综上,西达本胺能够在T-ALL/LBL中抑制HDAC1/2/3的活性,组蛋白H3的乙酰化水平增加,染色质开放;FOXO1蛋白上调且转录活性增加,作为GSDME基因的转录因子,在开放的染色质上与GSDME基因启动子的结合增加,促进GSDME转录上调;GSDME总蛋白表达增加...
GSDME蛋白质属于Gasdermin家族,它与其他成员一样具有一个保守的N端域(N-terminal domain)和一个C端域(C-terminal domain)。GSDME的N端域包含一个疱疹样DNA结合域(pyrin domain, PYD),而C端域则包含一个疱疹样蛋白结合域(pyrin domain, PYD)和一个疱疹样蛋白疱疹样DNA结合域(Gasdermin domain, GSD)。 GSDME的...
储存: -15°C to -25°C/1 year(Do not lower than -25°C) 实测条带: 36 55kD 功能: Cleavage at Asp-270 by CASP3 (mature and uncleaved precursor forms) or granzyme B (GZMB) relieves autoinhibition and is sufficient to initiate pyroptosis. 细胞定位: [Gasdermin-E, N-terminal]: Cell...
Interestingly, GSDME was found to be palmitoylated on its C-terminal (GSDME-C) during chemotherapy-induced pyroptosis, while 2-bromopalmitate (2-BP) could inhibit the GSDME-C palmitoylation and chemotherapy-induced pyroptosis. Mutation of palmitoylation sites on GSDME also diminished the pyroptosis ...
When GSDME is highly expressed, the active caspase-3 cleaves GSDME to the N-terminal domain, which can execute pyroptosis by forming nonselective pores in the membrane, shifting the mode of cell death from apoptosis to pyroptosis [48,49,50]. Shen et al. suggested that activation of caspase-...
1E–H). Additionally, we found that aerobic exercise and Igfbp2 OE could reduce the levels of N-terminal fragment of gasdermin E (N-GSDME) in myocardial cells, suggesting the involvement of GSDME in IGFBP2-mediated regulation of myocardial cell pyroptosis (Fig. 1F and H). Fig. 1 Aerobic...
The non-N-terminal fragment of GSDME within macrophages combines with PDPK1, thereby activating the PI3K-AKT pathway and facilitating M2-like polarization. The small-molecule Eliprodil inhibited the increase in PDPK1 phosphorylation mediated by GSDME site 1. The combination of Eliprodil and anti-...
种属反应性Human,Mouse,Rat 验证应用WB,IHC-P,FC 抗体类型兔多抗 免疫原Recombinant protein within N-terminal human DFNA5/GSDME. 偶联Non-conjugated 性能 形态Liquid 浓度1 mg/mL. 存放说明Store at +4℃ after thawing. Aliquot store at -20℃. Avoid repeated freeze / thaw cycles. ...
cytotoxic GSDME N-terminal fragments are generated after stimulation because of GSDME transcriptional repression, resulting in drug resistance (Fig.3E, F). Intriguingly, decreased protein level but not mRNA level of caspase 3 is also found in Sp1-shRNA or Sp1 inhibitor-treated cells. In contrast,...
Spleen tyrosine kinase promotes NLR family pyrin domain containing 3 inflammasome‑mediated IL‑1β secretion via c‑Jun N‑terminal kinase activation and cell apoptosis during diabetic nephropathy. Mol Med Rep. 2018;18:1995–2008. 56. Rubin JD, Nguyen TV, Allen KL, Ayasoufi K, Barry ...