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...
细胞定位: [Gasdermin-E, N-terminal]: Cell membrane ; Multi-pass membrane protein .; [Gasdermin-E]: Cytoplasm, cytosol . 组织表达: Expressed in cochlea (PubMed:9771715). Low level of expression in heart, brain, placenta, lung, liver, skeletal muscle, kidney and pancreas, with highest expre...
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...
细胞焦亡的关键效应因子―GSDMs 家族 | 细胞焦亡 (Pyroptosis) 是一种裂解性的细胞程序性死亡,由gasdermin (GSDM) 蛋白受上游信号激活后释放其 N 端结构域在细胞膜上打孔引发,具有高度促炎的免疫学特征。 人类GSDMs 蛋白家族拥有 6名成员,包括 GSDMA、GSDMB、GSDMC、GSDMD、GSDME ( 又名 DFNA5) 和 DFNB59 (...
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-...
熔点: 密度: 储存条件:-20℃ Anti-DFNA5/GSDME antibody 概述 产品描述Plays a role in the TP53-regulated cellular response to DNA damage probably by cooperating with TP53. Gasdermin-E, N-terminal: Switches CASP3-mediated apoptosis induced by TNF or danger signals, such as chemotherapy drugs, to ...
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...
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-...
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,...
chemotherapy agents [22]. Caspase-3 was previously regarded as one of the primary apoptosis biomarkers. Interestingly, emerging evidence reveals that caspase-3 specifically splits GSDME at the linker region, thereby releasing the N-terminal domain and generate membrane holes [23]. This process leads...