53-deficient mice. BH 3 61-64 BCL2-like 1 Mus musculus 35-43 21997189-0 2012 Pharmacological blockade of Bcl-2, Bcl-x(L) and Bcl-w by the BH3 mimetic ABT-737 has only minor impact on tumour development in p53-deficient mice. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 73-76 BCL2-like 1 Mus musculus 35-43 22134971-2 2012 Exposure of cells to taxol induced time-dependent cytotoxicity and cytoplasmic vacuolization without the involvement of Bax, Bak, Mcl-1, Bcl-XL, and caspase-3. Paclitaxel 21-26 BCL2-like 1 Mus musculus 137-143 22281782-3 2012 DPHC slightly reduced the expression of Bax induced by H(2)O(2) but recovered the expression of Bcl-xL as well as caspase-9 and -3 mediated PARP cleavage by H(2)O(2). diphlorethohydroxycarmalol 0-4 BCL2-like 1 Mus musculus 96-102 22467373-6 2012 Furthermore, treatment of PNMC increased expression of the pro-apoptotic protein Bax and decreased expression of the anti-apoptotic protein Bcl-XL in germ cells. pnmc 26-30 BCL2-like 1 Mus musculus 140-146 23213401-1 2012 The BH3 mimetic ABT-737 is a potent inhibitor of the anti-apoptotic proteins Bcl-2, Bcl-X(L), and Bcl-w. BH 3 4-7 BCL2-like 1 Mus musculus 84-92 21768359-4 2012 To determine whether the BH3 mimetic ABT-737 that neutralizes BCL-2, BCL-XL, and BCL-W had potential efficacy in targeting BCL-2-expressing basal-like triple-negative tumors, we generated a panel of primary breast tumor xenografts in immunocompromised mice and treated recipients with either ABT-737, docetaxel, or a combination. BH 3 25-28 BCL2-like 1 Mus musculus 69-75 21768359-4 2012 To determine whether the BH3 mimetic ABT-737 that neutralizes BCL-2, BCL-XL, and BCL-W had potential efficacy in targeting BCL-2-expressing basal-like triple-negative tumors, we generated a panel of primary breast tumor xenografts in immunocompromised mice and treated recipients with either ABT-737, docetaxel, or a combination. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 37-40 BCL2-like 1 Mus musculus 69-75 21768359-4 2012 To determine whether the BH3 mimetic ABT-737 that neutralizes BCL-2, BCL-XL, and BCL-W had potential efficacy in targeting BCL-2-expressing basal-like triple-negative tumors, we generated a panel of primary breast tumor xenografts in immunocompromised mice and treated recipients with either ABT-737, docetaxel, or a combination. ABT-737 37-44 BCL2-like 1 Mus musculus 69-75 23213401-1 2012 The BH3 mimetic ABT-737 is a potent inhibitor of the anti-apoptotic proteins Bcl-2, Bcl-X(L), and Bcl-w. ABT-737 16-23 BCL2-like 1 Mus musculus 84-92 23240061-5 2012 Z-VAD-fmk (caspase inhibitor), pifithrin-alpha (p53 inhibitor), or overexpressed Bcl-xl decreased the effects of quercetin on DOX-mediated apoptosis. Quercetin 113-122 BCL2-like 1 Mus musculus 81-87 22072391-0 2012 The BH4 domain of Bcl-X(L) rescues astrocyte degeneration in amyotrophic lateral sclerosis by modulating intracellular calcium signals. sapropterin 4-7 BCL2-like 1 Mus musculus 18-26 22072391-0 2012 The BH4 domain of Bcl-X(L) rescues astrocyte degeneration in amyotrophic lateral sclerosis by modulating intracellular calcium signals. Calcium 119-126 BCL2-like 1 Mus musculus 18-26 22038096-0 2012 Simvastatin suppresses apoptosis in vulnerable atherosclerotic plaques through regulating the expression of p(53), Bcl-2 and Bcl-xL. Simvastatin 0-11 BCL2-like 1 Mus musculus 125-131 22038096-8 2012 Moreover, we found that simvastatin administration led to reduced TUNEL-positive cells in the aortic root lesions, accompanied by up-regulation of Bcl-2 and Bcl-xL expression, and decreased P(53) expression as shown by Western blot. Simvastatin 24-35 BCL2-like 1 Mus musculus 157-163 22038096-9 2012 CONCLUSION: In the present study, we show novel data to suggest that simvastatin could suppress apoptosis in vulnerable atherosclerotic plaques of apoE(-/-) mice by regulating the expression of apoptosis-related proteins, such as p(53), Bcl-2 and Bcl-xL. Simvastatin 69-80 BCL2-like 1 Mus musculus 247-253 22040025-2 2012 Here we describe a comprehensive evaluation of diverse alpha/beta-peptide homologues of the Bim BH3 domain in terms of their ability to bind to the BH3-recognition sites on two partner proteins, Bcl-x(L) and Mcl-1. BH 3 96-99 BCL2-like 1 Mus musculus 195-203 22037186-4 2012 Protein expression levels of Bcl-x(L) but not Bcl-2 were elevated in VSMCs isolated from db/db compared with db/m age-matched controls. vsmcs 69-74 BCL2-like 1 Mus musculus 29-37 23240061-0 2012 Quercetin potentiates doxorubicin mediated antitumor effects against liver cancer through p53/Bcl-xl. Quercetin 0-9 BCL2-like 1 Mus musculus 94-100 23240061-0 2012 Quercetin potentiates doxorubicin mediated antitumor effects against liver cancer through p53/Bcl-xl. Doxorubicin 22-33 BCL2-like 1 Mus musculus 94-100 23240061-4 2012 The increase in DOX-mediated apoptosis in hepatoma cells by quercetin was p53-dependent and occurred by downregulating Bcl-xl expression. Doxorubicin 16-19 BCL2-like 1 Mus musculus 119-125 22687777-7 2012 Quantitative real-time PCR analysis demonstrated that the administration of AMC and AAC down-regulated the expression of Bcl-2, Bcl-xL, while on the other hand, up-regulated Bax, Cytochrome c, caspase-9 and caspase-3 mRNA level of the S180 ascites tumor cells. 7-amino-4-methylcoumarin 76-79 BCL2-like 1 Mus musculus 128-134 23288995-0 2012 Bcl-xL-mediated remodeling of rod and cone synaptic mitochondria after postnatal lead exposure: electron microscopy, tomography and oxygen consumption. Oxygen 132-138 BCL2-like 1 Mus musculus 0-6 23240061-5 2012 Z-VAD-fmk (caspase inhibitor), pifithrin-alpha (p53 inhibitor), or overexpressed Bcl-xl decreased the effects of quercetin on DOX-mediated apoptosis. Doxorubicin 126-129 BCL2-like 1 Mus musculus 81-87 23240061-4 2012 The increase in DOX-mediated apoptosis in hepatoma cells by quercetin was p53-dependent and occurred by downregulating Bcl-xl expression. Quercetin 60-69 BCL2-like 1 Mus musculus 119-125 21998213-6 2011 These findings identify Bcl-x(L) as a prerequisite for the emergence of c-Myc-driven pre-B/B lymphoma and suggest that BH3 mimetic drugs may provide a prophylactic strategy for c-Myc-driven tumors. BH 3 119-122 BCL2-like 1 Mus musculus 24-32 22384256-9 2012 Treatment with the JAK2 inhibitor TG101209 abrogated BCR-JAK2 and STAT5 phosphorylation, decreased Bcl-xL expression and triggered apoptosis of transformed Ba/F3 cells. TG101209 34-42 BCL2-like 1 Mus musculus 99-105 22015602-11 2011 Importantly, hydrogen inhibited the activation of P-JNK, and also reversed changes in Bax, Bcl-xl and caspase-3. Hydrogen 13-21 BCL2-like 1 Mus musculus 91-97 21903769-8 2011 Although both MLN2238 and bortezomib prolonged overall survival, reduced splenomegaly, and attenuated IgG2a levels in the iMyc(Calpha)/Bcl-X(L) GEM model, only MLN2238 alleviated osteolytic bone disease in the DP54-Luc model. Bortezomib 26-36 BCL2-like 1 Mus musculus 135-140 21857260-9 2011 While histologic lung injury was variable, both sulfide and hypothermia attenuated the trauma-related increase in heme oxygenase-1 expression and activated caspase-3 staining, which coincided with increased Bad phosphorylation and Bcl-Xl expression. Sulfides 48-55 BCL2-like 1 Mus musculus 231-237 21552152-9 2011 Exposure of myoblasts and myotubes for 48 and 72 h at high salmeterol concentrations induced apoptosis by the activation of the intrinsic apoptotic pathway, as confirmed by the modulation of the apoptotic proteins Bcl-xL, caspase-9, and poly (ADP-ribose) polymerase and by the cytoplasmic release of Smac/DIABLO. Salmeterol Xinafoate 59-69 BCL2-like 1 Mus musculus 214-220 21719460-3 2011 In this study, we demonstrate that treatment of DBA/1 mice, prior to the onset of CIA with ABT-737, a BH3 mimetic targeting Bcl-2, Bcl-w, and Bcl-x(L), ameliorated disease development. 1,2,5,6-dibenzanthracene 48-51 BCL2-like 1 Mus musculus 142-150 21843953-6 2011 Moreover, IL-22 treatment significantly enhanced activation of STAT3 and up-regulated the expression of Bcl-xL, heme oxygenase-1 (HO-1) and redox factor-1 (Ref-1) in the liver injury induced by GalN/LPS. Galactosamine 194-198 BCL2-like 1 Mus musculus 104-110 21723861-0 2011 Dexamethasone induces transcriptional activation of Bcl-xL gene and inhibits cardiac injury by myocardial ischemia. Dexamethasone 0-13 BCL2-like 1 Mus musculus 52-58 21723861-10 2011 In studying the mechanism of such protection, we found that dexamethasone induces the expression of Bcl-xL gene in the myocardium. Dexamethasone 60-73 BCL2-like 1 Mus musculus 100-106 21723861-12 2011 The glucocorticoid receptor antagonist mifepristone prevented dexamethasone from inducing cardiac protection or Bcl-xL expression. Mifepristone 39-51 BCL2-like 1 Mus musculus 112-118 21723861-12 2011 The glucocorticoid receptor antagonist mifepristone prevented dexamethasone from inducing cardiac protection or Bcl-xL expression. Dexamethasone 62-75 BCL2-like 1 Mus musculus 112-118 21719460-3 2011 In this study, we demonstrate that treatment of DBA/1 mice, prior to the onset of CIA with ABT-737, a BH3 mimetic targeting Bcl-2, Bcl-w, and Bcl-x(L), ameliorated disease development. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 91-94 BCL2-like 1 Mus musculus 142-150 21719460-3 2011 In this study, we demonstrate that treatment of DBA/1 mice, prior to the onset of CIA with ABT-737, a BH3 mimetic targeting Bcl-2, Bcl-w, and Bcl-x(L), ameliorated disease development. BH 3 102-105 BCL2-like 1 Mus musculus 142-150 21630270-10 2011 Renal cell apoptosis induced by IR was decreased in kidneys of mice pretreated by clopidogrel, with an increase in Bcl-2 and Bcl-xL expression and a decrease in caspase-3, caspase-8, and Bax expression. Clopidogrel 82-93 BCL2-like 1 Mus musculus 125-131 21683644-0 2011 Expression of Bcl2l1, Clcf1, IL-28ra and Pias1 in the mouse heart after single and repeated administration of chlorpromazine. Chlorpromazine 110-124 BCL2-like 1 Mus musculus 14-20 21737642-6 2011 Results from Western blotting indicated that etomidate enhanced the levels of cytochrome c, apoptosis-inducing factor (AIF), endonuclease G (Endo G), caspase-9, caspase-3 active form and Bax proteins, but it inhibited the expression of Bcl-xl, leading to apoptosis. Etomidate 45-54 BCL2-like 1 Mus musculus 236-242 21631112-4 2011 The results indicate that mogrosides can inhibit inflammation induced by lipopolysaccharides (LPS) in RAW 264.7 cells by down-regulating the expression of key inflammatory genes iNOS, COX-2, and IL-6 and up-regulating some inflammation protective genes such as PARP1, BCL2l1, TRP53, and MAPK9. mogrosides 26-36 BCL2-like 1 Mus musculus 268-274 21631112-5 2011 Similarly, in the murine ear edema model, 12-O-tetradecanoylphorbol-13-acetate-induced inflammation was inhibited by mogrosides by down-regulating COX-2 and IL-6 and up-regulating PARP1, BCL2l1, TRP53, MAPK9, and PPARdelta gene expression. Tetradecanoylphorbol Acetate 42-78 BCL2-like 1 Mus musculus 187-193 21631112-5 2011 Similarly, in the murine ear edema model, 12-O-tetradecanoylphorbol-13-acetate-induced inflammation was inhibited by mogrosides by down-regulating COX-2 and IL-6 and up-regulating PARP1, BCL2l1, TRP53, MAPK9, and PPARdelta gene expression. mogrosides 117-127 BCL2-like 1 Mus musculus 187-193 21505478-7 2011 Increased levels of the prosurvival factor Bcl-xL were evident 24 hours after injury in AraS-treated mice, followed by a 30% reduction in caspase-3 activity, measured 3 days after injury. N-arachidonoyl L-serine 88-92 BCL2-like 1 Mus musculus 43-49 21325633-5 2011 Further, Akt, NF-kappaB and NF-kappaB regulated Bcl-2, Bcl-xL, survivin and cIAP1 appear to be the molecular targets of CDDO for inhibiting the progression of prostate cancer in TRAMP mice. 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid 120-124 BCL2-like 1 Mus musculus 55-61 21193457-13 2011 It was shown that arginine induced expression of Bcl-2 and Bcl-xL, while rReg4 upregulated Bcl-2 and Bcl-xL expression by activating the EGFR/Akt pathway. Arginine 18-26 BCL2-like 1 Mus musculus 59-65 21052840-6 2011 Under the same experimental condition, the expression of both Bcl-2 and Bcl-xl was clearly induced by GM-CSF regardless of staurosporine treatment in RT-PCR and Western blot analyses. Staurosporine 123-136 BCL2-like 1 Mus musculus 72-78 21074598-7 2011 The levels of the pro-apoptotic proteins p53 and Bax and the anti-apoptotic protein Bcl-xL were significantly increased in Dox-treated mice compared with the control group. Doxorubicin 123-126 BCL2-like 1 Mus musculus 84-90 21337715-7 2011 In addition, cadmium provoked germ cell apoptosis by upregulating expression of the proapoptotic proteins Bax and caspase-3 and downregulating expression of the antiapoptotic protein Bcl-XL. Cadmium 13-20 BCL2-like 1 Mus musculus 183-189 21337715-10 2011 Additionally, quercetin protected germ cells from cadmium-induced apoptosis by downregulating the expression of Bax and caspase-3 and upregulating Bcl-XL expression. Quercetin 14-23 BCL2-like 1 Mus musculus 147-153 21337715-10 2011 Additionally, quercetin protected germ cells from cadmium-induced apoptosis by downregulating the expression of Bax and caspase-3 and upregulating Bcl-XL expression. Cadmium 50-57 BCL2-like 1 Mus musculus 147-153 20885444-0 2011 Single-point mutations of a lysine residue change function of Bax and Bcl-xL expressed in Bax- and Bak-less mouse embryonic fibroblasts: novel insights into the molecular mechanisms of Bax-induced apoptosis. Lysine 28-34 BCL2-like 1 Mus musculus 70-76 20885444-6 2011 To gain insight into the mechanism of Bax-Kv1.3 interaction, we mutated Glu158 of Bcl-x(L) (corresponding to K128 in Bax) to lysine. cloricromen 109-113 BCL2-like 1 Mus musculus 82-90 20885444-6 2011 To gain insight into the mechanism of Bax-Kv1.3 interaction, we mutated Glu158 of Bcl-x(L) (corresponding to K128 in Bax) to lysine. Lysine 125-131 BCL2-like 1 Mus musculus 82-90 20671748-8 2011 Therefore, we propose that Bcl-xL/Bax H5 disturbs mitochondrial morphology by binding and inhibiting Mfn1 and Mfn2 activity, supporting the hypothesis that Bcl-2 family members have the capacity to regulate mitochondrial morphology through binding to the mitofusins in healthy cells. mitofusins 255-265 BCL2-like 1 Mus musculus 27-33 20886344-7 2011 Furthermore, the phosphorylated form of STAT3 and the levels of STAT3"s target gene products such as Bcl-xl and Bcl-2, which are essential for cell growth and survival, were also decreased in aspirin-treated mice. Aspirin 192-199 BCL2-like 1 Mus musculus 101-107 20676141-6 2010 SAHA downregulated Bcl-XL and upregulated proapoptotic BH3-only protein Bim, whose expression was further enhanced by E1A in cancer cells. Vorinostat 0-4 BCL2-like 1 Mus musculus 19-25 26760337-3 2010 Antiapoptotic members of the Bcl-2 family (B cell CLL/lymphoma 2), that belong to the intrinsic route of the activation of caspases, such as Bcl-xL (extra-large B-cell lymphoma) and Bcl-w (Bcl-2-like 2), act predominantly to prevent that pro-apoptotic members, such as Bax (Bcl-2-associated X protein) and Bak (Bcl-2 relative bak) lead to cell death. bakuchiol 326-329 BCL2-like 1 Mus musculus 141-147 21138522-6 2010 Doxycycline treatment of adult mice carrying both transgenes induces shRNA expression, depletes Bcl-x(L) in megakaryocytes and triggers severe thrombocytopenia, whereas doxycycline withdrawal shuts off shRNA expression, normalizes Bcl-x(L) levels and restores platelet numbers. Doxycycline 0-11 BCL2-like 1 Mus musculus 96-101 21138522-6 2010 Doxycycline treatment of adult mice carrying both transgenes induces shRNA expression, depletes Bcl-x(L) in megakaryocytes and triggers severe thrombocytopenia, whereas doxycycline withdrawal shuts off shRNA expression, normalizes Bcl-x(L) levels and restores platelet numbers. Doxycycline 0-11 BCL2-like 1 Mus musculus 96-104 21033669-4 2010 Compound 6f inhibits the binding of BH3 peptides to Bcl-X(L), Bcl-2, and Mcl-1 with IC(50) values of 3.10, 3.12, and 2.05 muM, respectively. BH 3 36-39 BCL2-like 1 Mus musculus 52-60 20692331-12 2010 Activation of JNK and decreased levels of Bcl-2 and Bcl-XL were observed in the ethanol-fed KI mice compared to the other groups. Ethanol 80-87 BCL2-like 1 Mus musculus 52-58 20718735-4 2010 KEY RESULTS: We demonstrated that carboplatin initiated an intrinsic apoptotic pathway of activating caspase-3 and -9, accompanied by a decrease in the ratio of Bcl-XL/Bax and a significant increase in Bcl-XS. Carboplatin 34-45 BCL2-like 1 Mus musculus 161-167 20655905-7 2010 Both mitochondrion-dependent and endoplasmic reticulum stress-induced apoptotic pathways were also activated in the hearts of doxorubicin-treated mice as reflected by decreased Bcl-2/Bcl-(XL) and elevated Bax/Bad, p53/Apaf-1, endoplasmic reticulum glucose-related protein 78, C/EBP homologous protein, cytochrome c release from mitochondria, caspases-9/-3 cleavage, and cardiomyocyte apoptosis. Doxorubicin 126-137 BCL2-like 1 Mus musculus 183-191 19880821-0 2010 Epithelial ablation of Bcl-XL increases sensitivity to oxygen without disrupting lung development. Oxygen 55-61 BCL2-like 1 Mus musculus 23-29 19880821-9 2010 Intriguingly, increased 8-oxoguanine lesions seen during hyperoxia were also evident as lungs transitioned to room air at birth, a time when perinatal lethality in some mice lacking Bcl-X(L) was observed. 