Cell death was assessed using FluoroJade C (FJC) staining and the expression of the p38 mitogen-activated protein kinase (p38), phosphorylated-c-Jun amino-terminal kinase (p-JNK), c-Jun amino-terminal kinase (JNK), protein kinase B (Akt), phosphorylated-protein kinase B (p-Akt), glycogen synthase kinase-3β (Gsk3β), B-cell lymphoma 2 (Bcl2) and Bcl2-associated X protein (Bax) protein were measured by Western blotting.
There were decreases of B cell lymphoma-2 (Bcl-2)-associated X protein (Bax), Caspase-3, and Caspase-8 expressions but increases in Bcl-2 induced by silenced HSG.
The B16 cells were cultured in various concentrations of LY-15 (5, 15 and 25 µM), and the ameliorating effect of LY-15 was evaluated using apoptotic protein markers B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3 and caspase-9.
The effects of cisplatin include activation of caspases, proteolysis of enzyme poly ADP ribose polymerase (PARP), control of apoptosis modulators B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and BH3-interacting domain death agonist (Bid), and cell cycle arrest in G2/M phase.
Diabetes-related physical and biochemical parameters, pancreatic histopathological changes, immunohistochemical staining, quantitative real-time polymerase chain reaction, and western blot were used to measure the expression of apoptosis signal-regulating kinase 1 (ASK1), Jun N-terminal kinase (JNK), Bcl-2 associated X protein (BAX), and B-cell lymphoma-2 (Bcl-2).
Notably, western blot results suggested that this antioxidant reduced the expression levels of apoptosis‑related proteins cytochrome c and B‑cell lymphoma‑2 (Bcl‑2)‑associated X protein, whereas the anti‑apoptotic protein Bcl‑extra large was increased following MitoQ10 treatment.
The differential proteins were verified to be B cell lymphoma‑2 associated X, apoptosis regulator (Bax)‑α, apoptosis‑associated speck‑like protein containing a CARD (ASC) and myeloid cell leukemia sequence (Mcl)‑1.
Western blot analysis was conducted to detect protein expression of ERα36; tau protein; phosphorylated- tau (p-tau) at site Thr231 [p-tau (Thr231)]; glycogen synthase kinase (GSK)3β and its specificity sites (Tyr216 and Ser9); Cyclin Dl; proliferating cell nuclear antigen (PCNA); B-cell lymphoma (Bcl)-2; and Bcl-2-associated X protein (Bax).
Western blot analysis was performed to assess changes in the levels of proteins, including B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3, Akt and phosphorylated Akt.
The protein expression levels of apoptosis-related genes, including B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), C-Caspase and T-Caspase, were detected via Western blotting.
Western blot analysis showed that QLQX significantly reduced the expressions of AngII, non-phagocytic cell oxidase (NOX)2, and B-cell lymphoma (Bcl)2 associated X protein (Bax), and increased the expressions of Bcl2 and Angiotensin II Type 1 receptor (ATR) in the kidney as compared with the CRS-C group.
B-cell lymphoma 2 (BCL2) and BCL2-associated X protein (BAX) proteins are anti-apoptotic and pro-apoptotic determinants of mitochondrial-mediated apoptosis, and their relative expression determines the cell fate.
The protein expression of phosphorylated (p)‑AKT and caspase 3, B‑cell lymphoma 2 (Bcl2) and Bcl‑2‑associated X protein apoptosis‑associated genes, were detected using western blotting.
Apoptosis markers, including B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein (Bax), caspase‑3, caspase‑8 and caspase‑9 were estimated by western blot analysis at various time points.
Furthermore, the effects of bufalin on the expression of potential genes involved in MDR of BEL-7402/5-FU cells, including thymidylate synthase (TS), P-glycoprotein (P-gp), multidrug resistance protein 1 (MRP1), B-cell lymphoma-extra large (Bcl-xL) and Bcl-2-associated X protein (Bax), were determined using real-time PCR and western blot analysis.
Alterations in the apoptosis-related regulators B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), Bcl-2-interacting mediator of cell death (Bim), apoptotic protease-activating facter-1 (Apaf-1), caspase-9 and caspase-3 were determined using reverse transcription-polymerase chain reaction (PCR) and quantitative PCR methods.
The protein expression of PRMT6, H3R2me2a, and H3K4me3 in human and mouse samples, as well as B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), and endothelial nitric oxide synthase (eNOS) in mice were detected in lung homogenates by Western blotting.
Western blot analysis analyzed p53 and B‑cell lymphoma 2 (Bcl‑2)‑associated X protein/Bcl‑2, and induced the expression of peroxisome proliferator‑activated receptor‑γ (PPAR‑γ).
The increased mRNA and protein expression of the pro‑fibrogenic factors collagen I, connective tissue growth factor and α‑smooth muscle actin (SMA) stimulated by TGF‑β1 were reduced by eRF3b‑37 via the following mechanisms: i) Inhibiting LX‑2 cell proliferation, leading to G0/G1 cell cycle arrest and inhibition of DNA synthesis by downregulating the mRNA expressions of Cyclin D1 and cyclin dependent kinase‑4, and upregulating the levels of P21; ii) increasing cell apoptosis by upregulating the mRNA level of B‑cell lymphoma-2 (Bcl‑2)‑associated X protein (Bax) and Fas, and downregulating the expression of Bcl‑2; and iii) reducing cell migration by downregulating the mRNA and protein expression of α‑SMA.
The nature of adaptable change of B-cell lymphoma-2 (BCL-2) and/or Bcl2-associated X protein (BAX) gene expression in the human peripheral blood mononuclear cells (PBMCs) irradiated by radioiodine in thyroid diseases therapy is not fully understood.
The expression levels of apoptosis-related proteins B cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3, and poly-ADP-ribose polymerase 1 (PARP1) were analyzed in both in vivo and in vitro models.
Western blot was used to estimate the expression level of death receptor-5 (DR5), Fas-associated protein with death domain (FADD), caspase 8, B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax).
Furthermore, the expression levels of apoptosis-related proteins, including B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and phosphorylated (p)-p53, and angiogenesis-related proteins, including vascular endothelial growth factor (VEGF) and angiopoietin 2 (Ang-2), were measured by RT-qPCR and western blotting.
Overexpression of Fmr1 attenuated LPS-associated increases in the apoptosis-activating factors B-cell lymphoma 2 (Bcl-2)-associated X protein and caspase-3 and decreases in apoptosis inhibitors, including Bcl-2 and X-linked inhibitor of apoptosis protein.