phosphorylated bcl 2 associated death promoter p bad (Cell Signaling Technology Inc)
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Phosphorylated Bcl 2 Associated Death Promoter P Bad, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 131 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Incubation:Article Title: PROM2 promotes gemcitabine chemoresistance via activating the Akt signaling pathway in pancreatic cancer Article Snippet: Cell lysates were separated by 10% sodium dodecyl sulfate-polyacrylamide gel electrophoresis and then transferred to polyvinylidene fluoride membranes (Millipore, Billerica, MA, USA). .. The membranes were incubated with antibodies against PROM2 (1:500, Abcam, Cambridge, MA, USA), p-Akt (Ser473) (1:2000, Cell Signaling Technology, Danvers, MA, USA), Akt1 (1:1000, Cell Signaling Technology), Isolation:Article Title: Sweroside attenuates podocyte injury and proteinuria in part by activating Akt/BAD signaling in mice. Article Snippet: Funding information Science and Technology Plan Project of Huaihua, Grant/Award Number: 2021R3103; Hunan Provincial Natural Science Foundation of China, Grant/Award Number: 2023JJ50434; Scientific Research Fund of Hunan Provincial Education Department, Grant/Award Number: 22A0705; Doctoral Scientific Research Foundation of Hunan University of Medicine, Grant/Award Number: 2020122001 Abstract In this study, we investigated the effects of sweroside on podocyte injury in diabetic nephropathy (DN) mice and elucidated its molecular mechanisms.. We conducted in vivo experiments using a C57BL/6 mice model of DN to explore the effects of sweroside on proteinuria and podocyte injury in DN mice.. In in vitro experiments, conditionally immortalized mouse podocytes were treated with high glucose and sweroside, and the protective effects of sweroside on podocyte injury were analyzed. other:Article Title: ROR1 Regulates Chemoresistance in Triple Negative Breast Cancer and Can Be Targeted with Strictinin for Selective Anti-Cancer Therapy Article Snippet: BT—549 cells were cultured in RPMI (Lonza, Basel, Switzerland), with FBS (10%), insulin (’lOug/ml), and penicillin (100 U/ml) and streptomycin (0.1 mg/ml). |
![Figure 4. PGG inhibits ROR1 intracellular domain phosphorylation, ROR1 expression, down- stream oncogenic signaling, and anti-apoptotic signaling in PC3 cells. (A) Representative western blot of phospho-ROR1 (Tyr786) and ROR1 on PC3 cells treated with vehicle or 31.25 µM PGG for 24 h. (B) Quantification of immunoblot bands phospho-ROR1 (Tyr786) and ROR1, all nor- malized to GAPDH. Data are expressed as the mean +/−SEM from three independent western blots. (C) Representative western blot of phospho-AKT (ser473), phospho-GSK3β (ser9), AKT, and GSK3β on PC3 cells treated with vehicle or 31.25 µM PGG for 24 h. (D) Quantification of im- munoblot bands phospho-AKT (ser473), phospho-GSK3β (ser9), AKT, and GSK3β, all normalized to GAPDH. (E) Representative western blot of apoptotic markers XIAP, phospho-Bad <t>(ser136),</t> and Bad after treatment of PC3 cells with vehicle or 31.25 µM PGG for 24 h. (F) Quantification of immunoblot bands XIAP, phospho-Bad (ser136), and Bad, all normalized to GAPDH. Data are ex- pressed as the mean +/−SEM from three independent western blots. [N = 3. *** = p value < 0.001; * = p value < 0.05; ns = not significant].](https://pub-med-unpaywalled-images-cdn.bioz.com/pub_med_ids_ending_with_0112/pm39000112/pm39000112__page7_image1.jpg)