8-hydroxyguanine 24-36 BCL2-like 1 Mus musculus 182-190 19880821-10 2010 These findings reveal that the epithelial-specific expression of Bcl-X(L) is not required for proper lung development, but functions to protect respiratory epithelial cells against oxygen-induced toxicity, such as during hyperoxia and the lung"s first exposure to ambient air. Oxygen 181-187 BCL2-like 1 Mus musculus 65-73 20684596-4 2010 One of the derivatives, compound 7 (6-aminopenicillanic acid sodium-gossypolone), was identified with great water solubility and anticancer property, suggested by inducing a dramatically decrease in Bcl-2 and Bcl-xL protein expression level found in vitro and growth inhibition of murine colon tumor in vivo. 6-aminopenicillanic acid gossypolone 36-79 BCL2-like 1 Mus musculus 209-215 20534453-3 2010 We examined the effects of the drug ABT-737, a mimetic of the killer BH3 domain of the Bcl-2 family of proteins that induces apoptosis by antagonizing Bcl-2, Bcl-X(L), and Bcl-W (but not Mcl-1 and A1), on the mouse immune system. ABT-737 36-43 BCL2-like 1 Mus musculus 158-166 20413732-3 2010 METHODS AND RESULTS: We demonstrate that 6-MP induces apoptosis of THP-1 monocytes, involving decreased expression of the intrinsic antiapoptotic factors B-cell CLL/Lymphoma-2 (Bcl-2) and Bcl2-like 1 (Bcl-x(L)). Mercaptopurine 41-45 BCL2-like 1 Mus musculus 188-199 20413732-3 2010 METHODS AND RESULTS: We demonstrate that 6-MP induces apoptosis of THP-1 monocytes, involving decreased expression of the intrinsic antiapoptotic factors B-cell CLL/Lymphoma-2 (Bcl-2) and Bcl2-like 1 (Bcl-x(L)). Mercaptopurine 41-45 BCL2-like 1 Mus musculus 201-209 20535152-6 2010 To improve on this approach, we combined in vitro targeting of STAT5-mediated AKT/mTOR using rapamycin with inhibition of the STAT5 direct target genes bcl-2 and bcl-X(L) using ABT-737. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 177-180 BCL2-like 1 Mus musculus 162-170 20516119-5 2010 Therapeutically, deficiency of Taspase1 synergizes with chemotherapeutic agents and ABT-737, an inhibitor of BCL-2/BCL-X(L), to kill cancer cells. ABT-737 84-91 BCL2-like 1 Mus musculus 115-123 20353770-4 2010 Results showed a massive impairment of erythropoiesis early post paclitaxel administration (1-2 days), which involved induction of high Bax/Bcl-x(L) ratio, caspase-3 activation, disruptions of the medullar niche and cell death by both apoptosis and necrosis. Paclitaxel 65-75 BCL2-like 1 Mus musculus 140-148 20590594-7 2010 Western blot analysis of the tumour samples of mice who received both cucurbitacin B and gemcitabine, revealed stronger inhibition of Bcl-XL, Bcl-2 and c-myc, and higher activation of the caspase cascades, than mice treated with either agent alone. cucurbitacin B 70-84 BCL2-like 1 Mus musculus 134-140 20590594-7 2010 Western blot analysis of the tumour samples of mice who received both cucurbitacin B and gemcitabine, revealed stronger inhibition of Bcl-XL, Bcl-2 and c-myc, and higher activation of the caspase cascades, than mice treated with either agent alone. gemcitabine 89-100 BCL2-like 1 Mus musculus 134-140 19726085-4 2010 Silvestrol shows synergy with standard-of-care agents in AML cell lines and synergizes with ABT-737, a small molecule inhibitor of Bcl-X(L) and Bcl-2. silvestrol 0-10 BCL2-like 1 Mus musculus 131-139 20428789-5 2010 Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner. Desipramine 125-128 BCL2-like 1 Mus musculus 275-281 20428789-5 2010 Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner. Desipramine 223-226 BCL2-like 1 Mus musculus 275-281 20405005-11 2010 Further, curcumin down-regulated the pro-survival protein Bcl-xL, depolarized the mitochondrial membrane, increased PARP cleavage, which led to apoptotic cell death. Curcumin 9-17 BCL2-like 1 Mus musculus 58-64 20144634-0 2010 Silymarin modulates doxorubicin-induced oxidative stress, Bcl-xL and p53 expression while preventing apoptotic and necrotic cell death in the liver. Silymarin 0-9 BCL2-like 1 Mus musculus 58-64 20144634-0 2010 Silymarin modulates doxorubicin-induced oxidative stress, Bcl-xL and p53 expression while preventing apoptotic and necrotic cell death in the liver. Doxorubicin 20-31 BCL2-like 1 Mus musculus 58-64 20144634-3 2010 This in vivo study was designed to explore the hepatotoxic potential of Doxorubicin (Dox), the well-known cardiotoxin, and in particular whether pre-exposures to SMN can prevent hepatotoxicity by reducing Dox-induced free radical mediated oxidative stress, by modulating expression of apoptotic signaling proteins like Bcl-xL, and by minimizing liver cell death occurring by apoptosis or necrosis. Silymarin 162-165 BCL2-like 1 Mus musculus 319-325 20144634-16 2010 The effects of SMN on Dox were broad, including the ability to modulate changes in both Bcl-xL and p53 expression. Silymarin 15-18 BCL2-like 1 Mus musculus 88-94 20144634-16 2010 The effects of SMN on Dox were broad, including the ability to modulate changes in both Bcl-xL and p53 expression. Doxorubicin 22-25 BCL2-like 1 Mus musculus 88-94 20144634-17 2010 In animals treated with SMN, tissue Bcl-xL expression exceeded control values after Dox treatment. Doxorubicin 84-87 BCL2-like 1 Mus musculus 36-42 20144634-18 2010 Taken together, these results demonstrated that SMN (i) reduced, delayed onset, or prevented toxic effects of Dox which are typically associated with hydroxyl radical production, (ii) performed as an antioxidant limiting oxidative stress, (iii) protected the integrity of the genome, and (iv) antagonized apoptotic and necrotic cell death while increasing antiapoptotic Bcl-xL protein levels and minimizing the leakage of proapoptotic cytochrome c from liver mitochondria. Silymarin 48-51 BCL2-like 1 Mus musculus 370-376 20459769-10 2010 Stimulation of apoptosis in lapatinib-treated A549 cells was correlated with increased cleaved PARP, active caspase-3, and proapoptotic Bak-1 levels, and reduction in the antiapoptotic IAP-2 and Bcl-xL protein levels. Lapatinib 28-37 BCL2-like 1 Mus musculus 195-201 19726085-4 2010 Silvestrol shows synergy with standard-of-care agents in AML cell lines and synergizes with ABT-737, a small molecule inhibitor of Bcl-X(L) and Bcl-2. ABT-737 92-99 BCL2-like 1 Mus musculus 131-139 19887573-6 2010 Cadmium-induced apoptosis involved a mitochondria-mediated mechanism but not caspase-dependent pathway in that the critical apoptotic events induced by cadmium, such as the decrease of Bcl-2/Bcl-xL, the increase of GADD45alpha, and the nuclear translocation of apoptosis inducing factor, were not affected by the inhibition of executive caspases. Cadmium 0-7 BCL2-like 1 Mus musculus 191-197 20074638-6 2010 Additionally, WISP1 reverses DOX-induced suppression of Bcl-2 and Bcl-xL expression and Akt inhibition. Doxorubicin 29-32 BCL2-like 1 Mus musculus 66-72 19997066-7 2010 Expression levels of pro-survival proteins Bcl-xL and heme oxygenase-1 (HO-1), which are downstream of Stat3, were substantially lower in PXR-null than wild-type mouse livers after LPS/GalN treatment. Galactosamine 185-189 BCL2-like 1 Mus musculus 43-49 19997066-12 2010 Increases of LPS/GalN-induced hepatocyte apoptosis and liver injury in PXR-null mice are due to deregulated mitogen-activated protein (MAP) kinase activation as well as delayed Jak2/Stat3 activation, which lead to a compromise in defense mechanisms that involve Bcl-xL-, HO-1, and autophagy-mediated pathways. Galactosamine 17-21 BCL2-like 1 Mus musculus 262-268 21088703-7 2010 However, metaxin deficiency and Bcl-X(L) overexpression apparently affect Rh123 release from a site(s) different from that of CsA, as CsA can overcome their effect. Rhodamine 123 74-79 BCL2-like 1 Mus musculus 32-40 21088703-10 2010 The alteration of the mitochondrial outer membrane properties by metaxin deficiency and Bcl-X(L) overexpression, as indicated by a quicker Rh123 release, may be helpful in maintaining mitochondrial integrity. Rhodamine 123 139-144 BCL2-like 1 Mus musculus 88-96 19887573-6 2010 Cadmium-induced apoptosis involved a mitochondria-mediated mechanism but not caspase-dependent pathway in that the critical apoptotic events induced by cadmium, such as the decrease of Bcl-2/Bcl-xL, the increase of GADD45alpha, and the nuclear translocation of apoptosis inducing factor, were not affected by the inhibition of executive caspases. Cadmium 152-159 BCL2-like 1 Mus musculus 191-197 19676108-8 2009 In contrast, bcl-x(flox/flox) mcl-1(flox/+) AlbCre, bcl-x(flox/+) mcl-1(flox/flox) AlbCre, and bcl-x(flox/flox) mcl-1(flox/flox) AlbCre mice displayed a decreased number of hepatocytes and a reduced volume of the liver on day 18.5 of embryogenesis and rapidly died within 1 day after birth, developing hepatic failure evidenced by increased levels of blood ammonia and bilirubin. Ammonia 357-364 BCL2-like 1 Mus musculus 13-18 19839062-7 2009 tBid was capable of binding to Bcl-xL and displacing Bak and Bax from Bcl-xL, leading to release of cytochrome c from wild-type mitochondria. tBID 0-4 BCL2-like 1 Mus musculus 31-37 19839062-7 2009 tBid was capable of binding to Bcl-xL and displacing Bak and Bax from Bcl-xL, leading to release of cytochrome c from wild-type mitochondria. tBID 0-4 BCL2-like 1 Mus musculus 70-76 19839062-8 2009 Bcl-xL-deficient mitochondria were more susceptible to tBid-induced cytochrome c release. tBID 55-59 BCL2-like 1 Mus musculus 0-6 19839062-9 2009 Finally, administration of ABT-737, a pharmacological inhibitor of Bcl-2/Bcl-xL, caused Bak/Bax-dependent liver injury, but this was clearly ameliorated with a Bid KO background. ABT-737 27-34 BCL2-like 1 Mus musculus 73-79 19875169-7 2009 In addition, pro-survival signaling including activation of mitogen-activated protein kinases (MAPKs) such as the extracellular signal-regulated protein kinases, c-Jun NH(2) terminal kinases and p38 and the expression of Bcl-x(L) were significantly prolonged in me-BMMCs compared with WT-BMMCs. methionylglutamic acid 262-264 BCL2-like 1 Mus musculus 221-229 19676108-8 2009 In contrast, bcl-x(flox/flox) mcl-1(flox/+) AlbCre, bcl-x(flox/+) mcl-1(flox/flox) AlbCre, and bcl-x(flox/flox) mcl-1(flox/flox) AlbCre mice displayed a decreased number of hepatocytes and a reduced volume of the liver on day 18.5 of embryogenesis and rapidly died within 1 day after birth, developing hepatic failure evidenced by increased levels of blood ammonia and bilirubin. Bilirubin 369-378 BCL2-like 1 Mus musculus 13-18 19309000-5 2009 A significant increase in apoptosis induced by either UVB irradiation or 7,12-dimethylbenz[a]anthracene (DMBA) treatment was observed in the epidermis of Bcl-x(L)-deficient mice. 7,12-dimethylbenz[a 73-92 BCL2-like 1 Mus musculus 154-162 19581414-6 2009 RESULTS: Bcl-xL-deficient beta-cells developed but were abnormally sensitive to apoptosis induced in vivo by low-dose STZ. Streptozocin 118-121 BCL2-like 1 Mus musculus 9-15 19309000-8 2009 Bcl-x(L)-deficient mice were more resistant than wild-type controls to skin tumor development with delayed onset and reduced number of tumors using either UVB or the DMBA/TPA two-stage regimen. 9,10-Dimethyl-1,2-benzanthracene 166-170 BCL2-like 1 Mus musculus 0-8 19309000-8 2009 Bcl-x(L)-deficient mice were more resistant than wild-type controls to skin tumor development with delayed onset and reduced number of tumors using either UVB or the DMBA/TPA two-stage regimen. Tetradecanoylphorbol Acetate 171-174 BCL2-like 1 Mus musculus 0-8 19608979-8 2009 During the late preconditioning period, H(2)S increased the expression of antioxidants (heme oxygenase-1 and thioredoxin 1), increased the expression of heat shock protein 90, heat shock protein 70, Bcl-2, Bcl-xL, and cyclooxygenase-2 and also inactivated the proapoptogen Bad. Hydrogen Sulfide 40-45 BCL2-like 1 Mus musculus 206-212 19309000-5 2009 A significant increase in apoptosis induced by either UVB irradiation or 7,12-dimethylbenz[a]anthracene (DMBA) treatment was observed in the epidermis of Bcl-x(L)-deficient mice. anthracene 93-103 BCL2-like 1 Mus musculus 154-162 19309000-5 2009 A significant increase in apoptosis induced by either UVB irradiation or 7,12-dimethylbenz[a]anthracene (DMBA) treatment was observed in the epidermis of Bcl-x(L)-deficient mice. 9,10-Dimethyl-1,2-benzanthracene 105-109 BCL2-like 1 Mus musculus 154-162 19398586-3 2009 Mutation of the proximal tyrosine motif interrupted PI3-kinase binding and prevented CD28-dependent phosphorylation of protein kinase B (PKB)/Akt; however, there was no detectable effect on interleukin-2 (IL-2) secretion, expression of Bcl-X(L), or on T-cell function in vivo. Tyrosine 25-33 BCL2-like 1 Mus musculus 236-244 19584264-5 2009 In addition, depletion of Bcl-xl rescued the apoptotic response to Taxol. Paclitaxel 67-72 BCL2-like 1 Mus musculus 26-32 19023096-7 2009 RESULTS: Leptin treatment activated the nuclear translocation of nuclear transcription factors kappaB dimers containing the c-Rel subunit, induced the expression of the antiapoptotic c-Rel target gene Bcl-xL in both control and oxygen-glucose deprivation conditions, and counteracted the oxygen-glucose deprivation-mediated apoptotic death of cultured cortical neurons. oxygen-glucose 228-242 BCL2-like 1 Mus musculus 201-207 18807035-3 2009 ABT-737, a small molecule inhibitor of the antiapoptotic proteins Bcl-2, Bcl-w and Bcl-x(L), was tested for the ability to increase antitumor immune responses in two tumor immunotherapy animal models. ABT-737 0-7 BCL2-like 1 Mus musculus 83-91 19368804-6 2009 Further examination of the B16F10 cells showed that curcumin effectively suppresses Cyclin D1, P-NF-kB, BclXL, P-Akt, and VEGF, which explains its efficacy in blocking proliferation, survival, and invasion of the B16F10 cells in the brain. Curcumin 52-60 BCL2-like 1 Mus musculus 104-109 19063961-13 2009 NF-kappaB activation products such as Bcl-2, Bcl-X(L), cFLIP(S), cFLIP(L), and Mn-SOD were reduced by TNFalpha plus PY and restored by 1400W or NAC. N-((3-(aminomethyl)phenyl)methyl)ethanimidamide 135-140 BCL2-like 1 Mus musculus 45-53 18349030-7 2008 RESULTS: As(2)O(3)-induced apoptosis was paralleled by a reduction of the DNA-binding activities of transcription factors of the NFkB and signal transducer and activator of transcription gene families and reduced expression of the antiapoptotic proteins bcl-1, bcl-xL and mcl-1. (2)o(3) 11-18 BCL2-like 1 Mus musculus 261-267 18755736-8 2008 In wild-type testes, MEHP-induced Akt1-dependent transcription of the antiapoptotic mitochondrial target gene, Bcl-xL. mono-(2-ethylhexyl)phthalate 21-25 BCL2-like 1 Mus musculus 111-117 19004807-4 2008 ABT-737 selectively targets certain prosurvival proteins (Bcl-2, Bcl-x(L), and Bcl-w) but not others (Mcl-1 and A1). 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 0-3 BCL2-like 1 Mus musculus 65-70 18841882-2 2008 We recently described the discovery of 1 (ABT-737), which binds Bcl-2, Bcl-X L, and Bcl-w with high affinity, shows robust antitumor activity in murine tumor xenograft models, but is not orally bioavailable. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 42-45 BCL2-like 1 Mus musculus 71-78 18649067-8 2008 VPA also increased levels of anti-apoptotic factors, Bcl-2 and Bcl-x(L), in spinal neurons. Valproic Acid 0-3 BCL2-like 1 Mus musculus 63-71 18591385-3 2008 ABT-737 is a BH3-only mimetic and potent inhibitor of the antiapoptotic Bcl-2 family members Bcl-2, Bcl-X(L), and Bcl-w. ABT-737 0-7 BCL2-like 1 Mus musculus 100-108 18802088-7 2008 Additionally, the ADAP proline-rich domain is required for optimal Ag-induced activation of CD69, CD25, and Bcl-x(L), but is not required for assembly of the CARMA1/Bcl10/Malt1 (caspase-recruitment domain (CARD) membrane-associated guanylate kinase (MAGUK) protein 1/B-cell CLL-lymphoma 10/mucosa-associated lymphoid tissue lymphoma translocation protein 1) signaling complex and subsequent TCR-dependent NF-kappaB activity. Proline 23-30 BCL2-like 1 Mus musculus 108-113 18543336-4 2008 Histological studies show an attenuation of motor neuron loss and a decrease in the number of cleaved caspase 9-, cleaved caspase 3-, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells in the lumbar cords of TAT-modified Bcl-X(L)-treated G93A mice. deoxyuridine triphosphate 185-189 BCL2-like 1 Mus musculus 267-275 18586292-0 2008 Involvement of Bcl-xL degradation and mitochondrial-mediated apoptotic pathway in pyrrolizidine alkaloids-induced apoptosis in hepatocytes. Pyrrolizidine Alkaloids 82-105 BCL2-like 1 Mus musculus 15-21 18586292-4 2008 Western-blot results showed that clivorine induced caspase-3/-9 activation, mitochondrial release of cytochrome c and decreased anti-apoptotic Bcl-xL in a time (8-48 h)- and concentration (1-100 microM)-dependent manner. clivorine 33-42 BCL2-like 1 Mus musculus 143-149 18586292-6 2008 Polyubiquitination of Bcl-xL was detected after incubation with 100 microM clivorine for 40 h in the presence of proteasome specific inhibitor MG132, indicating possible degradation of Bcl-xL protein. clivorine 75-84 BCL2-like 1 Mus musculus 22-28 18586292-6 2008 Polyubiquitination of Bcl-xL was detected after incubation with 100 microM clivorine for 40 h in the presence of proteasome specific inhibitor MG132, indicating possible degradation of Bcl-xL protein. clivorine 75-84 BCL2-like 1 Mus musculus 185-191 18586292-6 2008 Polyubiquitination of Bcl-xL was detected after incubation with 100 microM clivorine for 40 h in the presence of proteasome specific inhibitor MG132, indicating possible degradation of Bcl-xL protein. