PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18455702-7 2008 Our results also show that quercetin decreases the Bcl-xL:Bax ratio and increases translocation and multimerization of Bax to the mitochondrial membrane. Quercetin 27-36 BCL2 like 1 Homo sapiens 51-57 18455702-6 2008 Protein interaction assay revealed that during treatment with quercetin, Bcl-xL dissociated from Bax and then associated with Bad. Quercetin 62-71 BCL2 like 1 Homo sapiens 73-79 18455702-11 2008 Our results indicate that the apoptotic processes caused by quercetin are mediated by the dissociation of Bax from Bcl-xL and the activation of caspase families in human prostate cancer cells. Quercetin 60-69 BCL2 like 1 Homo sapiens 115-121 18359480-3 2008 Co-treatment with ATO plus quercetin caused mitochondrial transmembrane potential dissipation, stimulated the mitochondrial apoptotic pathway, as indicated by cytochrome c and Omi/Htra2 release, XIAP and Bcl-X(L) down-regulation, and Bax activation, and caused caspase-8/Bid activation. Quercetin 27-36 BCL2 like 1 Homo sapiens 204-212 31827702-1 2019 A flavonoid antioxidant quercetin promotes dose-dependent activation of the ATM-CHK-p53 pathway, downregulation of antiapoptotic survivin, and upregulation of proapoptotic NOXA in human T cell acute lymphoblastic leukemia Jurkat clones (J/Neo and J/BCL-XL). Quercetin 24-33 BCL2 like 1 Homo sapiens 249-255 16898267-7 2006 In quercetin-treated PC-3 cells, an increase in Bax protein expression and a decrease in Bcl-x(L) protein and Bcl-2 protein were observed. Quercetin 3-12 BCL2 like 1 Homo sapiens 89-97 34311541-6 2021 The most appreciated route of quercetin effect on prostate cancer cells is the detachment of Bax from Bcl-xL and the stimulation of caspase families. Quercetin 30-39 BCL2 like 1 Homo sapiens 102-108 31827702-4 2019 Both cytosolic and mitochondrial ROS levels were elevated in quercetin-treated J/Neo cells; however, the ROS elevations were almost completely abrogated in J/BCL-XL cells, suggesting the ROS elevations were downstream of BCL-XL-sensitive mitochondrial damage and dysfunction. Quercetin 61-70 BCL2 like 1 Homo sapiens 158-164 31827702-4 2019 Both cytosolic and mitochondrial ROS levels were elevated in quercetin-treated J/Neo cells; however, the ROS elevations were almost completely abrogated in J/BCL-XL cells, suggesting the ROS elevations were downstream of BCL-XL-sensitive mitochondrial damage and dysfunction. Quercetin 61-70 BCL2 like 1 Homo sapiens 221-227 28902204-0 2017 Rational design and structure-activity relationship studies of quercetin-amino acid hybrids targeting the anti-apoptotic protein Bcl-xL. Quercetin 63-72 BCL2 like 1 Homo sapiens 129-135 30991286-9 2019 Moreover, in vitro experiments showed that rhein, kaempferol and quercetin treatments remarkably decreased the protein levels of cleaved caspase-3 and increased p-ERK1/2, PI3K and Bcl-XL protein expression in TNF-alpha-stimulated L02 cells. Quercetin 65-74 BCL2 like 1 Homo sapiens 180-186 31362681-8 2019 On the other hand, RT-PCR results showed a reduction in some of the candidate genes expression, especially HSP70, Bcl-X(L) and FOXM1, when cells were treated with quercetin 40 and 80microM. Quercetin 163-172 BCL2 like 1 Homo sapiens 114-122 30152185-5 2018 Results from western blotting showed that quercetin decreased anti-apoptotic protein of Mcl-1, Bcl-2, and Bcl-x but increased pro-apoptotic protein of Bad, Bax, and Bid. Quercetin 42-51 BCL2 like 1 Homo sapiens 106-111 29472583-5 2018 Quercetin and green tea reduced tumor growth in HL-60 xenografts accompanied by decreased expression of anti-apoptotic proteins, BCL-2, BCL-XL and MCL-1 and increased expression of BAX, a pro-apoptotic protein. Quercetin 0-9 BCL2 like 1 Homo sapiens 136-142 28902204-4 2017 Herein, Induced Fit Docking (IFD) and Molecular Dynamics (MD) simulations were performed to rationally design quercetin analogues that bind in the BH3 site of the Bcl-xL protein. Quercetin 110-119 BCL2 like 1 Homo sapiens 163-169 28902204-6 2017 The quercetin analogues were synthesized and their binding to Bcl-xL was verified with fluorescence spectroscopy. Quercetin 4-13 BCL2 like 1 Homo sapiens 62-68 28902204-8 2017 2D 1H-15N HSQC NMR chemical shift perturbation mapping was used to chart the binding site of the quercetin analogues in the Bcl-xL that overlapped with the predicted poses generated by both IFD and MD calculations. Quercetin 97-106 BCL2 like 1 Homo sapiens 124-130 25211642-4 2014 It may be concluded that, quercetin binds directly to the BH3 domain of Bcl-2 and Bcl-xL proteins, thereby inhibiting their activity and promoting cancer cell apoptosis. Quercetin 26-35 BCL2 like 1 Homo sapiens 82-88 25084985-4 2014 In addition, the simultaneous treatments for 24 h with quercetin plus ELF-MF increased Bcl-2 protein expression and prevented quercetin-induced downregulation of Mcl-1 and Bcl-xL. Quercetin 55-64 BCL2 like 1 Homo sapiens 172-178 25293876-3 2014 Quercetin caused pronounced apoptosis in P39 leukemia cells, followed by Bcl-2, Bcl-xL, Mcl-1 downregulation, Bax upregulation, and mitochondrial translocation, triggering cytochrome c release and caspases activation. Quercetin 0-9 BCL2 like 1 Homo sapiens 80-86 25084985-4 2014 In addition, the simultaneous treatments for 24 h with quercetin plus ELF-MF increased Bcl-2 protein expression and prevented quercetin-induced downregulation of Mcl-1 and Bcl-xL. Quercetin 126-135 BCL2 like 1 Homo sapiens 172-178