有研究表明EA可诱导人脐静脉内皮细胞的动脉粥样硬化;通过促进炎症和氧化应激(OS)加速小鼠动脉粥样硬化;可诱导多种细胞凋亡,增加糖尿病小鼠的内质网应激(ERS)和OS,并激活巨噬细胞中的NLRP3炎性小体,但其在慢性疾病中的具体致病机制有待...
Intracellular Ca2+ increase by ω-3 PUFAs in human colonic epithelial cells Because FFA4 couples to G proteins and increases [Ca2+]i in FFA4-overexpressing cells, this Ca2+ response was measured in colonic epithelial cells endogenously expressing FFA4. As shown Figure 2A, the ω-3 PUFAs, ...
DNA 复制压力应激反应(replication stress response)是细胞应对复制压力的重要机制, 应答失败是造成癌细胞中基因突变和基因组不稳定的主要原因之一。 圣路易斯华盛顿大学医学院(Washington University in St. Louis, School of Medicine)尤忠...
内质网应激(ER stress)是由于内源或外源的刺激(如Ca2+稳态的破坏、病毒感染和氧化还原平衡等)导致内质网中错误折叠蛋白的积累而引发。为了应对细胞遭受的内质网应激,细胞会产生未折叠蛋白反应(Unfolded protein response, UPR)[1]。细胞通过启动UPR来抑制翻译过程,减弱蛋白质合成从而减轻内质网蛋白合成负担、同时促进内质网...
[5] J. Shan, A. Kushnir, M.J. Betzenhauser, S. Reiken, J. Li, S.E. Lehnart, N. Lindegger, M. Mongillo, P.J. Mohler, A.R. Marks, Phosphorylation of the ryanodine receptor mediates the cardiac fight or flight response in mice, J Clin Invest, 120 (2010) 4388-4398. ...
c, Ca2+ concentration response curves of Gi3, Gq and Gs activation by CaSRΔ894 using the BRET-based G-protein-activation assay. d, G-protein-activation assays measuring the functional responses of 15 Gα subtypes by full-length CaSR (WT) and CaSRΔ894 after stimulation with 10 mM...
(3D representative of calcium transients in 300 s over defined threshold level, Line 4CX1), and their significant change showing the spontaneous Ca2+ transient activity of the cells and their response after the application of DL-AP5 (50 μM, a) and CNQX (50 μM, b), Nifedipine (...
BclxL-ER evoked a CD95-mediated cytosolic Ca2+ response similar to that in MEFs reconstituted with BclxL-WT (Figure 2b). By contrast, BclxL-MT failed to restore the cytosolic Ca2+ response in these cells (Figure 2b). Importantly, although MEFBclxL−/− did not migrate in the ...
[5] J. Shan, A. Kushnir, M.J. Betzenhauser, S. Reiken, J. Li, S.E. Lehnart, N. Lindegger, M. Mongillo, P.J. Mohler, A.R. Marks, Phosphorylation of the ryanodine receptor mediates the cardiac fight or ...
These observations molecularly define a feature ofthe inflammatory response to hemodynamic overload that protects against heart failure development. Inflammation’s beneficial traits need to be consideredwhen developing inflammation as a...