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 143-148 BCL2-like 1 Mus musculus 22-28 18586292-6 2008 Polyubiquitination of Bcl-xL was detected after incubation with 100 microM clivorine for 40 h in the presence of proteasome specific inhibitor MG132, indicating possible degradation of Bcl-xL protein. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 143-148 BCL2-like 1 Mus musculus 185-191 18586292-7 2008 Furthermore, pretreatment with MG132 or calpain inhibitor I for 2 h significantly enhanced clivorine-decreased Bcl-xL level and cell viability. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 31-36 BCL2-like 1 Mus musculus 111-117 18586292-7 2008 Furthermore, pretreatment with MG132 or calpain inhibitor I for 2 h significantly enhanced clivorine-decreased Bcl-xL level and cell viability. clivorine 91-100 BCL2-like 1 Mus musculus 111-117 18586292-9 2008 Clivorine (10 microM) induced caspase-3 activation and decreased Bcl-xL was also confirmed in mouse hepatocytes. clivorine 0-9 BCL2-like 1 Mus musculus 65-71 18586292-10 2008 Meanwhile, another PA senecionine isolated from Senecio vulgaris L also induced apoptosis, caspase-3 activation and decreased Bcl-xL in mouse hepatocytes. Pyrrolizidine Alkaloids 19-21 BCL2-like 1 Mus musculus 126-132 18586292-10 2008 Meanwhile, another PA senecionine isolated from Senecio vulgaris L also induced apoptosis, caspase-3 activation and decreased Bcl-xL in mouse hepatocytes. senecionine 22-33 BCL2-like 1 Mus musculus 126-132 18586292-11 2008 In conclusion, our results suggest that PAs may share the same hepatotoxic signal pathway, which involves degradation of Bcl-xL protein and thus leading to the activation of mitochondrial-mediated apoptotic pathway. Pyrrolizidine Alkaloids 40-43 BCL2-like 1 Mus musculus 121-127 18673421-17 2009 After treatment with melatonin, the levels of Bcl-XL and procaspase-3 increased when compared with LPS + SD. Melatonin 21-30 BCL2-like 1 Mus musculus 46-52 19011510-6 2008 Here we demonstrate that in murine melanocytes activation of STAT5 measured by its tyrosine phosphorylation and translocation to the nucleus parallels upregulation with its target gene bcl-XL. Tyrosine 83-91 BCL2-like 1 Mus musculus 185-191 18786174-5 2008 In the present study, we investigated the potential of cystamine (CYS), an anti-oxidant and anti-apoptotic compound, to prevent HAL-induced reduction in BDNF, GSH, and Bcl-xl protein levels in mice and the signaling mechanism(s) involved in the beneficial effects of CYS. Cystamine 55-64 BCL2-like 1 Mus musculus 168-174 18786174-5 2008 In the present study, we investigated the potential of cystamine (CYS), an anti-oxidant and anti-apoptotic compound, to prevent HAL-induced reduction in BDNF, GSH, and Bcl-xl protein levels in mice and the signaling mechanism(s) involved in the beneficial effects of CYS. Cystamine 66-69 BCL2-like 1 Mus musculus 168-174 18786174-5 2008 In the present study, we investigated the potential of cystamine (CYS), an anti-oxidant and anti-apoptotic compound, to prevent HAL-induced reduction in BDNF, GSH, and Bcl-xl protein levels in mice and the signaling mechanism(s) involved in the beneficial effects of CYS. Haloperidol 128-131 BCL2-like 1 Mus musculus 168-174 18786174-7 2008 CYS co-treatment prevented chronic HAL treatment-induced reduction in BDNF, GSH, and Bcl-xl protein levels. Cystamine 0-3 BCL2-like 1 Mus musculus 85-91 18786174-7 2008 CYS co-treatment prevented chronic HAL treatment-induced reduction in BDNF, GSH, and Bcl-xl protein levels. Haloperidol 35-38 BCL2-like 1 Mus musculus 85-91 18070358-8 2007 Interestingly, L-glutamine supplementation prevented Gadd153 up-regulation in cells ectopically expressing Bcl-xL, but had no effect on cell viability. Glutamine 15-26 BCL2-like 1 Mus musculus 107-113 18381954-8 2008 Moreover, curcumin suppressed NF-kappaB activity and the expression of NF-kappaB-regulated gene products (cyclin D1, c-myc, Bcl-2, Bcl-xL, cellular inhibitor of apoptosis protein-1, cyclooxygenase-2, matrix metalloproteinase-9, and vascular endothelial growth factor), many of which were induced by radiation therapy and mediate radioresistance. Curcumin 10-18 BCL2-like 1 Mus musculus 131-137 18230621-2 2008 Chelerythrine has recently been identified as a Bcl-xL inhibitor that is capable of triggering apoptosis via direct action on mitochondria. chelerythrine 0-13 BCL2-like 1 Mus musculus 48-54 18006096-11 2008 CONCLUSIONS: The radiosensitization effect of DCQ occurs through enhancement of radiation-induced apoptosis, which correlates to the inhibition of p-Akt kinase and Bcl-X(L) and the activation of Erk and Jnk kinases, but appears independent of p53 induction or modulation of Bax/Bcl-2 gene expression. 2-benzoyl-3-phenyl-6,7-dichloroquinoxaline-1,4-dioxide 46-49 BCL2-like 1 Mus musculus 164-172 17995935-0 2008 Membrane-permeable Bcl-xL prevents MPTP-induced dopaminergic neuronal loss in the substantia nigra. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 35-39 BCL2-like 1 Mus musculus 19-25 17995935-4 2008 Cell-permeable Bcl-xL protected neuroblastoma cells from the selective neurotoxin 1-methyl-4-phenylpyridinium. 1-Methyl-4-phenylpyridinium 82-109 BCL2-like 1 Mus musculus 15-21 18226269-5 2008 In xenogrfated tumors, curcumin upregulated the expression of TRAIL-R1/DR4, TRAIL-R2/DR5, Bax, Bak, p21/WAF1, and p27/KIP1, and inhibited the activation of NFkappaB and its gene products such as cyclin D1, VEGF, uPA, MMP-2, MMP-9, Bcl-2 and Bcl-XL. Curcumin 23-31 BCL2-like 1 Mus musculus 241-247 18472640-7 2008 Further, CDDO-Me inhibited NF-kappaB-regulated antiapoptotic Bcl-2, Bcl-xL, and XIAP and proangiogenic VEGF. bardoxolone methyl 9-16 BCL2-like 1 Mus musculus 68-74 17998390-2 2007 We asked if AID is required for accelerated tumor development in pristane-treated Bcl-xL transgenic BALB/c mice deficient in AID (pBxAicda-/-). pristane 65-73 BCL2-like 1 Mus musculus 82-88 18180697-0 2008 Edaravone prevents Fas-induced fulminant hepatic failure in mice by regulating mitochondrial Bcl-xL and Bax. Edaravone 0-9 BCL2-like 1 Mus musculus 93-99 18180697-0 2008 Edaravone prevents Fas-induced fulminant hepatic failure in mice by regulating mitochondrial Bcl-xL and Bax. ammonium ferrous sulfate 19-22 BCL2-like 1 Mus musculus 93-99 18180697-13 2008 Western blotting showed that the Bcl-xL-Bax ratio of the edaravone group was much higher than that of the control group. Edaravone 57-66 BCL2-like 1 Mus musculus 33-39 18180697-14 2008 In conclusion, edaravone might protect hepatocytes from Fas-induced mitochondria-dependent apoptosis by regulating mitochondrial Bcl-xL and Bax. Edaravone 15-24 BCL2-like 1 Mus musculus 129-135 18180697-14 2008 In conclusion, edaravone might protect hepatocytes from Fas-induced mitochondria-dependent apoptosis by regulating mitochondrial Bcl-xL and Bax. ammonium ferrous sulfate 56-59 BCL2-like 1 Mus musculus 129-135 18360826-0 2008 Bcl-xL antisense oligonucleotide and cisplatin combination therapy extends survival in SCID mice with established mesothelioma xenografts. Oligonucleotides 17-32 BCL2-like 1 Mus musculus 0-6 18360826-3 2008 Moreover, upon introduction of antisense oligonucleotides specific to Bcl-xL mRNA, MPM cells are sensitized to chemotherapeutic agents. Oligonucleotides 41-57 BCL2-like 1 Mus musculus 70-76 18360826-4 2008 Here we describe the therapeutic effects of a novel combination therapy, Bcl-xL antisense oligonucleotide (ASO 15999) and cisplatin, on mesothelioma cell lines in vitro and in vivo; in addition, efficacy of ASO 15999 in decreasing tumor load as well as its effect on survival in an animal model. Oligonucleotides 90-105 BCL2-like 1 Mus musculus 73-79 18645028-5 2008 (-)-Gossypol blocked the interactions of Bcl-xL with Bax or Bad in cancer cells by fluorescence resonance energy transfer assay and overcame the Bcl-xL protection of FL5.12 model cells on interleukin-3 withdrawal. Gossypol 0-12 BCL2-like 1 Mus musculus 41-47 18645028-5 2008 (-)-Gossypol blocked the interactions of Bcl-xL with Bax or Bad in cancer cells by fluorescence resonance energy transfer assay and overcame the Bcl-xL protection of FL5.12 model cells on interleukin-3 withdrawal. Gossypol 0-12 BCL2-like 1 Mus musculus 145-151 18292288-3 2008 AT-101 is a BH3 mimetic known to be a potent inhibitor of antiapoptotic Bcl-2 family members including Bcl-2, Bcl-X(L), and Mcl-1. gossypol acetic acid 0-6 BCL2-like 1 Mus musculus 110-118 18292288-3 2008 AT-101 is a BH3 mimetic known to be a potent inhibitor of antiapoptotic Bcl-2 family members including Bcl-2, Bcl-X(L), and Mcl-1. BH 3 12-15 BCL2-like 1 Mus musculus 110-118 18483296-5 2008 Using the Emu-myc mouse model of B-cell lymphoma, we showed previously that overexpression of the prosurvival proteins Bcl-2 and Bcl-XL inhibited the apoptotic and therapeutic activities of the vorinostat. Vorinostat 194-204 BCL2-like 1 Mus musculus 129-135 18299995-6 2008 Treatments with the antioxidant N-acetyl-cysteine (NAC) were needed to promote survival in cell recovering from mild proteasome inhibition while overexpression of the antiapoptotic protein Bcl-xL together with NAC attenuated cell death during recovery from potent inhibition. Acetylcysteine 32-49 BCL2-like 1 Mus musculus 189-195 18281560-8 2008 Honokiol-induced apoptosis correlated with induction of Bax, Bak, and Bad and a decrease in Bcl-xL and Mcl-1 protein levels. honokiol 0-8 BCL2-like 1 Mus musculus 92-98 18281560-9 2008 Transient transfection of PC-3 cells with Bak- and Bax-targeted siRNAs and Bcl-xL plasmid conferred partial yet significant protection against honokiol-induced apoptosis. honokiol 143-151 BCL2-like 1 Mus musculus 75-81 17975011-10 2008 Furthermore, signal transducer and activator of transcription factor (STAT) 3 and associated Bcl-xL induction was observed in ethanol-fed wild-type mice but not in ethanol-fed hepatocyte RXRalpha-deficient mice. Ethanol 126-133 BCL2-like 1 Mus musculus 93-99 17728251-9 2007 Bcl-XL-specific siRNA significantly inhibits lactogen-mediated protection against DEX-induced beta cell death. Dexamethasone 82-85 BCL2-like 1 Mus musculus 0-6 17541981-5 2007 Treatment of wild-type A20 cells with phosphatidic acid (PA), the metabolic end product of PLD2 derived from phosphatidylcholin, markedly increased levels of anti-apoptotic Bcl-2 and Bcl-xL proteins. Phosphatidic Acids 38-55 BCL2-like 1 Mus musculus 183-189 17850585-4 2007 Fas-mediated death of mitogen-activated T cells was caspase dependent and could be blocked by FLIP(L) overexpression only with the minor involvement of Bcl-x(L) or RIPDeltakin inhibitable pathways. ammonium ferrous sulfate 0-3 BCL2-like 1 Mus musculus 152-160 17541981-5 2007 Treatment of wild-type A20 cells with phosphatidic acid (PA), the metabolic end product of PLD2 derived from phosphatidylcholin, markedly increased levels of anti-apoptotic Bcl-2 and Bcl-xL proteins. Phosphatidic Acids 57-59 BCL2-like 1 Mus musculus 183-189 17541981-6 2007 Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels. Phosphatidic Acids 10-12 BCL2-like 1 Mus musculus 46-52 17541981-6 2007 Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels. Phosphatidic Acids 10-12 BCL2-like 1 Mus musculus 298-304 17541981-6 2007 Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels. Propranolol 70-81 BCL2-like 1 Mus musculus 46-52 17541981-6 2007 Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels. Propranolol 70-81 BCL2-like 1 Mus musculus 298-304 17541981-6 2007 Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels. Quinacrine 156-165 BCL2-like 1 Mus musculus 298-304 17541981-6 2007 Moreover, PA-induced expressions of Bcl-2 and Bcl-xL were enhanced by propranolol, an inhibitor of PA phospholydrolase (PAP), whereas completely blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), suggesting that PLA(2) metabolite of PA is responsible for the increases in Bcl-2 and Bcl-xL protein levels. Phosphatidic Acids 99-101 BCL2-like 1 Mus musculus 46-52 17541981-7 2007 We further confirmed the involvement of arachidonic acid (AA) in PA-induced survival signals by showing that 1,2-dipalmitoyl-sn-glycero-3-phosphate (DPPA), PA without AA, was unable to increase Bcl-2 and Bcl-xL proteins. Phosphatidic Acids 65-67 BCL2-like 1 Mus musculus 204-210 17541981-8 2007 Moreover, PA notably increased cyclooxygenase (COX)-2 protein expression, and PA-induced expression of both Bcl-2 and Bcl-xL was inhibited by NS-398, a specific inhibitor of COX-2. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 142-148 BCL2-like 1 Mus musculus 118-124 17541981-9 2007 Taken together, these findings demonstrate that PA generated by PLD2 plays an important role in cell survival during Fas-mediated apoptosis through the increased Bcl-2 and Bcl-xL protein levels which resulted from PLA(2) and AA-COX2 pathway. Phosphatidic Acids 48-50 BCL2-like 1 Mus musculus 172-178 17415663-5 2007 However, depletions in glutathione and Bcl-xL with potent proteasome inhibition exacerbated this response whereupon survival required the cooperative protection of NAC with Bcl-xL overexpression. Glutathione 23-34 BCL2-like 1 Mus musculus 173-179 17415663-5 2007 However, depletions in glutathione and Bcl-xL with potent proteasome inhibition exacerbated this response whereupon survival required the cooperative protection of NAC with Bcl-xL overexpression. Acetylcysteine 164-167 BCL2-like 1 Mus musculus 39-45 17697574-0 2007 Adeno-associated virus-mediated Bcl-xL prevents aminoglycoside-induced hearing loss in mice. Aminoglycosides 48-62 BCL2-like 1 Mus musculus 32-38 17697574-3 2007 The aim of this study was to determine the potential cochlear protective effect of Bcl-x(L) as a therapeutic agent in the murine model of aminoglycoside ototoxicity. Aminoglycosides 138-152 BCL2-like 1 Mus musculus 83-91 17448893-8 2007 The mitochondria from the ethanol-fed Sod1-/- mice had elevated levels of cleaved Bax, Bak, Bcl-xl, and adenine nucleotide translocator. Ethanol 26-33 BCL2-like 1 Mus musculus 92-98 17384938-1 2007 OBJECTIVES: This study analyzes the effects of prolonged administration of methadone and withdrawal on sensorimotor and cognitive performance in mice and explores the associated changes in brain expression of proteins regulating the extrinsic (FasL, Fas, and caspase-8) and the mitochondrial (Bcl-2, Bcl-x(L), Bad, and Bax) apoptotic pathways. Methadone 75-84 BCL2-like 1 Mus musculus 300-308 17055152-1 2007 L1210 murine leukemia cells exposed to an LD(90) concentration of the Bcl-2/Bcl-x(L) antagonist HA14-1 rapidly undergo apoptosis but also develop numerous intracellular vacuoles with double membranes, exhibit enhanced labeling by monodansylcadaverine, and convert the cytosolic protein LC3-I to LC3-II. monodansylcadaverine 230-250 BCL2-like 1 Mus musculus 76-84 17307150-2 2007 Here it is demonstrated that the BH4 peptide domain of the anti-apoptotic protein Bcl-xL can be delivered to cells by covalent attachment to the TAT peptide transduction domain (TAT-BH4) and provide protection in vitro and in vivo from radiation-induced apoptotic cell death. sapropterin 33-36 BCL2-like 1 Mus musculus 82-88 17136322-7 2007 The anti-apoptotic proteins Bcl-2 and Bcl-x(L) have the ability to block the MPT, and can therefore block MPT-dependent necrosis in addition to their well-established ability to inhibit apoptosis. mpt 77-80 BCL2-like 1 Mus musculus 38-46 17307150-2 2007 Here it is demonstrated that the BH4 peptide domain of the anti-apoptotic protein Bcl-xL can be delivered to cells by covalent attachment to the TAT peptide transduction domain (TAT-BH4) and provide protection in vitro and in vivo from radiation-induced apoptotic cell death. sapropterin 182-185 BCL2-like 1 Mus musculus 82-88 17404107-6 2007 Hence, TW-37 is a potent inhibitor of Bcl-2 and has >3-fold selectivity over Bcl-X(L). TW-37 7-12 BCL2-like 1 Mus musculus 80-88 16909118-7 2007 The U0126-mediated inhibition of ERK1/2 activation impaired proliferation and viability of the ALK+ TCL cells and expression of antiapoptotic factor Bcl-xL and cell cycle-promoting CDK4 and phospho-RB. U 0126 4-9 BCL2-like 1 Mus musculus 149-155 17439357-11 2007 The induction of antioxidant HO-1 and anti-apoptotic Bcl-2/Bcl-x(L) by vIL-10 exerts synergistic cytoprotective function against antigen-independent hepatic inflammatory response triggered by IRI. vil-10 71-77 BCL2-like 1 Mus musculus 59-67 17287506-9 2007 Altogether, these results suggest that high levels of serotonin, acting through 5-HT2 receptors, have neuroprotective action on cortical neurons by controlling Bcl-X(L) mRNA levels and that this action is independent of trkB signaling. Serotonin 54-63 BCL2-like 1 Mus musculus 160-168 17366662-7 2007 Instead, leflunomide inhibited APAP-induced activation (phosphorylation) of c-jun NH2-terminal protein kinase (JNK), thus preventing downstream Bcl-2 and Bcl-XL inactivation and protecting from mitochondrial permeabilization and cytochrome c release. Leflunomide 9-20 BCL2-like 1 Mus musculus 154-160 17366662-7 2007 Instead, leflunomide inhibited APAP-induced activation (phosphorylation) of c-jun NH2-terminal protein kinase (JNK), thus preventing downstream Bcl-2 and Bcl-XL inactivation and protecting from mitochondrial permeabilization and cytochrome c release. Acetaminophen 31-35 BCL2-like 1 Mus musculus 154-160 17508927-0 2007 Small molecule inhibition of the Bcl-X(L)-BH3 protein-protein interaction: proof-of-concept of an in vivo chemopotentiator ABT-737. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 123-126 BCL2-like 1 Mus musculus 33-45 17135272-9 2007 Carbon monoxide inhibited the activation of Bid and the expression and mitochondrial translocation of Bax, whereas promoted Bcl-X(L)/Bax interaction and increased Bad phosphorylation. Carbon Monoxide 0-15 BCL2-like 1 Mus musculus 124-132 17508927-2 2007 Bcl-2 and its closely related Bcl-X(L) counterpart are one of several pro-survival proteins which can share up to four highly conserved domains known as the BH1, BH2, BH3 and BH4 domains. bh1 157-160 BCL2-like 1 Mus musculus 30-38 17240030-5 2007 1,3-DNP caused pro-apoptotic events, including increased phosphorylation and accumulation of p53 in the nucleus, cleavage of bid and of caspases 8 and 3, down-regulation of bcl-x(L) and phosphorylation of p38 and JNK MAPK. 1,3-dinitropyrene 0-7 BCL2-like 1 Mus musculus 173-181 17254689-0 2007 EPO receptor, Bax and Bcl-x(L) expressions in murine erythropoiesis after cyclophosphamide treatment. Cyclophosphamide 74-90 BCL2-like 1 Mus musculus 22-30 17508927-2 2007 Bcl-2 and its closely related Bcl-X(L) counterpart are one of several pro-survival proteins which can share up to four highly conserved domains known as the BH1, BH2, BH3 and BH4 domains. bh2 162-165 BCL2-like 1 Mus musculus 30-38 17508927-2 2007 Bcl-2 and its closely related Bcl-X(L) counterpart are one of several pro-survival proteins which can share up to four highly conserved domains known as the BH1, BH2, BH3 and BH4 domains. BH 3 167-170 BCL2-like 1 Mus musculus 30-38 17508927-2 2007 Bcl-2 and its closely related Bcl-X(L) counterpart are one of several pro-survival proteins which can share up to four highly conserved domains known as the BH1, BH2, BH3 and BH4 domains. sapropterin 175-178 BCL2-like 1 Mus musculus 30-38 17237296-6 2007 Cultures treated with XK469 or SH80 readily underwent apoptosis upon exposure to the Bcl-2/Bcl-x(L) antagonist ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate. ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate 111-190 BCL2-like 1 Mus musculus 91-99 17177603-7 2007 Our results define a signalling pathway leading from DNA damage to up-regulation of the NHE-1 antiport, to intracellular alkalanisation to Bcl-xL deamidation, to apoptosis, representing the first example, to our knowledge, of how deamidation of internal asparagine residues can be regulated in a protein in vivo. Asparagine 254-264 BCL2-like 1 Mus musculus 139-145 17182546-8 2007 Moreover, we show that overexpression of Akt, a target of Syk, or Bcl-x(L), a target of Akt can overcome curcumin-induced apoptosis of B lymphoma cells. Curcumin 105-113 BCL2-like 1 Mus musculus 66-74 17046822-0 2006 CpG-B oligodeoxynucleotide promotes cell survival via up-regulation of Hsp70 to increase Bcl-xL and to decrease apoptosis-inducing factor translocation. Oligodeoxyribonucleotides 6-26 BCL2-like 1 Mus musculus 89-95 17202839-4 2006 We also demonstrated that truncated Bad to Bcl-xL interaction in genistein- treated cells was prevented by BocD-fmk but not by zVAD-fmk treatment. Genistein 65-74 BCL2-like 1 Mus musculus 43-49 17202839-4 2006 We also demonstrated that truncated Bad to Bcl-xL interaction in genistein- treated cells was prevented by BocD-fmk but not by zVAD-fmk treatment. bocd-fmk 107-115 BCL2-like 1 Mus musculus 43-49 17202839-4 2006 We also demonstrated that truncated Bad to Bcl-xL interaction in genistein- treated cells was prevented by BocD-fmk but not by zVAD-fmk treatment. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 127-135 BCL2-like 1 Mus musculus 43-49 17046822-6 2006 Additional experiments demonstrated that quercetin and anti-sense hsp70 modulated CpG-B ODN-induced anti-apoptosis via a caspase-3-independent pathway by down-regulating the survival gene bcl-x(L) and by increasing translocation of apoptosis-inducing factor. Quercetin 41-50 BCL2-like 1 Mus musculus 188-196 16716514-3 2006 The purpose of the present study was to analyse the effects of naltrexone on the expression levels of proteins regulating the extrinsic (FasL and Fas) and the mitochondrial (Bcl-2, Bcl-xL, Bad and Bax) apoptotic pathways, as well as the active fragment of the executioner caspase-3 in the mouse brain. Naltrexone 63-73 BCL2-like 1 Mus musculus 181-187 16862141-3 2006 To determine the impact of this p53 activity on normal tissue radiosensitivity, we isolated a small molecule named pifithrin-mu (PFTmu, 1) that inhibits p53 binding to mitochondria by reducing its affinity to antiapoptotic proteins Bcl-xL and Bcl-2 but has no effect on p53-dependent transactivation. 2-phenylacetylenesulfonamide 129-134 BCL2-like 1 Mus musculus 232-238 16904964-0 2006 Bcl-XL antisense oligonucleotides coupled with antennapedia enhances radiation-induced apoptosis in pancreatic cancer. Oligonucleotides 17-33 BCL2-like 1 Mus musculus 0-6 16904964-3 2006 The aim of this study was to examine the effects of the Bcl-XL antisense oligonucleotide for radiosensitivity of in vitro and in vivo pancreatic cancer using oligonucleotide conjugated with antennapedia. Oligonucleotides 73-88 BCL2-like 1 Mus musculus 56-62 16904964-3 2006 The aim of this study was to examine the effects of the Bcl-XL antisense oligonucleotide for radiosensitivity of in vitro and in vivo pancreatic cancer using oligonucleotide conjugated with antennapedia. Oligonucleotides 158-173 BCL2-like 1 Mus musculus 56-62 16904964-21 2006 CONCLUSIONS: The results suggest that, when coupled with antennapedia, the antisense oligonucleotide against Bcl-XL could be a good therapeutic tool for radiosensitization of pancreatic cancer. Oligonucleotides 85-100 BCL2-like 1 Mus musculus 109-115 16678846-8 2006 DFMO inhibits several of the molecular events of apoptosis that follow simulated ischemia, such as the release of cytochrome c from mitochondria, caspase activation, downregulation of Bcl-xL, and DNA fragmentation. Eflornithine 0-4 BCL2-like 1 Mus musculus 184-190 16254573-6 2006 Dox stimulation of BCL-xL-inducible LNT-229 cells conferred infiltrative growth to BCL-xL-positive glioma cells in vivo and reduced the survival of tumor-bearing mice. Doxycycline 0-3 BCL2-like 1 Mus musculus 19-25 16254573-6 2006 Dox stimulation of BCL-xL-inducible LNT-229 cells conferred infiltrative growth to BCL-xL-positive glioma cells in vivo and reduced the survival of tumor-bearing mice. Doxycycline 0-3 BCL2-like 1 Mus musculus 83-89 16617327-6 2006 Furthermore, we show that p38 inhibition enhances the bortezomib-induced MM apoptosis by upregulation of p53 and downregulation of Bcl-X(L) and Mcl-1. Bortezomib 54-64 BCL2-like 1 Mus musculus 131-139 16225850-0 2005 Cisplatin and TNF-alpha downregulate transcription of Bcl-xL in murine malignant mesothelioma cells. Cisplatin 0-9 BCL2-like 1 Mus musculus 54-60 16585548-3 2006 In this study, we report that oral nickel administration increased the nickel content of splenic Ni(high) B cells and up-regulated their Fas expression while down-regulating expression of bcl-2 and Bcl-xL, thus giving rise to an Ag-carrying, apoptosis-prone B cell phenotype. Nickel 35-41 BCL2-like 1 Mus musculus 198-204 16509771-5 2006 We also show evidence suggesting that IAN4 and IAN5 are associated with anti-apoptotic proteins Bcl-2 and Bcl-xL, whereas IAN1 is associated with pro-apoptotic Bax. ian5 47-51 BCL2-like 1 Mus musculus 106-112 16225850-6 2005 In the AC29 and AB1 models, both cisplatin and TNF-alpha downregulated Bcl-xL gene expression, indicating that this gene was a common transcriptional target in these cells. Cisplatin 33-42 BCL2-like 1 Mus musculus 71-77 16018998-4 2005 In adriamycin-treated BALB/3T3 cells, the down-shift in temperature from 37 degrees C to 32 degrees C increased the Bcl-xL protein level and decreased the mRNA level of Puma and mitochondrial translocation of Bax, suppressing caspase-9-mediated apoptosis. Doxorubicin 3-13 BCL2-like 1 Mus musculus 116-122 16142752-0 2005 Tumor necrosis factor prevents alendronate-induced osteoclast apoptosis in vivo by stimulating Bcl-xL expression through Ets-2. Alendronate 31-42 BCL2-like 1 Mus musculus 95-101 16142752-5 2005 The effect of overexpression of Bcl-xL and Ets-2 proteins on ALN-induced osteoclast apoptosis was determined using an in vitro osteoclast survival assay and retrovirus transfer approach. Alendronate 61-64 BCL2-like 1 Mus musculus 32-38 16142752-8 2005 Bcl-xL or Ets-2 overexpression protected osteoclasts from ALN-induced apoptosis, and TNF stimulated Bcl-xL and Ets-2 expression in osteoclasts. Alendronate 58-61 BCL2-like 1 Mus musculus 0-6 16142752-9 2005 Overexpression of Ets-2 increased Bcl-xL messenger RNA in osteoclasts, while a dominant-negative form of the Ets-2 blocked the protective effect of Bcl-xL or TNF on ALN-induced apoptosis. Alendronate 165-168 BCL2-like 1 Mus musculus 148-154 15899920-1 2005 The long form of B-cell lymphoma-x (Bcl-x(L)), an outer mitochondrial membrane protein, has been proposed to mediate the antiapoptotic action of erythropoietin on erythroid progenitor cells and to be necessary for heme synthesis in erythroblasts. Heme 214-218 BCL2-like 1 Mus musculus 36-44 15899920-7 2005 The bcl-x(-/-) erythroblasts synthesized heme, but at reduced rates compared to bled littermate erythroblasts. Heme 41-45 BCL2-like 1 Mus musculus 4-9 15987750-10 2005 Dexamethasone also lowered the increase in the proapoptotic Bax, which was increased by PA, and increased expression of the antiapoptotic Bcl-xL protein. Dexamethasone 0-13 BCL2-like 1 Mus musculus 138-144 15987750-11 2005 Moreover, the decrease in p53 by dexamethasone was associated with increased Bcl-xL levels. Dexamethasone 33-46 BCL2-like 1 Mus musculus 77-83 15987750-15 2005 The protective effects of dexamethasone on PA-induced apoptosis were associated with decreasing p53, increasing Bcl-xL, and inhibition of AIF translocation. Dexamethasone 26-39 BCL2-like 1 Mus musculus 112-118 15987750-15 2005 The protective effects of dexamethasone on PA-induced apoptosis were associated with decreasing p53, increasing Bcl-xL, and inhibition of AIF translocation. Puromycin Aminonucleoside 43-45 BCL2-like 1 Mus musculus 112-118 15967790-5 2005 Further characterization of GATA-1 phosphorylation site mutants revealed that the antiapoptotic function of GATA-1 is strongly dependent upon its phosphorylation at the Ser-26 position and is probably mediated through its up-regulation of Bcl-X(L) expression. Serine 169-172 BCL2-like 1 Mus musculus 239-247 16098092-10 2005 Co-treatment with melatonin restored phosphorylated Akt levels, increased Bcl-X(L) expression and reduced caspase-3 activity. Melatonin 18-27 BCL2-like 1 Mus musculus 74-82 15861188-1 2005 Bcl-x(S), a proapoptotic member of the Bcl-2 protein family, is localized in the mitochondria and induces apoptosis in a caspase- and BH3-dependent manner by a mechanism involving cytochrome c release. BH 3 134-137 BCL2-like 1 Mus musculus 0-5 16447871-8 2005 The number of CFU-E, BFU-E and CFU-Meg as well as expression of anti-apoptosis protein BcL-XL of BMC in treated group I also were significantly higher than that of anemic control (P <0. S-benzyl-N-malonylcysteine 97-100 BCL2-like 1 Mus musculus 87-93 16447871-10 2005 01), while numbers of CFU-E as well as expression of anti-apoptosis protenin BcL-XL of BMC in treated group II were higher than that of anemic control (P < 0.05). S-benzyl-N-malonylcysteine 87-90 BCL2-like 1 Mus musculus 77-83 16131858-12 2005 Of 12,423 transcripts analyzed for >or= two-fold changes, several related to apoptosis were influenced by CHOP: Gadd45 and cathepsin B were up-regulated in ethanol-fed wild-type mice but not in CHOP null (-/-) mice, whereas Jun D and Bcl-xL were down-regulated in ethanol-fed wild-type mice but not in ethanol-fed CHOP null (-/-) mice. Ethanol 159-166 BCL2-like 1 Mus musculus 237-243 15939587-5 2005 CD4+ T lymphocyte and splenocyte counts were also reduced following 1,25-dihydroxyvitamin D3 treatment and a marked induction of apoptosis, accompanied with down-regulation of the anti-apoptotic proteins Bcl-2 and Bcl-X(L), was observed. Calcitriol 68-92 BCL2-like 1 Mus musculus 214-222 15683736-5 2005 Furthermore, that the MAPK kinase (MEK) 1/2 inhibitor, U0126, blocked proliferation and induced death of B9 cells indicate that IL-6 may not exert its survival effect primarily through bcl-XL and emphasizes the key role of Ras-MAPK cascade elements in the regulation of myeloma growth/viability. U 0126 55-60 BCL2-like 1 Mus musculus 185-191 15824117-8 2005 Even a single injection of paraquat + maneb in the non-transgenic treated group modulated several key pro- and anti-apoptotic proteins, including Bax, Bad, Bcl-xL, and upstream stress-induced cascade. Paraquat 27-35 BCL2-like 1 Mus musculus 156-162 16251044-4 2005 RESULTS: MTT assay showed that the proliferation of esophageal carcinoma cells in the ASODN group decreased significantly as compared with control (P < 0.05), along with a 57.3% inhibitory rate of Bcl-XL mRNA, a significant decrease of Bcl-XL protein and the apoptosis rates of (31.1 +/- 5.8)% and 35.0% by flow cytometry and TUNEL assay, respectively (P < 0.01, as compared with controls). asodn 86-91 BCL2-like 1 Mus musculus 200-206 16251044-4 2005 RESULTS: MTT assay showed that the proliferation of esophageal carcinoma cells in the ASODN group decreased significantly as compared with control (P < 0.05), along with a 57.3% inhibitory rate of Bcl-XL mRNA, a significant decrease of Bcl-XL protein and the apoptosis rates of (31.1 +/- 5.8)% and 35.0% by flow cytometry and TUNEL assay, respectively (P < 0.01, as compared with controls). asodn 86-91 BCL2-like 1 Mus musculus 239-245 16251044-5 2005 The growth of human esophageal carcinoma in nude mice was also significantly inhibited in the ASODN group (P < 0.05), along with a significant decrease of Bcl-XL mRNA and protein expression, and also an enhanced apoptosis of the tumor cells in nude mice. asodn 94-99 BCL2-like 1 Mus musculus 158-164 15792999-6 2005 Further, introgression of a Bcl-x(L) transgene into ROR gamma(0/0) mice, which promotes survival and permits secondary rearrangements of distal V alpha and J alpha gene segments at the DP stage, rescues V alpha 14-to-J alpha 18 recombination. dp 185-187 BCL2-like 1 Mus musculus 28-36 15806010-7 2005 RESULTS: SP600125 at 10 microM drastically inhibited JNK phosphorylation but had little effect on CD40-mediated p38 phosphorylation and expression of the NF-kappaB dependent genes c-Myc and bcl-xL. pyrazolanthrone 9-17 BCL2-like 1 Mus musculus 190-196 15523684-5 2005 DHMEQ inhibition of NF-kappaB triggers activation of caspases 8 and 9, as well as G0/G1 cell cycle arrest accompanied by downregulation of antiapoptotic genes Bcl-XL and c-FLIP and cell cycle progression gene cyclins D1 and D2. dehydroxymethylepoxyquinomicin 0-5 BCL2-like 1 Mus musculus 159-165 15558033-5 2004 This non-apoptotic death of double knockout cells was suppressed by inhibitors of autophagy, including 3-methyl adenine, was dependent on autophagic proteins APG5 and Beclin 1 (capable of binding to Bcl-2/Bcl-x(L)), and was also modulated by Bcl-x(L). 3-methyladenine 103-119 BCL2-like 1 Mus musculus 205-213 15588723-0 2005 BCL-xL overexpression effectively protects against tetrafluoroethylcysteine-induced intramitochondrial damage and cell death. tetrafluoroethylcysteine 51-75 BCL2-like 1 Mus musculus 0-6 15588723-7 2005 Significantly, TAMH cells overexpressing BCL-xL preserved cell viability even to supratoxicological concentrations of TFEC (< or =600 microM), and this cytoprotection was associated with decreased HSP70i upregulation, indicating suppression of TFEC-induced proteotoxicity. S-(1,1,2,2-Tetrafluoroethyl)cysteine 118-122 BCL2-like 1 Mus musculus 41-47 15588723-7 2005 Significantly, TAMH cells overexpressing BCL-xL preserved cell viability even to supratoxicological concentrations of TFEC (< or =600 microM), and this cytoprotection was associated with decreased HSP70i upregulation, indicating suppression of TFEC-induced proteotoxicity. S-(1,1,2,2-Tetrafluoroethyl)cysteine 247-251 BCL2-like 1 Mus musculus 41-47 15588723-8 2005 Hence, TFEC-induced necrotic cell death in the TAMH cell line is mediated by BAX and antagonized by the anti-apoptotic BCL-2 family member, BCL-xL. S-(1,1,2,2-Tetrafluoroethyl)cysteine 7-11 BCL2-like 1 Mus musculus 140-146 15657349-0 2005 Preclinical studies of a nonpeptidic small-molecule inhibitor of Bcl-2 and Bcl-X(L) [(-)-gossypol] against diffuse large cell lymphoma. Gossypol 85-97 BCL2-like 1 Mus musculus 75-83 15657349-3 2005 (-)-Gossypol, a natural product isolated from cottonseeds, was discovered as a potent small-molecule inhibitor of Bcl-2 and Bcl-X(L) proteins, with a Ki value in the nanomole per liter range for both. Gossypol 0-12 BCL2-like 1 Mus musculus 124-132 15558033-5 2004 This non-apoptotic death of double knockout cells was suppressed by inhibitors of autophagy, including 3-methyl adenine, was dependent on autophagic proteins APG5 and Beclin 1 (capable of binding to Bcl-2/Bcl-x(L)), and was also modulated by Bcl-x(L). 3-methyladenine 103-119 BCL2-like 1 Mus musculus 242-250 15492835-5 2004 Whereas TSA treatment increased the expression level of Bad, it decreased the level of Bcl-2, Bcl-xL, and X-linked inhibitor of apoptosis protein. trichostatin A 8-11 BCL2-like 1 Mus musculus 94-100 12842996-11 2003 FLT3 kinase inhibitor, AG1296, alone not only dephosphorylated Bad but also down-regulated Bcl-XL, leading FLT3/ITD-32D cells into apoptosis. 6,7-dimethoxy-3-phenylquinoxaline 23-29 BCL2-like 1 Mus musculus 91-97 15172982-3 2004 DETA-NO-treated DCs became resistant to tumor-induced apoptosis because DETA-NO prevented tumor-induced changes in the expression of Bcl-2, Bax, and Bcl-xL; activation of caspase-9; and a reduction in the mitochondrial membrane potential. DETA-NO 0-7 BCL2-like 1 Mus musculus 149-155 15172982-3 2004 DETA-NO-treated DCs became resistant to tumor-induced apoptosis because DETA-NO prevented tumor-induced changes in the expression of Bcl-2, Bax, and Bcl-xL; activation of caspase-9; and a reduction in the mitochondrial membrane potential. DETA-NO 72-79 BCL2-like 1 Mus musculus 149-155 15161370-3 2004 Using a tetracycline-repressible system, we found that removal of tetracycline for 16 h induced Bcl-X(S) and reduced the surviving fraction of NIH 3T3 cells to 25%. Tetracycline 8-20 BCL2-like 1 Mus musculus 96-101 15161370-3 2004 Using a tetracycline-repressible system, we found that removal of tetracycline for 16 h induced Bcl-X(S) and reduced the surviving fraction of NIH 3T3 cells to 25%. Tetracycline 66-78 BCL2-like 1 Mus musculus 96-101 14701943-5 2004 This is achieved, at least in part, by transcriptional regulation of apoptosis-related genes such as Bcl-X(L) via a calcium- and phosphatidylinositol 3 kinase-dependent pathway. Calcium 116-123 BCL2-like 1 Mus musculus 101-109 15279625-5 2004 In addition, interestingly, pre-treatment with caspase inhibitors, Boc-D-FMK and Z-DEVD-FMK, significantly abolished T. vaginalis-induced down-regulation of Bcl-x(L), suggesting that caspase-3 may play a pivotal role in the process of apoptosis as well as the down-regulation of Bcl-x(L)by T. vaginalis. Boc-D-FMK 67-76 BCL2-like 1 Mus musculus 157-164 15279625-5 2004 In addition, interestingly, pre-treatment with caspase inhibitors, Boc-D-FMK and Z-DEVD-FMK, significantly abolished T. vaginalis-induced down-regulation of Bcl-x(L), suggesting that caspase-3 may play a pivotal role in the process of apoptosis as well as the down-regulation of Bcl-x(L)by T. vaginalis. benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone 81-91 BCL2-like 1 Mus musculus 157-164 15279625-5 2004 In addition, interestingly, pre-treatment with caspase inhibitors, Boc-D-FMK and Z-DEVD-FMK, significantly abolished T. vaginalis-induced down-regulation of Bcl-x(L), suggesting that caspase-3 may play a pivotal role in the process of apoptosis as well as the down-regulation of Bcl-x(L)by T. vaginalis. benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone 81-91 BCL2-like 1 Mus musculus 279-286 14718643-10 2004 Finally, thymocytes from mice exposed perinatally to TCDD showed higher levels of Fas, TRAIL, and DR5 mRNA, but the levels of Bcl-2, Bcl-xL, and Bax were either unaltered or changed moderately. Polychlorinated Dibenzodioxins 53-57 BCL2-like 1 Mus musculus 133-139 14743399-7 2004 Additionally, we found that cycloheximide treatment appeared to downregulate the Bcl-xL mRNA level but not the Bax mRNA level by RNase protection assay. Cycloheximide 28-41 BCL2-like 1 Mus musculus 81-87 14743399-8 2004 Because the upregulation of CD40 mRNA and the downregulation of Bcl-xL correlated with CT26 cell death, our results suggest that chemotherapeutic agents, including cycloheximide, may exert their synergistic effects on the TNF family treatment of cancer cells by regulating the mRNA levels of apoptosis-related genes. Cycloheximide 164-177 BCL2-like 1 Mus musculus 64-70 14749429-0 2004 Enhanced in vitro midbrain dopamine neuron differentiation, dopaminergic function, neurite outgrowth, and 1-methyl-4-phenylpyridium resistance in mouse embryonic stem cells overexpressing Bcl-XL. 1-methyl-4-phenylpyridium 106-131 BCL2-like 1 Mus musculus 188-194 14749429-4 2004 In vitro differentiation of Bcl-XL overexpressing ES (Bcl-ES) cells resulted in higher expression of genes related to midbrain dopamine (DA) neuron development and increased the number of ES-derived neurons expressing midbrain DA markers compared with differentiation of wild-type ES cells. Dopamine 127-135 BCL2-like 1 Mus musculus 28-34 12969969-6 2004 Moreover, overexpression of Bcl-xL protects WEHI-231 B cells from mitochondrial disruption and apoptosis resulting from culture with exogenous arachidonic acid, the product of phospholipase A2 action, suggesting that Bcl-xL may act to antagonize arachidonic acid-mediated disruption of mitochondrial integrity. Arachidonic Acid 143-159 BCL2-like 1 Mus musculus 28-34 12969969-6 2004 Moreover, overexpression of Bcl-xL protects WEHI-231 B cells from mitochondrial disruption and apoptosis resulting from culture with exogenous arachidonic acid, the product of phospholipase A2 action, suggesting that Bcl-xL may act to antagonize arachidonic acid-mediated disruption of mitochondrial integrity. Arachidonic Acid 143-159 BCL2-like 1 Mus musculus 217-223 12969969-6 2004 Moreover, overexpression of Bcl-xL protects WEHI-231 B cells from mitochondrial disruption and apoptosis resulting from culture with exogenous arachidonic acid, the product of phospholipase A2 action, suggesting that Bcl-xL may act to antagonize arachidonic acid-mediated disruption of mitochondrial integrity. Arachidonic Acid 246-262 BCL2-like 1 Mus musculus 28-34 15971583-10 2003 The increased culture longevity by inhibition of NaBu-induced apoptosis by inducible expression of Bcl-XL combined with the enhanced secretion of antibody by NaBu contributed to the enhancement of final antibody concentration in the stably transfected H18 cells culture. sethoxydim 49-53 BCL2-like 1 Mus musculus 99-105 15971583-13 2003 NaBu-induced apoptosis of hybridoma cells could be inhibited by inducible expression of Bcl-XL. sethoxydim 0-4 BCL2-like 1 Mus musculus 88-94 15347599-4 2004 Between docetaxel-treated and non-treated 435/Bcl-x(L).luc mice significant differences in the metastatic burden of lymph nodes (P = 0.02) and viscera (P = 0.02) were observed. Docetaxel 8-17 BCL2-like 1 Mus musculus 46-51 15377864-4 2004 Overexpression of Bcl-x(L) improves mitochondrial respiratory function, normalizes mitochondrial membrane potential, and reduces production of free radicals early after the imposition of a stress in primary cultured murine astrocytes. Free Radicals 143-156 BCL2-like 1 Mus musculus 18-26 14656879-7 2004 To elucidate the role of Bcl-XL in vivo, Ba/F3-NPM/ALK+ cells expressing a doxycycline (Dox)-inducible Bcl-XL antisense transgene (pTet-ON) were injected into nude mice. Doxycycline 75-86 BCL2-like 1 Mus musculus 103-109 14656879-7 2004 To elucidate the role of Bcl-XL in vivo, Ba/F3-NPM/ALK+ cells expressing a doxycycline (Dox)-inducible Bcl-XL antisense transgene (pTet-ON) were injected into nude mice. Doxycycline 88-91 BCL2-like 1 Mus musculus 103-109 14656879-8 2004 Doxycycline administration prevented a fatal systemic disease in 15 of 15 intravenously injected mice and the appearance of subcutaneous tumor xenografts in 9 of 12 mice; in vivo down-regulation of Bcl-XL was also documented. Doxycycline 0-11 BCL2-like 1 Mus musculus 198-204 14750167-6 2004 The impact of Bax/Bcl-xL expression on gemcitabine-sensitivity in vivo was evaluated in orthotopic Colo357 tumors in SCID mice. gemcitabine 39-50 BCL2-like 1 Mus musculus 18-24 14679196-0 2004 Steroid hormones induce bcl-X gene expression through direct activation of distal promoter P4. Steroids 0-16 BCL2-like 1 Mus musculus 24-29 15059344-9 2004 The expression level of bcl-xl mRNA and protein was decreased in the ASODN group, whereas in the SCODN group there was no significant difference in contrast with saline-treated control group. Sodium Chloride 162-168 BCL2-like 1 Mus musculus 24-30 14636693-2 2003 Our research showed that cadmium could directly lead to the dysfunction of isolated mitochondria from mouse liver, including the inhibition of respiration, the opening of permeability transition pore (PTP), the loss of transmembrane potential, and the release of cytochrome c. These mitochondrial changes were completely suppressed by Bcl-xL and Ruthenium Red (RR). Cadmium 25-32 BCL2-like 1 Mus musculus 335-341 12972296-9 2003 Expression of bcl-XL protein level was upregulated by DEX. Dexamethasone 54-57 BCL2-like 1 Mus musculus 14-20 14572633-4 2003 In nude mice growth of melanoma xenotransplants derived from stably transfected cells was significantly reduced after induction of Bcl-X(S) by doxycycline. Doxycycline 143-154 BCL2-like 1 Mus musculus 131-136 12893848-0 2003 Antisense oligonucleotide inhibition of Bcl-xL and Bid expression in liver regulates responses in a mouse model of Fas-induced fulminant hepatitis. Oligonucleotides 10-25 BCL2-like 1 Mus musculus 40-46 12893848-0 2003 Antisense oligonucleotide inhibition of Bcl-xL and Bid expression in liver regulates responses in a mouse model of Fas-induced fulminant hepatitis. ammonium ferrous sulfate 115-118 BCL2-like 1 Mus musculus 40-46 12893848-3 2003 To do this, we have developed chemically modified 2"-O-(2-methoxy) ethyl antisense inhibitors of both Bid and Bcl-xL expression. 2"-o-(2-methoxy) ethyl 50-72 BCL2-like 1 Mus musculus 110-116 12893848-6 2003 Reduction of Bcl-xL expression resulted in a potentiation of Fas-mediated apoptosis in liver and significant increase of the lethality of Fas-mediated fulminant hepatitis (p < 0.0001). ammonium ferrous sulfate 61-64 BCL2-like 1 Mus musculus 13-19 12893848-6 2003 Reduction of Bcl-xL expression resulted in a potentiation of Fas-mediated apoptosis in liver and significant increase of the lethality of Fas-mediated fulminant hepatitis (p < 0.0001). ammonium ferrous sulfate 138-141 BCL2-like 1 Mus musculus 13-19 12972296-5 2003 Ribonuclease protection assays (RPA) revealed that DEX upregulated mRNA levels of caspases-1, -3, -6, -8, -11, -12, and bcl-XL. Dexamethasone 51-54 BCL2-like 1 Mus musculus 120-126 12907145-0 2003 RU486-inducible retrovirus-mediated caspase-3 overexpression is cytotoxic to bcl-xL-expressing myeloma cells in vitro and in vivo. Mifepristone 0-5 BCL2-like 1 Mus musculus 77-83 12721288-8 2003 Replacement of the BCL-2 BH4 domain with the related BCL-XL BH4 sequence resulted in a switch of FDCP-Mix BCL-2 cells to erythroid fate accompanied by persistence of Raf-1 protein expression. sapropterin 60-63 BCL2-like 1 Mus musculus 53-59 12787408-4 2003 METHODS: Apoptosis induced by simvastatin was measured in murine tubular cells with and without overexpressing Bcl-xL. Simvastatin 30-41 BCL2-like 1 Mus musculus 111-117 12787408-12 2003 Simvastatin appears to alter the balance between cell-life and death-promoting genes, as reflected by the decreased Bcl-xL/Bax ratio. Simvastatin 0-11 BCL2-like 1 Mus musculus 116-122 12787408-13 2003 Supporting this hypothesis, overexpression of Bcl-xL reduced the amount of apoptosis induced by simvastatin by 80% when compared with control vector-expressing cells. Simvastatin 96-107 BCL2-like 1 Mus musculus 46-52 12707337-3 2003 Bcl-x(L) overexpression in A/WySnJ B cells decreased the turnover of transitional B cells, as determined by 5-bromo-2"-deoxyuridine labeling, and restored follicular B cell development. Bromodeoxyuridine 108-131 BCL2-like 1 Mus musculus 0-8 12880486-11 2003 Selegiline and its metabolite, desmethylselegiline, reduce apoptosis by altering the expression of a number of genes, for instance, superoxide dismutase, Bcl-2, Bcl-xl, NOS, c-Jun, and nicotinamide adenine nucleotide dehydrogenase. Selegiline 0-10 BCL2-like 1 Mus musculus 161-167 12880486-11 2003 Selegiline and its metabolite, desmethylselegiline, reduce apoptosis by altering the expression of a number of genes, for instance, superoxide dismutase, Bcl-2, Bcl-xl, NOS, c-Jun, and nicotinamide adenine nucleotide dehydrogenase. desmethylselegiline 31-50 BCL2-like 1 Mus musculus 161-167 12782000-9 2003 BH4 treatment led to increases in the ratio of Bax/Bcl-x(L) mRNA and protein levels. sapropterin 0-3 BCL2-like 1 Mus musculus 51-59 12118121-1 2002 An oligonucleotide-based microarray analysis of 9,500 genes and expressed sequence tags (ESTs) demonstrated that the type 1 inositol 1,4,5-trisphosphate receptor (IP(3)R) was significantly down-regulated in Bcl-X(L)-expressing as compared with control cells. Oligonucleotides 3-18 BCL2-like 1 Mus musculus 207-214 12614196-12 2003 The overexpression of bcl-2 or bcl-x(L) in FL5.12 cells inhibited apoptosis induced by MK886 as well as the enhancement of apoptosis by WY14643. MK-886 87-92 BCL2-like 1 Mus musculus 31-36 12614196-12 2003 The overexpression of bcl-2 or bcl-x(L) in FL5.12 cells inhibited apoptosis induced by MK886 as well as the enhancement of apoptosis by WY14643. pirinixic acid 136-143 BCL2-like 1 Mus musculus 31-36 12474250-0 2003 Bcl-xL expression interferes with the effects of L-glutamine supplementation on hybridoma cultures. Glutamine 49-60 BCL2-like 1 Mus musculus 0-6 12474250-7 2003 Interestingly, Sp2/0-Ag14 cells over-expressing Bcl-xL showed a culture behavior upon L-Gln complementation that was similar to the P3x63-Ag8.653 myeloma. Glutamine 86-91 BCL2-like 1 Mus musculus 48-54 12232794-3 2002 Bcl-X(L)-deficient primary telencephalic neuron cultures were highly susceptible to the apoptotic effects of cytosine arabinoside (AraC), a known genotoxic agent. Cytarabine 109-129 BCL2-like 1 Mus musculus 0-8 12232794-3 2002 Bcl-X(L)-deficient primary telencephalic neuron cultures were highly susceptible to the apoptotic effects of cytosine arabinoside (AraC), a known genotoxic agent. Cytarabine 131-135 BCL2-like 1 Mus musculus 0-8 12232794-4 2002 In contrast, neurons lacking p53, or both Bcl-X(L) and p53, were markedly, and equivalently, resistant to AraC-induced caspase-3 activation and death in vitro indicating that Bcl-X(L) lies downstream of p53 in DNA damage-induced neuronal death. Cytarabine 106-110 BCL2-like 1 Mus musculus 42-50 12232794-4 2002 In contrast, neurons lacking p53, or both Bcl-X(L) and p53, were markedly, and equivalently, resistant to AraC-induced caspase-3 activation and death in vitro indicating that Bcl-X(L) lies downstream of p53 in DNA damage-induced neuronal death. Cytarabine 106-110 BCL2-like 1 Mus musculus 175-183 12160936-0 2002 Effect of Bcl-x(L) overexpression on reactive oxygen species, intracellular calcium, and mitochondrial membrane potential following injury in astrocytes. Reactive Oxygen Species 37-60 BCL2-like 1 Mus musculus 10-18 12160936-0 2002 Effect of Bcl-x(L) overexpression on reactive oxygen species, intracellular calcium, and mitochondrial membrane potential following injury in astrocytes. Calcium 76-83 BCL2-like 1 Mus musculus 10-18 12160936-2 2002 This work analyzed effects of Bcl-x(L) overexpression on cellular levels of reactive oxygen species (ROS), intracellular calcium ([Ca(2+)](i)), and mitochondrial membrane potential (DeltaPsi(m)) in cultured mouse primary astrocytes after exposure to glucose deprivation (GD) or hydrogen peroxide (H(2)O(2)). Reactive Oxygen Species 76-99 BCL2-like 1 Mus musculus 30-38 12160936-3 2002 Upon exposure to GD or H(2)O(2), uninfected and Lac-Z-expressing astrocytes showed an immediate, rapid increase in ROS accumulation that was slowed and or reduced by Bcl-x(L). Water 23-28 BCL2-like 1 Mus musculus 166-174 12160936-10 2002 These data thus dissociate the effect of Bcl-x(L) on calcium homeostasis from effects on ROS, DeltaPsi(m,) and for H(2)O(2) exposure, cell survival. Calcium 53-60 BCL2-like 1 Mus musculus 41-49 12446462-0 2003 Bcl-XL is required for heme synthesis during the chemical induction of erythroid differentiation of murine erythroleukemia cells independently of its antiapoptotic function. Heme 23-27 BCL2-like 1 Mus musculus 0-6 12446462-3 2003 We have previously shown that dimethyl sulfoxide (DMSO) induction of erythroid differentiation in murine erythroleukemia (MEL) cells correlates with delay of apoptosis and specific induction of Bcl-X(L). Dimethyl Sulfoxide 30-48 BCL2-like 1 Mus musculus 194-202 12446462-3 2003 We have previously shown that dimethyl sulfoxide (DMSO) induction of erythroid differentiation in murine erythroleukemia (MEL) cells correlates with delay of apoptosis and specific induction of Bcl-X(L). Dimethyl Sulfoxide 50-54 BCL2-like 1 Mus musculus 194-202 12446462-7 2003 Inhibition of Bcl-X(L) by antisense transcripts accelerated apoptosis in DMSO-treated MEL cells and blocked the synthesis of hemoglobin without altering the growth arrest associated with terminal erythroid differentiation. Dimethyl Sulfoxide 73-77 BCL2-like 1 Mus musculus 14-22 12446462-8 2003 An antisense oligonucleotide to Bcl-X(L) did not induce apoptosis in MEL cells overexpressing Bcl-2 but greatly decreased their hemoglobin synthesis when treated with DMSO, suggesting that Bcl-X(L) is necessary for erythroid differentiation independently of its antiapoptotic function. Oligonucleotides 13-28 BCL2-like 1 Mus musculus 32-40 12446462-8 2003 An antisense oligonucleotide to Bcl-X(L) did not induce apoptosis in MEL cells overexpressing Bcl-2 but greatly decreased their hemoglobin synthesis when treated with DMSO, suggesting that Bcl-X(L) is necessary for erythroid differentiation independently of its antiapoptotic function. Oligonucleotides 13-28 BCL2-like 1 Mus musculus 189-197 12446462-8 2003 An antisense oligonucleotide to Bcl-X(L) did not induce apoptosis in MEL cells overexpressing Bcl-2 but greatly decreased their hemoglobin synthesis when treated with DMSO, suggesting that Bcl-X(L) is necessary for erythroid differentiation independently of its antiapoptotic function. Dimethyl Sulfoxide 167-171 BCL2-like 1 Mus musculus 32-40 12446462-8 2003 An antisense oligonucleotide to Bcl-X(L) did not induce apoptosis in MEL cells overexpressing Bcl-2 but greatly decreased their hemoglobin synthesis when treated with DMSO, suggesting that Bcl-X(L) is necessary for erythroid differentiation independently of its antiapoptotic function. Dimethyl Sulfoxide 167-171 BCL2-like 1 Mus musculus 189-197 12446462-9 2003 Importantly, Bcl-X(L) antisense transcripts prevented heme synthesis but not globin mRNA induction in DMSO-treated MEL cells. Heme 54-58 BCL2-like 1 Mus musculus 13-21 12446462-11 2003 Finally, Bcl-X(L) localized to mitochondria during MEL erythroid differentiation, suggesting that it may mediate a critical mitochondrial transport function related to heme biosynthesis. Heme 168-172 BCL2-like 1 Mus musculus 9-17 12639928-8 2003 Inhibition of the GLP-1-dependent increase of cAMP by Rp-cAMP blocked the antiapoptotic action of GLP-1, as determined by DNA fragmentation and poly-(ADP-ribose)-polymerase assays and by detection of Bcl-2 and Bcl-xL protein levels. Cyclic AMP 46-50 BCL2-like 1 Mus musculus 210-216 12639928-8 2003 Inhibition of the GLP-1-dependent increase of cAMP by Rp-cAMP blocked the antiapoptotic action of GLP-1, as determined by DNA fragmentation and poly-(ADP-ribose)-polymerase assays and by detection of Bcl-2 and Bcl-xL protein levels. Cyclic AMP 57-61 BCL2-like 1 Mus musculus 210-216 12654481-7 2003 The paraquat-mediated gene or protein expression of proapoptotic Bax, Bcl-w, and Bcl-X(S), cell survival/death factors GADD45, MDM2, c-Myc, and caspase-3 was upregulated, but that of antiapoptotic Bcl-2 was downregulated in the GPX1-/- mice vs. the WT mice. Paraquat 4-12 BCL2-like 1 Mus musculus 81-86 12665473-4 2003 Bcl-xL-deficient keratinocytes cultured in vitro readily underwent apoptosis in the absence of growth factors, but the addition of HGF or EGF resulted in restoration of cell survival, which was reversed by treatment with wortmannin, an inhibitor of phosphoinositide-3 kinase (PI3K). Wortmannin 221-231 BCL2-like 1 Mus musculus 0-6 12665473-5 2003 Topical treatment of K5.Bcl-xL-/- mice with wortmannin sensitized the skin for apoptosis induced by UV (UV) B, although wild-type epidermis was only marginally affected by this treatment, suggesting that the resistance to UVB largely depended on PI3K-Akt signaling in Bcl-xL-deficient mice but not in wild-type mice. Wortmannin 44-54 BCL2-like 1 Mus musculus 24-30 12665473-5 2003 Topical treatment of K5.Bcl-xL-/- mice with wortmannin sensitized the skin for apoptosis induced by UV (UV) B, although wild-type epidermis was only marginally affected by this treatment, suggesting that the resistance to UVB largely depended on PI3K-Akt signaling in Bcl-xL-deficient mice but not in wild-type mice. Wortmannin 44-54 BCL2-like 1 Mus musculus 268-274 12621302-0 2003 Bcl-XL maintains mitochondrial function in murine astrocytes deprived of glucose. Glucose 73-80 BCL2-like 1 Mus musculus 0-6 12406902-8 2003 At the biochemical level, SU5614 down-regulated the activity of the hyperphosphorylated FLT3 receptor and its downstream targets, signal transducer and activator of (STAT) 3, STAT5, and mitogen-activated protein kinase (MAPK), and the STAT5 target genes BCL-X(L) and p21. SU 5614 26-32 BCL2-like 1 Mus musculus 254-262 12429713-6 2002 Activation of T cells with PMA and ionomycin together with CTLA4-CD80/CD86 blockade results in decreased induction of CD25 and Bcl-X(L), reduced interleukin (IL)-2, and enhanced transforming growth factor-beta (TGF-beta) production. Ionomycin 35-44 BCL2-like 1 Mus musculus 127-135 12115434-9 2002 The level of Bcl-X(L) expressed after ZnSO(4) induction was sufficient to prevent apoptosis experimentally induced by cycloheximide and allowed 4G1.D9 cells to grow at higher densities and remain viable for prolonged periods in suboptimal culture conditions. znso 38-42 BCL2-like 1 Mus musculus 13-21 12115434-9 2002 The level of Bcl-X(L) expressed after ZnSO(4) induction was sufficient to prevent apoptosis experimentally induced by cycloheximide and allowed 4G1.D9 cells to grow at higher densities and remain viable for prolonged periods in suboptimal culture conditions. Cycloheximide 118-131 BCL2-like 1 Mus musculus 13-21 12121614-8 2002 Importantly, sustained proliferation of Bcl-X(L)-expressing immature erythroblasts still required respective factors (Epo, stem cell factor [SCF], and the glucocorticoid receptor ligand dexamethasone [Dex]). Dexamethasone 186-199 BCL2-like 1 Mus musculus 40-48 12121614-8 2002 Importantly, sustained proliferation of Bcl-X(L)-expressing immature erythroblasts still required respective factors (Epo, stem cell factor [SCF], and the glucocorticoid receptor ligand dexamethasone [Dex]). Dexamethasone 201-204 BCL2-like 1 Mus musculus 40-48 11964391-14 2002 Nevertheless, Mn(II), in part, exerts its effect via its ability to replace Ca(II) in the activation of m-calpain, which in turn activates caspase-12 and degrades Bcl-xL. Manganese(2+) 14-20 BCL2-like 1 Mus musculus 163-169 11964391-14 2002 Nevertheless, Mn(II), in part, exerts its effect via its ability to replace Ca(II) in the activation of m-calpain, which in turn activates caspase-12 and degrades Bcl-xL. ca(ii) 76-82 BCL2-like 1 Mus musculus 163-169 11861645-4 2002 Bcl-X(L) protected cells from nitric oxide-induced apoptosis during hypoxia by preventing the release of cytochrome c, caspase-9 activation, and by maintaining a mitochondrial membrane potential. Nitric Oxide 30-42 BCL2-like 1 Mus musculus 0-7 11746439-11 2001 Taken together, our data suggest that Bcl-X(L) prevents etoposide-induced neuronal death by exerting its anticaspase and anticalpain effect on cellular events after the formation of topoisomerase II-DNA cleavable complex that may not be a major contributor to cell death. Etoposide 56-65 BCL2-like 1 Mus musculus 38-46 12479265-2 2002 Here, we report the ability of a novel family of nonnuclear targeted anthracyclines to induce rapid apoptosis in cells despite Bcl-2 or Bcl-X(L) expression. Anthracyclines 69-83 BCL2-like 1 Mus musculus 136-144 11739725-4 2002 Bcl-X(L) prevented oxygen deprivation-induced cell death by inhibiting the release of cytochrome c and caspase-9 activation. Oxygen 19-25 BCL2-like 1 Mus musculus 0-8 11739725-5 2002 The ability of Bcl-X(L) to prevent cell death was dependent on allowing the import of glycolytic ATP into the mitochondria to generate an inner mitochondrial membrane potential through the F(1)F(0)-ATP synthase. Adenosine Triphosphate 97-100 BCL2-like 1 Mus musculus 15-23 11705740-9 2001 Furthermore, LY-294002 pretreatment blocks TNF-alpha- and Jo2-induced Bcl-xL levels in hepatocytes, with no effect on the phosphorylation levels of Bad. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 13-22 BCL2-like 1 Mus musculus 70-76 11705740-11 2001 Together, the PI3K/Akt pathway has a protective role in Fas-mediated apoptosis, which requires NF-kappa B activation, partially through the subsequent induction of Bcl-xL. ammonium ferrous sulfate 56-59 BCL2-like 1 Mus musculus 164-170 11589424-7 2001 Targeted gene disruptions of p53 and bax inhibited and bcl-x potentiated chloroquine-induced neuron death. Chloroquine 73-84 BCL2-like 1 Mus musculus 55-60 11583580-4 2001 IL-3 stimulation induced Bad phosphorylation at Ser-112, impairing its binding to Bcl-x(L) and resulting in its association with 14-3-3 proteins in the cytosol. Serine 48-51 BCL2-like 1 Mus musculus 82-90 11481222-5 2001 Moreover, the amphetamines can cause differential changes in the expression of Bcl-X splice variants in primary cortical cell cultures. Amphetamines 14-26 BCL2-like 1 Mus musculus 79-84 11461765-0 2001 Ca(2+)-calmodulin antagonist chlorpromazine and poly(ADP-ribose) polymerase modulators 4-aminobenzamide and nicotinamide influence hepatic expression of BCL-XL and P53 and protect against acetaminophen-induced programmed and unprogrammed cell death in mice. Chlorpromazine 29-43 BCL2-like 1 Mus musculus 153-159 11461765-0 2001 Ca(2+)-calmodulin antagonist chlorpromazine and poly(ADP-ribose) polymerase modulators 4-aminobenzamide and nicotinamide influence hepatic expression of BCL-XL and P53 and protect against acetaminophen-induced programmed and unprogrammed cell death in mice. 4-aminobenzamide 87-103 BCL2-like 1 Mus musculus 153-159 11461765-0 2001 Ca(2+)-calmodulin antagonist chlorpromazine and poly(ADP-ribose) polymerase modulators 4-aminobenzamide and nicotinamide influence hepatic expression of BCL-XL and P53 and protect against acetaminophen-induced programmed and unprogrammed cell death in mice. Niacinamide 108-120 BCL2-like 1 Mus musculus 153-159 11461765-0 2001 Ca(2+)-calmodulin antagonist chlorpromazine and poly(ADP-ribose) polymerase modulators 4-aminobenzamide and nicotinamide influence hepatic expression of BCL-XL and P53 and protect against acetaminophen-induced programmed and unprogrammed cell death in mice. Acetaminophen 188-201 BCL2-like 1 Mus musculus 153-159 11485388-0 2001 Proteolytic loss of bcl-x(L) in FL5.12 Cells undergoing apoptosis induced by MK886. MK-886 77-82 BCL2-like 1 Mus musculus 20-28 11485388-1 2001 Apoptosis induced in the IL3-dependent murine pro-B lymphocytic (FL5.12) cell line by the 5-lipoxygenase activating protein inhibitor MK886 is accompanied by the rapid loss of the anti-apoptotic bcl-x(L) and bcl-2, but not the proapoptotic bax proteins (Datta et al., J. Biol. MK-886 134-139 BCL2-like 1 Mus musculus 195-203 11485388-6 2001 The disappearance of bcl-x(L) from FL5.12 cells upon MK886 treatment was prevented in a dose-dependent manner by pretreatment with leupeptin, pepstatin, phenylmethylsulfonyl fluoride, or the broad-spectrum caspase inhibitor Boc-D-FMK. MK-886 53-58 BCL2-like 1 Mus musculus 21-29 11485388-6 2001 The disappearance of bcl-x(L) from FL5.12 cells upon MK886 treatment was prevented in a dose-dependent manner by pretreatment with leupeptin, pepstatin, phenylmethylsulfonyl fluoride, or the broad-spectrum caspase inhibitor Boc-D-FMK. leupeptin 131-140 BCL2-like 1 Mus musculus 21-29 11485388-6 2001 The disappearance of bcl-x(L) from FL5.12 cells upon MK886 treatment was prevented in a dose-dependent manner by pretreatment with leupeptin, pepstatin, phenylmethylsulfonyl fluoride, or the broad-spectrum caspase inhibitor Boc-D-FMK. pepstatin 142-151 BCL2-like 1 Mus musculus 21-29 11485388-6 2001 The disappearance of bcl-x(L) from FL5.12 cells upon MK886 treatment was prevented in a dose-dependent manner by pretreatment with leupeptin, pepstatin, phenylmethylsulfonyl fluoride, or the broad-spectrum caspase inhibitor Boc-D-FMK. Phenylmethylsulfonyl Fluoride 153-182 BCL2-like 1 Mus musculus 21-29 11485388-6 2001 The disappearance of bcl-x(L) from FL5.12 cells upon MK886 treatment was prevented in a dose-dependent manner by pretreatment with leupeptin, pepstatin, phenylmethylsulfonyl fluoride, or the broad-spectrum caspase inhibitor Boc-D-FMK. Boc-D-FMK 224-233 BCL2-like 1 Mus musculus 21-29 11485388-12 2001 This pathway may be unique to MK886 since these same protease inhibitors had only minimal effects on etoposide-induced apoptosis and the accompanying moderate loss of bcl-x(L) in FL5.12 cells. MK-886 30-35 BCL2-like 1 Mus musculus 167-175 11141501-8 2001 CsA also decreased Bcl-xL levels. Cyclosporine 0-3 BCL2-like 1 Mus musculus 19-25 11391533-12 2001 In addition, etoposide treatment enhanced the mRNA and protein expression of Bcl-xL, an antiapoptotic molecule in the liver. Etoposide 13-22 BCL2-like 1 Mus musculus 77-83 11391533-13 2001 The present findings suggest that etoposide prevents endotoxin-induced lethal liver injury by up-regulation of Bcl-xL, and that etoposide could be useful for the treatment of TNF-alpha-mediated liver diseases. Etoposide 34-43 BCL2-like 1 Mus musculus 111-117 11343245-6 2001 The level of the antiapoptotic protein bcl-x(L) was increased greater than tenfold in the mutant animals (P < .04), which can, at least in part, account for the protection from Fas-mediated apoptosis. ammonium ferrous sulfate 180-183 BCL2-like 1 Mus musculus 39-47 11343245-8 2001 These observations link C/EBPbeta to Fas-induced hepatocyte apoptosis through a mechanism that likely involves translational or posttranslational regulation of bcl-x(L). ammonium ferrous sulfate 37-40 BCL2-like 1 Mus musculus 160-168 11313368-5 2001 Mutation of C-terminal proline residues abrogated the proliferative and cytokine regulatory features of CD28 costimulation while preserving Bcl-X(L) induction. Proline 23-30 BCL2-like 1 Mus musculus 140-148 11482458-4 2001 The cytokine-dependent cell lines (THS119/IL-3 and THS119/IL-7) showed induction of STAT5 phosphorylation and target genes for STAT5 such as CIS, pim-1, p21 and bcl-xL upon addition of IL-3 or IL-7. ths119 35-41 BCL2-like 1 Mus musculus 161-167 11482458-4 2001 The cytokine-dependent cell lines (THS119/IL-3 and THS119/IL-7) showed induction of STAT5 phosphorylation and target genes for STAT5 such as CIS, pim-1, p21 and bcl-xL upon addition of IL-3 or IL-7. ths119 51-57 BCL2-like 1 Mus musculus 161-167 11349125-0 2001 Interleukin-6 protects against Fas-mediated death by establishing a critical level of anti-apoptotic hepatic proteins FLIP, Bcl-2, and Bcl-xL. ammonium ferrous sulfate 31-34 BCL2-like 1 Mus musculus 135-141 11356068-10 2001 A possible role for inhibition of Bcl-2 or Bcl-x(L) expression in the apoptosis induced by GCV was observed in the tk-transduced TonB210.1 cells but not in the 32D or 32Dp210 cells. Ganciclovir 91-94 BCL2-like 1 Mus musculus 43-51 11254887-5 2001 The expression of Bcl-2 and Bax proteins were high in LBC cells and following CsA treatment the expression of these proteins as well as Bcl-XL decreased. Cyclosporine 78-81 BCL2-like 1 Mus musculus 136-142 11259472-6 2001 The in vivo activity of oligonucleotide 4625 was determined by the inhibition of growth of established tumor xenografts in nude mice, immunohistochemical staining of Bcl-2 and Bcl-x proteins in the tumors, and western blotting of tumor lysates. Oligonucleotides 24-39 BCL2-like 1 Mus musculus 176-181 12549008-7 2001 However, the H2O2-induced N-2a cell death can be inhibited by Bcl-XL. Hydrogen Peroxide 13-17 BCL2-like 1 Mus musculus 62-68 19003387-5 2000 Bcl-xL-transfected Sp2/0-Ag14cells were more resistant than the wild type and theplasmid-containing cells to apoptosis induced by CHXand by glutamine depletion. Glutamine 140-149 BCL2-like 1 Mus musculus 0-6 11150333-8 2001 AraC caused extensive apoptosis of wild-type and Bcl-X(L)-deficient neurons. Cytarabine 0-4 BCL2-like 1 Mus musculus 49-57 11140697-4 2000 Adult mice exposed to greater than 95% oxygen concentrations for 48 to 88 hours had increased whole-lung mRNA levels of Bax and Bcl-X(L), no change in Bak, Bad, or Bcl-2, and decreased levels of Bcl-w and Bfl-1. Oxygen 39-45 BCL2-like 1 Mus musculus 128-136 10979952-5 2000 Expression of Bcl-X(L) and BAD phosphorylation are critical for the survival of erythroid cells, and orthovanadate in the absence of EPO both maintained expression levels of antiapoptotic Bcl-X(L) and induced BAD phosphorylation at serine 112. Serine 232-238 BCL2-like 1 Mus musculus 14-22 10946304-3 2000 Bcl-xL-transfected RAW 264 macrophages were protected from gliotoxin-induced apoptosis, indicating the presence of functional Bcl-xL. Gliotoxin 59-68 BCL2-like 1 Mus musculus 0-6 11201044-2 2000 The present study examines the contributions of apoptosis-related proteins (Bcl-2, Bcl-XL, Bax, and p21WAF1/CIP1) in the regulation of T-cell death induced by butyric acid, using p53 knock-out (p53-/-) and wild-type (p53+/+) mice. Butyric Acid 159-171 BCL2-like 1 Mus musculus 83-89 10894153-4 2000 A bcl-x hypomorphic mouse was generated through the introduction of a neomycin (neo) gene into the promoter of the bcl-x gene by homologous recombination. Neomycin 70-78 BCL2-like 1 Mus musculus 2-7 11201044-7 2000 Western blotting analysis of splenic T-cells showed that butyric acid treatment decreased Bcl-2 and Bcl-XL expressions in p53+/+ and p53-/- cells. Butyric Acid 57-69 BCL2-like 1 Mus musculus 100-106 11201044-9 2000 These results suggest that butyric-acid-mediated apoptosis of murine T-cells takes place via a pathway that is independent of p53, and is followed by the p53-regulated proteins Bax and p21WAF1/CIP1, which lower the levels of the apoptosis antagonists Bcl-2 and Bcl-XL in cells. Butyric Acid 27-39 BCL2-like 1 Mus musculus 261-267 11006017-8 2000 TGF-beta-induced DNA fragmentation and cleavage of bcl-x(L) were inhibited by pretreatment with tetra peptide caspase 1 inhibitor, YVAD.cmk. YVAD 131-135 BCL2-like 1 Mus musculus 51-56 10894153-4 2000 A bcl-x hypomorphic mouse was generated through the introduction of a neomycin (neo) gene into the promoter of the bcl-x gene by homologous recombination. Neomycin 70-78 BCL2-like 1 Mus musculus 115-120 10842201-8 2000 Combined treatment of Shionogi cells with antisense Bcl-xL and Bcl-2 ODNs significantly enhanced taxol chemosensitivity compared with either agent alone, reducing the IC(50) of taxol by more than 1 log. Paclitaxel 97-102 BCL2-like 1 Mus musculus 52-58 10842201-8 2000 Combined treatment of Shionogi cells with antisense Bcl-xL and Bcl-2 ODNs significantly enhanced taxol chemosensitivity compared with either agent alone, reducing the IC(50) of taxol by more than 1 log. Paclitaxel 177-182 BCL2-like 1 Mus musculus 52-58 10663392-0 2000 A hepatotoxic dose of acetaminophen modulates expression of BCL-2, BCL-X(L), and BCL-X(S) during apoptotic and necrotic death of mouse liver cells in vivo. Acetaminophen 22-35 BCL2-like 1 Mus musculus 67-75 10662719-3 2000 After exposure to thapsigargin (10 microM for 48 h), losses of cell viability in islets of Fd 1 and Fd 2 Bcl-x(L) transgenic mice were significantly lower than in islets of wild-type mice. Thapsigargin 18-30 BCL2-like 1 Mus musculus 105-110 10662719-6 2000 However, Fd 2 Bcl-x(L) islets had impaired insulin secretory and intracellular free Ca(2+) ([Ca(2+)](i)) responses to glucose and KCl. Glucose 118-125 BCL2-like 1 Mus musculus 14-22 10662719-6 2000 However, Fd 2 Bcl-x(L) islets had impaired insulin secretory and intracellular free Ca(2+) ([Ca(2+)](i)) responses to glucose and KCl. Potassium Chloride 130-133 BCL2-like 1 Mus musculus 14-22 10662719-7 2000 Furthermore, insulin and [Ca(2+)](i) responses to pyruvate methyl ester (PME) were similarly reduced as glucose in Fd 2 Bcl-x(L) islets. Glucose 104-111 BCL2-like 1 Mus musculus 120-128 10662719-9 2000 Glucose-, PME-, and alpha-ketoisocaproate-induced hyperpolarization of mitochondrial membrane potential, NAD(P)H, and ATP production were also significantly reduced in Fd 2 Bcl-x(L) islets. Glucose 0-7 BCL2-like 1 Mus musculus 173-181 10662719-9 2000 Glucose-, PME-, and alpha-ketoisocaproate-induced hyperpolarization of mitochondrial membrane potential, NAD(P)H, and ATP production were also significantly reduced in Fd 2 Bcl-x(L) islets. pme 10-13 BCL2-like 1 Mus musculus 173-181 10662719-9 2000 Glucose-, PME-, and alpha-ketoisocaproate-induced hyperpolarization of mitochondrial membrane potential, NAD(P)H, and ATP production were also significantly reduced in Fd 2 Bcl-x(L) islets. alpha-ketoisocaproic acid 20-41 BCL2-like 1 Mus musculus 173-181 10662719-9 2000 Glucose-, PME-, and alpha-ketoisocaproate-induced hyperpolarization of mitochondrial membrane potential, NAD(P)H, and ATP production were also significantly reduced in Fd 2 Bcl-x(L) islets. nad(p)h 105-112 BCL2-like 1 Mus musculus 173-181 10662719-9 2000 Glucose-, PME-, and alpha-ketoisocaproate-induced hyperpolarization of mitochondrial membrane potential, NAD(P)H, and ATP production were also significantly reduced in Fd 2 Bcl-x(L) islets. Adenosine Triphosphate 118-121 BCL2-like 1 Mus musculus 173-181 10663392-0 2000 A hepatotoxic dose of acetaminophen modulates expression of BCL-2, BCL-X(L), and BCL-X(S) during apoptotic and necrotic death of mouse liver cells in vivo. Acetaminophen 22-35 BCL2-like 1 Mus musculus 67-72 10663392-6 2000 This study demonstrates that administration of a hepatotoxic dose of AAP to ICR mice results in severe liver injury (ALT leakage >200-fold at 6 h and >600-fold at 18 h) leading to massive cell death by apoptosis (diagnosed by nuclear ultrastructure, histopathology, and DNA ladder), in addition to necrosis coupled with spectacular changes in the BCL-X(L) expression (6 and 18 h after AAP administration). Acetaminophen 69-72 BCL2-like 1 Mus musculus 353-361 10663392-8 2000 As the toxicity progressed, during 6 and 18 h post-AAP administration, the BCL-X(L) protein band shifted to a slower mobility band which might represent a phosphorylated form of BCL-X(L). Acetaminophen 51-54 BCL2-like 1 Mus musculus 75-83 10663392-8 2000 As the toxicity progressed, during 6 and 18 h post-AAP administration, the BCL-X(L) protein band shifted to a slower mobility band which might represent a phosphorylated form of BCL-X(L). Acetaminophen 51-54 BCL2-like 1 Mus musculus 178-186 10663392-14 2000 However, this study may have demonstrated for the first time drug-induced changes in the expression of anti-apoptotic gene BCL-X(L), and a positive link between AAP-induced apoptotic death and modification of BCL-X(L) protein in vivo. Acetaminophen 161-164 BCL2-like 1 Mus musculus 209-217 10595916-4 1999 Bcl-x(L) conferred protection on SCK cells against methotrexate at certain drug concentrations, but not at all against 5-fluorouracil in clonogenic survival assays in vitro. Methotrexate 51-63 BCL2-like 1 Mus musculus 0-8 18521433-7 2000 Paclitaxel induced cell cycle arrest with an accumulation of cells in sub-G1.This was accompanied in vitro by various events typical of apoptosis: phosphorylation of two anti-apoptotic proteins Bcl-2 and Bcl-(xL) , release of cytochrome c into the cytoplasm, cleavage and activation of caspase-3. Paclitaxel 0-10 BCL2-like 1 Mus musculus 204-211 10585435-2 1999 Increased expression of Bcl-x protein was observed in native and silica-exposed p50(-/-) macrophages in which the NF-kappaB p65-containing complex was predominantly induced. Silicon Dioxide 65-71 BCL2-like 1 Mus musculus 24-29 10595916-7 1999 In addition, numbers of apoptotic cells were significantly higher in control tumors as compared to Bcl-x(L)-expressing tumors in animals treated with methotrexate or 5-fluorouracil. Methotrexate 150-162 BCL2-like 1 Mus musculus 99-104 10595916-7 1999 In addition, numbers of apoptotic cells were significantly higher in control tumors as compared to Bcl-x(L)-expressing tumors in animals treated with methotrexate or 5-fluorouracil. Fluorouracil 166-180 BCL2-like 1 Mus musculus 99-104 10567231-6 1999 At 24 h after treatment with 500 nM MG132, apoptosis in bcl-x(L) cells (22%) was less than that observed in control cells (34%). benzyloxycarbonylleucyl-leucyl-leucine aldehyde 36-41 BCL2-like 1 Mus musculus 56-64 10567231-8 1999 By 48 h after MG132 treatment, apoptosis and caspase activity in bcl-x(L) cells were similar to those observed in control cells at 24 h. Proteasome inhibition stimulated increases in hsp70 protein levels in control and bcl-x(L) cells by 12 h, although the maximal increases found in bcl-x(L) cells were less. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 14-19 BCL2-like 1 Mus musculus 65-73 10567231-8 1999 By 48 h after MG132 treatment, apoptosis and caspase activity in bcl-x(L) cells were similar to those observed in control cells at 24 h. Proteasome inhibition stimulated increases in hsp70 protein levels in control and bcl-x(L) cells by 12 h, although the maximal increases found in bcl-x(L) cells were less. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 14-19 BCL2-like 1 Mus musculus 219-227 14634326-2 1999 Ether lipid-resistant S49ar cells were cross-resistant to extracellular stress factors (cold shock, heat shock, H2O2, dimethylsulfoxide) and to radiation-induced apoptosis but not to physiological apoptotic signals (dexamethasone, growth factor deprivation, thapsigargin, C2-ceramide) and expressed similar levels of the apoptosis-regulating proteins Bcl-2, Bcl-X, Bax, Bad and Bak as did the parent S49wt cells. ether lipid 0-11 BCL2-like 1 Mus musculus 358-363 10606248-1 1999 Using a tetracycline-regulated expression system, we have shown that expression of bcl-X(s) is sufficient to induce acute cell death in 3T3 cells, and that the manner in which these cells die is both morphologically and biochemically different from Fas/CD95-induced apoptosis. Tetracycline 8-20 BCL2-like 1 Mus musculus 83-88 10728401-4 2000 METHODS: To test the hypothesis that antisense bcl-x oligodeoxynucleotide (ODN) is effective in preventing intimal hyperplasia through enhancing apoptosis after cardiac transplantation, we performed single intraluminal delivery of antisense bcl-x ODN into murine cardiac allografts (n = 9). Oligodeoxyribonucleotides 75-78 BCL2-like 1 Mus musculus 47-52 10567231-8 1999 By 48 h after MG132 treatment, apoptosis and caspase activity in bcl-x(L) cells were similar to those observed in control cells at 24 h. Proteasome inhibition stimulated increases in hsp70 protein levels in control and bcl-x(L) cells by 12 h, although the maximal increases found in bcl-x(L) cells were less. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 14-19 BCL2-like 1 Mus musculus 219-227 10484397-5 1999 The present study shows that transgenic mice overexpressing BCL-XL in hepatocytes are also protected from Fas-induced apoptosis in a dose-dependent manner. ammonium ferrous sulfate 106-109 BCL2-like 1 Mus musculus 60-66 10462439-0 1999 A novel proanthocyanidin IH636 grape seed extract increases in vivo Bcl-XL expression and prevents acetaminophen-induced programmed and unprogrammed cell death in mouse liver. proanthocyanidin 8-24 BCL2-like 1 Mus musculus 68-74 10532544-0 1999 FK506 markedly enhances apoptosis of antigen-stimulated peripheral T cells by down-regulation of Bcl-xL. Tacrolimus 0-5 BCL2-like 1 Mus musculus 97-103 10532544-10 1999 In contrast, the expression of Bcl-x(L) on Vgamma8+ T cells, which was markedly induced by SEB, was abrogated by FK506. Tacrolimus 113-118 BCL2-like 1 Mus musculus 31-39 10532544-11 1999 CONCLUSIONS: Our findings indicate FK506-induced enhancement of apoptosis of activated T cells is mediated by down-regulation of Bcl-X(L) expression on these cells. Tacrolimus 35-40 BCL2-like 1 Mus musculus 129-137 10385386-6 1999 Treatment of bcl-X(L)/Tag cells, cocultured with MC3T3E 1 cells, with the combination of 1,25-dihydroxyvitamin D3 and dexamethasone induced high levels of OCL formation. Calcitriol 89-113 BCL2-like 1 Mus musculus 13-21 10385386-6 1999 Treatment of bcl-X(L)/Tag cells, cocultured with MC3T3E 1 cells, with the combination of 1,25-dihydroxyvitamin D3 and dexamethasone induced high levels of OCL formation. Dexamethasone 118-131 BCL2-like 1 Mus musculus 13-21 10188775-6 1999 Furthermore, if ETX-tolerant/FasL-deficient CLP animals were administered the steroid receptor antagonist RU-38486 (s.c., immediately after CLP) the increase in Ao was markedly attenuated, along with restoration of the percentage of cells expressing Bcl-2 and Fas antigen as well as Bcl-2/Bcl-X(L/S) mRNA levels. Mifepristone 106-114 BCL2-like 1 Mus musculus 289-294 10349855-0 1999 Sequential cleavage of poly(ADP-ribose)polymerase and appearance of a small Bax-immunoreactive protein are blocked by Bcl-X(L) and caspase inhibitors during staurosporine-induced dopaminergic neuronal apoptosis. Staurosporine 157-170 BCL2-like 1 Mus musculus 118-126 10349855-1 1999 To assess the role of Bcl-X(L) and its splice derivative, Bcl-X(S), in staurosporine-induced cell death, we used a dopaminergic cell line, MN9D, transfected with bcl-xL (MN9D/Bcl-X(L)), bcl-xS (MN9D/Bcl-X(S)), or control vector (MN9D/Neo). Staurosporine 71-84 BCL2-like 1 Mus musculus 58-63 10349855-5 1999 Bcl-X(L) prevented morphologically apoptotic changes as well as cleavage of poly(ADP-ribose)polymerase (PARP) induced by staurosporine. Staurosporine 121-134 BCL2-like 1 Mus musculus 0-8 10349855-9 1999 Thus, our present study suggests that Bcl-X(L) but not Bcl-X(S) prevents staurosporine-induced apoptosis by inhibiting the caspase activation that may be directly or indirectly responsible for the appearance of the small Bax-immunoreactive protein in some types of neurons. Staurosporine 73-86 BCL2-like 1 Mus musculus 38-46 10349855-9 1999 Thus, our present study suggests that Bcl-X(L) but not Bcl-X(S) prevents staurosporine-induced apoptosis by inhibiting the caspase activation that may be directly or indirectly responsible for the appearance of the small Bax-immunoreactive protein in some types of neurons. Staurosporine 73-86 BCL2-like 1 Mus musculus 38-43 10200563-8 1999 DMSO or HMBA treatment of 745A cells induced a marked increase of Bcl-XL expression during the late phase of differentiation which persisted even when the cells began to die. Dimethyl Sulfoxide 0-4 BCL2-like 1 Mus musculus 66-72 10200563-8 1999 DMSO or HMBA treatment of 745A cells induced a marked increase of Bcl-XL expression during the late phase of differentiation which persisted even when the cells began to die. hexamethylene bisacetamide 8-12 BCL2-like 1 Mus musculus 66-72 10200563-10 1999 DMSO treatment induced a similar delay of apoptosis and enhancement of Bcl-XL expression in F-MEL (strain TFP10) cells which fail to synthesize haemoglobin in the presence of DMSO. Dimethyl Sulfoxide 0-4 BCL2-like 1 Mus musculus 71-77 10200563-11 1999 Dexamethasone, which blocks DMSO-induced differentiation of F-MEL cells, prevented the induction of Bcl-XL. Dexamethasone 0-13 BCL2-like 1 Mus musculus 100-106 10200563-11 1999 Dexamethasone, which blocks DMSO-induced differentiation of F-MEL cells, prevented the induction of Bcl-XL. Dimethyl Sulfoxide 28-32 BCL2-like 1 Mus musculus 100-106 10200563-13 1999 Taken together, these results indicate that DMSO treatment of F-MEL cells induces a marked increase in Bcl-XL expression suggesting a role for this anti-apoptotic protein in the process of erythroid differentiation in F-MEL cells. Dimethyl Sulfoxide 44-48 BCL2-like 1 Mus musculus 103-109 9774436-7 1998 bcl-xL and bcl-2 proteins, but not bax or FLAP, were decreased by 4 h after 5 nmol of MK886/10(6) cells in both cell lines, although the higher levels of bcl-xL in overexpressors took longer to disappear. MK-886 86-91 BCL2-like 1 Mus musculus 154-160 9926866-1 1998 BcL-xL and Bcl-2 proteins were identified by paraffin section immunohistochemistry in the neuropil core of the barrelettes of the caudalis spinal trigeminal nucleus 6 h after birth. Paraffin 45-53 BCL2-like 1 Mus musculus 0-6 9794391-3 1998 We found that at least one of these tyrosines (Y338) also mediates cell survival and induction of bcl-2, bcl-x, and c-myc in the murine T cell line CTLL-2. Tyrosine 36-45 BCL2-like 1 Mus musculus 105-110 9794391-3 1998 We found that at least one of these tyrosines (Y338) also mediates cell survival and induction of bcl-2, bcl-x, and c-myc in the murine T cell line CTLL-2. y338 47-51 BCL2-like 1 Mus musculus 105-110 9774436-12 1998 These data indicate that MK886 induces extensive apoptosis that is partially caspase-3 dependent and may be related to a rapid loss of bcl-xL. MK-886 25-30 BCL2-like 1 Mus musculus 135-141 9751125-3 1998 Bleomycin-induced apoptosis was accompanied by decreases in bcl-2 and bcl-xl and increases in p53, bak, and bax protein levels. Bleomycin 0-9 BCL2-like 1 Mus musculus 70-76 9531315-4 1998 The protective effect of C2-ceramide is achieved only in the early stages following cytokine deprivation and is related to the inhibition of bcl-xL degradation and the induction of a G0 arrest of cells. N-acetylsphingosine 25-36 BCL2-like 1 Mus musculus 141-147 9774436-2 1998 The current study examined the expression of FLAP and bcl family proteins and the induction of apoptosis in interleukin-3-dependent control and bcl-xL-overexpressing FL5.12 cell lines after treatment with MK886, a specific FLAP inhibitor. MK-886 205-210 BCL2-like 1 Mus musculus 144-150 9774436-6 1998 A dose- and time-response study revealed that 5 nmol of MK886/10(6) cells was sufficient to induce apoptosis both in control and bcl-xL cells, respectively, but to different degrees. MK-886 56-61 BCL2-like 1 Mus musculus 129-135 9774436-7 1998 bcl-xL and bcl-2 proteins, but not bax or FLAP, were decreased by 4 h after 5 nmol of MK886/10(6) cells in both cell lines, although the higher levels of bcl-xL in overexpressors took longer to disappear. MK-886 86-91 BCL2-like 1 Mus musculus 0-6 9637502-9 1998 A CpG ODN with a nuclease-resistant phosphorothioate backbone (S-ODN) was also active, and increased the levels of c-myc, egr-1, c-jun, bclXL, and bax mRNA and c-Myc, c-Jun, Bax, and BclXL protein in spleen B cells. Parathion 36-52 BCL2-like 1 Mus musculus 183-188 9605754-3 1998 Bcl-xL transgenics also failed to develop skin lesions following treatment with the chemical mutagen 9,10-dimethyl-1,2-benzanthracene, or the tumor promoter O-tetradecanoylphorbol-13-acetate. 9,10-Dimethyl-1,2-benzanthracene 101-133 BCL2-like 1 Mus musculus 0-6 9605754-3 1998 Bcl-xL transgenics also failed to develop skin lesions following treatment with the chemical mutagen 9,10-dimethyl-1,2-benzanthracene, or the tumor promoter O-tetradecanoylphorbol-13-acetate. o-tetradecanoylphorbol-13-acetate 157-190 BCL2-like 1 Mus musculus 0-6 9605754-4 1998 However, Bcl-xL transgenics developed a two-fold greater number of benign papillomas than control littermates following treatment with the combination of 9,10-dimethyl-1,2-benzanthracene and O-tetradecanoylphorbol-13-acetate. 9,10-Dimethyl-1,2-benzanthracene 154-186 BCL2-like 1 Mus musculus 9-15 9605754-4 1998 However, Bcl-xL transgenics developed a two-fold greater number of benign papillomas than control littermates following treatment with the combination of 9,10-dimethyl-1,2-benzanthracene and O-tetradecanoylphorbol-13-acetate. o-tetradecanoylphorbol-13-acetate 191-224 BCL2-like 1 Mus musculus 9-15 9366408-7 1997 Further, B cells from Bcl-x Tg mice were found to be resistant to Fas-mediated apoptosis. ammonium ferrous sulfate 66-69 BCL2-like 1 Mus musculus 22-27 9510156-6 1998 Since activated RAW264 were more resistant to NO-induced apoptosis mediated by the exposure to S-nitroso-N-acetyl-penicillamine (SNAP) than nonactivated RAW264, the inducible Bcl-xL may play a role in the protection from NO toxicity. S-Nitroso-N-Acetylpenicillamine 95-127 BCL2-like 1 Mus musculus 175-181 9242554-3 1997 Using four M-phase specific chemotherapeutic agents, Bcl-XL and Bcl-2 provided similar protection against vincristine and vinblastine whereas Bcl-XL afforded as much as 50% greater cell viability than Bcl-2 against etoposide and teniposide-induced cell death. Vincristine 106-117 BCL2-like 1 Mus musculus 53-59 9242554-3 1997 Using four M-phase specific chemotherapeutic agents, Bcl-XL and Bcl-2 provided similar protection against vincristine and vinblastine whereas Bcl-XL afforded as much as 50% greater cell viability than Bcl-2 against etoposide and teniposide-induced cell death. Etoposide 215-224 BCL2-like 1 Mus musculus 53-59 9427515-7 1997 Similarly, the Bcl-2 family member, Bcl-X(L) also blocked staurosporine-induced cell death in MN9D cells whereas overexpression of Bcl-X(S) or Bax did not. Staurosporine 58-71 BCL2-like 1 Mus musculus 36-44 9427515-7 1997 Similarly, the Bcl-2 family member, Bcl-X(L) also blocked staurosporine-induced cell death in MN9D cells whereas overexpression of Bcl-X(S) or Bax did not. Staurosporine 58-71 BCL2-like 1 Mus musculus 36-41 9362454-4 1997 In FL5.12 cells expressing Bcl-XL and Bak wt or Bak deltaBH3, both Bak wt or Bak deltaBH3 were able to antagonize the protective effect of Bcl-XL when treated with etoposide or fluorouracil. bakuchiol 38-41 BCL2-like 1 Mus musculus 139-145 9362454-4 1997 In FL5.12 cells expressing Bcl-XL and Bak wt or Bak deltaBH3, both Bak wt or Bak deltaBH3 were able to antagonize the protective effect of Bcl-XL when treated with etoposide or fluorouracil. bakuchiol 48-51 BCL2-like 1 Mus musculus 139-145 9362454-4 1997 In FL5.12 cells expressing Bcl-XL and Bak wt or Bak deltaBH3, both Bak wt or Bak deltaBH3 were able to antagonize the protective effect of Bcl-XL when treated with etoposide or fluorouracil. bakuchiol 48-51 BCL2-like 1 Mus musculus 139-145 9362454-4 1997 In FL5.12 cells expressing Bcl-XL and Bak wt or Bak deltaBH3, both Bak wt or Bak deltaBH3 were able to antagonize the protective effect of Bcl-XL when treated with etoposide or fluorouracil. bak deltabh3 48-60 BCL2-like 1 Mus musculus 139-145 9362454-4 1997 In FL5.12 cells expressing Bcl-XL and Bak wt or Bak deltaBH3, both Bak wt or Bak deltaBH3 were able to antagonize the protective effect of Bcl-XL when treated with etoposide or fluorouracil. Etoposide 164-173 BCL2-like 1 Mus musculus 27-33 9362454-4 1997 In FL5.12 cells expressing Bcl-XL and Bak wt or Bak deltaBH3, both Bak wt or Bak deltaBH3 were able to antagonize the protective effect of Bcl-XL when treated with etoposide or fluorouracil. Etoposide 164-173 BCL2-like 1 Mus musculus 139-145 9362454-4 1997 In FL5.12 cells expressing Bcl-XL and Bak wt or Bak deltaBH3, both Bak wt or Bak deltaBH3 were able to antagonize the protective effect of Bcl-XL when treated with etoposide or fluorouracil. Fluorouracil 177-189 BCL2-like 1 Mus musculus 27-33 9362454-4 1997 In FL5.12 cells expressing Bcl-XL and Bak wt or Bak deltaBH3, both Bak wt or Bak deltaBH3 were able to antagonize the protective effect of Bcl-XL when treated with etoposide or fluorouracil. Fluorouracil 177-189 BCL2-like 1 Mus musculus 139-145 9362454-6 1997 Immunoprecipitation studies revealed that deletion of BH3 disrupted heterodimerization between Bak and Bcl-XL and that both Bak wt and Bak deltaBH3 failed to interact with Bcl-2. BH 3 54-57 BCL2-like 1 Mus musculus 103-109 9393984-2 1997 Here we demonstrate that v-Abl PTK activation is followed by an approximately twofold increase in mRNA level of Bcl-XL by 6 h and a corresponding increase in Bcl-XL protein level by 24 h. Bcl-xL RNA and protein decreased in IL-3 deprived cells in the absence of v-Abl PTK activity. Vanadium 25-26 BCL2-like 1 Mus musculus 112-118 9393984-2 1997 Here we demonstrate that v-Abl PTK activation is followed by an approximately twofold increase in mRNA level of Bcl-XL by 6 h and a corresponding increase in Bcl-XL protein level by 24 h. Bcl-xL RNA and protein decreased in IL-3 deprived cells in the absence of v-Abl PTK activity. Vanadium 25-26 BCL2-like 1 Mus musculus 158-164 9393984-2 1997 Here we demonstrate that v-Abl PTK activation is followed by an approximately twofold increase in mRNA level of Bcl-XL by 6 h and a corresponding increase in Bcl-XL protein level by 24 h. Bcl-xL RNA and protein decreased in IL-3 deprived cells in the absence of v-Abl PTK activity. Vanadium 25-26 BCL2-like 1 Mus musculus 188-194 9393984-3 1997 Exposure of cells with v-Abl PTK active to the PKC inhbitor calphostin C (125 ng/ml) prevented the increase in Bcl-xL protein and resulted in apoptosis. calphostin C 60-72 BCL2-like 1 Mus musculus 111-117 9393984-6 1997 The data suggest that suppression of apoptosis by v-Abl PTK in the absence of IL-3 is associated with PKC signalling and the upregulation of Bcl-xL in IC.DP cells. dp 154-156 BCL2-like 1 Mus musculus 141-147 9242554-3 1997 Using four M-phase specific chemotherapeutic agents, Bcl-XL and Bcl-2 provided similar protection against vincristine and vinblastine whereas Bcl-XL afforded as much as 50% greater cell viability than Bcl-2 against etoposide and teniposide-induced cell death. Teniposide 229-239 BCL2-like 1 Mus musculus 53-59 9242554-3 1997 Using four M-phase specific chemotherapeutic agents, Bcl-XL and Bcl-2 provided similar protection against vincristine and vinblastine whereas Bcl-XL afforded as much as 50% greater cell viability than Bcl-2 against etoposide and teniposide-induced cell death. Vinblastine 122-133 BCL2-like 1 Mus musculus 53-59 9242554-4 1997 In addition, Bcl-XL provided significantly greater cell viability than Bcl-2 against methotrexate, fluorouracil, and hydroxyurea, three S-phase specific agents. Methotrexate 85-97 BCL2-like 1 Mus musculus 13-19 9242554-4 1997 In addition, Bcl-XL provided significantly greater cell viability than Bcl-2 against methotrexate, fluorouracil, and hydroxyurea, three S-phase specific agents. Fluorouracil 99-111 BCL2-like 1 Mus musculus 13-19 9242554-4 1997 In addition, Bcl-XL provided significantly greater cell viability than Bcl-2 against methotrexate, fluorouracil, and hydroxyurea, three S-phase specific agents. Hydroxyurea 117-128 BCL2-like 1 Mus musculus 13-19 9242554-5 1997 In apoptosis induced by gamma-irradiation and cisplatin, two antitumor treatments that are cell-cycle phase-nonspecific agents, both Bcl-XL and Bcl-2 conferred similar protection against gamma-irradiation, but Bcl-XL provided better protection than Bcl-2 against cisplatin. Cisplatin 46-55 BCL2-like 1 Mus musculus 133-139 9242554-5 1997 In apoptosis induced by gamma-irradiation and cisplatin, two antitumor treatments that are cell-cycle phase-nonspecific agents, both Bcl-XL and Bcl-2 conferred similar protection against gamma-irradiation, but Bcl-XL provided better protection than Bcl-2 against cisplatin. Cisplatin 263-272 BCL2-like 1 Mus musculus 133-139 9230108-10 1997 These results suggest a possible role for GSH in the mechanism by which bcl-xL prevents cell death. Glutathione 42-45 BCL2-like 1 Mus musculus 72-78 9230108-0 1997 Bcl-xL overexpression attenuates glutathione depletion in FL5.12 cells following interleukin-3 withdrawal. Glutathione 33-44 BCL2-like 1 Mus musculus 0-6 9096145-4 1997 bcl-x-/-/bax-/- mice demonstrate greatly reduced levels of apoptosis both in vivo and in vitro compared with the CNS of Bcl-xL-deficient mice, as assessed by histology and terminal deoxytransferase-mediated deoxyuridine triphosphate nick end-labeling. deoxyuridine triphosphate 207-232 BCL2-like 1 Mus musculus 0-5 9176392-8 1997 When C3H/HeN mice were pretreated with cycloheximide before hepatectomy, the early peak of Bcl-x mRNA at 4 hours was essentially abrogated whereas the immediate-early gene c-myc was hyperinduced, thus implicating Bcl-x as a delayed early response gene during liver regeneration. Cycloheximide 39-52 BCL2-like 1 Mus musculus 91-96 9176392-8 1997 When C3H/HeN mice were pretreated with cycloheximide before hepatectomy, the early peak of Bcl-x mRNA at 4 hours was essentially abrogated whereas the immediate-early gene c-myc was hyperinduced, thus implicating Bcl-x as a delayed early response gene during liver regeneration. Cycloheximide 39-52 BCL2-like 1 Mus musculus 213-218 9108035-4 1997 Induction of apoptosis in murine thymocytes by dexamethasone or gamma-irradiation shifts the subcellular locations of Bax and Bcl-X(L) from soluble to membrane-bound forms. Dexamethasone 47-60 BCL2-like 1 Mus musculus 126-134 9092523-16 1997 In this study, these bcl-xL transfectants also displayed increased resistance to exogenous N-acetylsphingosine (C2-ceramide) or N-hexanoylsphingosine (C6-ceramide). N-acetylsphingosine 91-110 BCL2-like 1 Mus musculus 21-27 9092523-16 1997 In this study, these bcl-xL transfectants also displayed increased resistance to exogenous N-acetylsphingosine (C2-ceramide) or N-hexanoylsphingosine (C6-ceramide). N-acetylsphingosine 112-123 BCL2-like 1 Mus musculus 21-27 9092523-16 1997 In this study, these bcl-xL transfectants also displayed increased resistance to exogenous N-acetylsphingosine (C2-ceramide) or N-hexanoylsphingosine (C6-ceramide). N-caproylsphingosine 128-149 BCL2-like 1 Mus musculus 21-27 9092523-16 1997 In this study, these bcl-xL transfectants also displayed increased resistance to exogenous N-acetylsphingosine (C2-ceramide) or N-hexanoylsphingosine (C6-ceramide). N-caproylsphingosine 151-162 BCL2-like 1 Mus musculus 21-27 9092523-17 1997 However, when challenged with anti-IgM the bcl-xL transfectants produced levels of ceramide similar to wild type cells, suggesting that ceramide formation is upstream of bcl-xL and that it is a major determinant of B-cell death. Ceramides 83-91 BCL2-like 1 Mus musculus 43-49 9092523-17 1997 However, when challenged with anti-IgM the bcl-xL transfectants produced levels of ceramide similar to wild type cells, suggesting that ceramide formation is upstream of bcl-xL and that it is a major determinant of B-cell death. Ceramides 136-144 BCL2-like 1 Mus musculus 43-49 9108035-6 1997 Inhibition of apoptosis with cycloheximide inhibits the movement of Bax and Bcl-X(L) in thymocytes from the cytosol into membranes induced by dexamethasone treatment. Cycloheximide 29-42 BCL2-like 1 Mus musculus 76-84 9108035-6 1997 Inhibition of apoptosis with cycloheximide inhibits the movement of Bax and Bcl-X(L) in thymocytes from the cytosol into membranes induced by dexamethasone treatment. Dexamethasone 142-155 BCL2-like 1 Mus musculus 76-84 8855292-9 1996 In vitro Bcl-XL induction following ligation of sIgM-required BTK, was cyclosporin A (CsA)-sensitive and dependent on extracellular Ca2+. Cyclosporine 71-84 BCL2-like 1 Mus musculus 9-15 14646567-7 1997 Although the cell death-suppressor bcl-2-family proteins (bcl-2 and bcl-XL) were recently found to suppress the activation of CPP32-like proteases, the expression levels of death-suppressor bcl-2-family proteins did not change when thiols were added. Sulfhydryl Compounds 232-238 BCL2-like 1 Mus musculus 68-74 9129161-11 1996 Moreover, in three of the four B lymphoma cell lines tested, Fas susceptibility correlated with the status of bcl-xL expression. ammonium ferrous sulfate 61-64 BCL2-like 1 Mus musculus 110-116 8855292-9 1996 In vitro Bcl-XL induction following ligation of sIgM-required BTK, was cyclosporin A (CsA)-sensitive and dependent on extracellular Ca2+. Cyclosporine 86-89 BCL2-like 1 Mus musculus 9-15 8605937-6 1996 To investigate the functional significance of bcl-x in activated B cells, we tested their sensitivity to apoptosis induced by the Ca2+ ATPase inhibitor thapsigargin: B cell blasts activated with anti-CD40 and anti-Ig were resistant to this agent. Thapsigargin 152-164 BCL2-like 1 Mus musculus 46-51 8774443-5 1996 bcl-x-/- telencephalic cells cultured in 0.5 or 2.0% fetal calf serum (FCS)-containing medium for 48 hr showed increased apoptosis, defined by abnormal bisbenzamide staining and terminal-deoxytransferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL), and decreased numbers of microtubule-associated protein-2-immunoreactive neurons compared with bcl-x+/- and bcl-x+/+ cultures. deoxyuridine triphosphate 213-238 BCL2-like 1 Mus musculus 0-5 8774443-6 1996 Cycloheximide treatment of bcl-x-/- telencephalic cell cultures failed to prevent the increased cell death observed in low FCS-containing medium, suggesting a protein synthesis-independent apoptosis. Cycloheximide 0-13 BCL2-like 1 Mus musculus 27-32 8910687-5 1996 This mechanism is supported by the data indicating that induction of the survival gene, bcl-xL, can override Fas induced cell death and that the kinetics of Bcl-xL expression correlate well with the susceptibility of normal T cells to apoptosis initiated by Fas-Fas ligand interactions. ammonium ferrous sulfate 109-112 BCL2-like 1 Mus musculus 88-94 7561075-6 1995 Antisense but not sense phosphorothioate oligonucleotide for bcl-x can partially block this CD40-mediated apoptotic rescue. Phosphorothioate Oligonucleotides 24-56 BCL2-like 1 Mus musculus 61-66 7539757-5 1995 We show here that ligation of CD40 rapidly induces the appearance of the bcl-XL protein in WEHI-231, while stimulation via sIgM, sIgD, CD5 or CD45 receptors, or with phorbol esters plus ionomycin does not. Ionomycin 186-195 BCL2-like 1 Mus musculus 73-79 7539757-6 1995 WEHI-231 cells also rapidly undergo massive apoptosis following culture with thapsigargin, a specific inhibitor of the Ca(2+)-ATPase of the endoplasmic reticulum: this is also reversed by anti-CD40, or by overexpression of bcl-XL. Thapsigargin 77-89 BCL2-like 1 Mus musculus 223-229 8774443-5 1996 bcl-x-/- telencephalic cells cultured in 0.5 or 2.0% fetal calf serum (FCS)-containing medium for 48 hr showed increased apoptosis, defined by abnormal bisbenzamide staining and terminal-deoxytransferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL), and decreased numbers of microtubule-associated protein-2-immunoreactive neurons compared with bcl-x+/- and bcl-x+/+ cultures. bisbenzamide 152-164 BCL2-like 1 Mus musculus 0-5 8521409-6 1995 The apoptosis induced by cisplatin treatment or murine ICE overexpression can be suppressed by the tetrapeptide ICE inhibitor Ac-YVAD-CMK or the apoptosis inhibitors bcl-2 or bcl-2-related bcl-XL gene. Cisplatin 25-34 BCL2-like 1 Mus musculus 189-195 8521409-6 1995 The apoptosis induced by cisplatin treatment or murine ICE overexpression can be suppressed by the tetrapeptide ICE inhibitor Ac-YVAD-CMK or the apoptosis inhibitors bcl-2 or bcl-2-related bcl-XL gene. ac-yvad 126-133 BCL2-like 1 Mus musculus 189-195 7602123-4 1995 bcl-xL-transfected cells were also resistant to apoptosis following incubation in low serum medium or exposure to gamma-irradiation, the sphingomyelin ceramide, or compounds that increase intracellular levels of oxidants. sphingomyelin ceramide 137-159 BCL2-like 1 Mus musculus 0-6 33787344-8 2021 In BNL.CL2 cells treated with ABT-737, Gab1 knockdown posttranscriptionally suppressed Bcl-xL expression, and p35-Gab1 overexpression enhanced Bcl-xL expression. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 30-33 BCL2-like 1 Mus musculus 87-93 33787344-8 2021 In BNL.CL2 cells treated with ABT-737, Gab1 knockdown posttranscriptionally suppressed Bcl-xL expression, and p35-Gab1 overexpression enhanced Bcl-xL expression. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 30-33 BCL2-like 1 Mus musculus 143-149 26629039-9 2015 Western blotting results showed that the protein expression levels of Bcl-xL were significantly higher, but the caspase-3 levels were significantly lower in the sevoflurane group than those in the control group and sham group (both P < 0.05). Sevoflurane 161-172 BCL2-like 1 Mus musculus 70-76