However, P2X7R knockdown aggravated osteoprotegerin-induced osteoclast adhesion damage via Ca2+ signaling. In conclusion, the P2X7R鈥揅a2+ NFATc1 signaling pathway has a key functional role in osteoprotegerin-induced osteoclast adhesion structure damage....
通讯作者:伊正君ꎬ电子信箱:ｙｉｚｈｅｎｇｊｕｎ＠１２６.ｃｏｍ Ｐ２Ｘ７Ｒ在结核分枝杆菌感染中的作用研究进展 赵荣兰㊀彭效祥㊀伊正君 摘㊀要㊀结核病是一种全球范围内的人畜共患病ꎬ由结核分枝杆菌(ＭｙｃｏｂａｃｔｅｒｉｕｍｔｕｂｅｒｃｕｌｏｓｉｓꎬＭＴＢ)引起ꎬ其防治形势日趋严峻ꎮ嘌呤能离子...
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Song S, Jacobson KN, McDermott KM, Reddy SP, Cress AE, Tang H, Dudek SM, Black SM, Garcia JG, Makino A, Yuan JX (2016) ATP promotes cell survival via regulation of cytosolic [Ca2+] and Bcl-2/Bax ratio in lung cancer cells. Am J Physiol Cell Physiol 310:C99–114. https://doi...
当ATP短暂或低浓度刺激时,被激活的P2X7R可以形成阳离子通道,使Na+、Ca2+内流和K+外流。当P2X7R受到ATP持续或高浓度刺激时,成为ATP敏感的P2X7R,在细胞膜上形成非选择性膜孔,允许分子量< 900 Da的大分子和阳离子通过,导致细胞死亡,因此P2X7R又被称为细胞死亡受体[15,19-20]。 2 P2X7R与RA 2.1 P2X7R表达...
Stimulation of P2X7 receptors elevates Ca2+ and kills retinal ganglion cells. Invest Ophthalmol Vis Sci. 2005;46(6):2183–2191. doi:10.1167/iovs.05-0052 11. Suzuki T, Hide I, Ido K, Kohsaka S, Inoue K, Nakata Y. Production and release of neuroprotective tumor ...
When there is ATP binding, P2X7R is gated to the open state to allow the influx of Ca2+ and Na+ ions and the efflux of K+ from cells (Khakh and North, 2006), and results in rapid depolarization of the cells. P2X7R can also promote the release of pro-inflammatory cytokines, ...
嘌呤受体P2X7是一种离子型配体门控通道受体,由配体ATP激活后,可使离子通道开放,促进Ca2+、Na+内流以及K+外流,进而介导一系列细胞信号转导,如可激活核苷酸结合寡聚化结构域样受体3(NLRP3、NLR炎性体家族中的重要一员),核转录因子kB(NF-kB)、转化生长因子-β(TGF-β)等多条通路,诱导成熟白细胞介素IL-1β...
目的观察黑逍遥散对阿尔茨海默病(AD)小鼠海马神经元Ca2+浓度和钙调蛋白(Ca M),钙调蛋白依赖性激酶Ⅱα(Ca MKⅡα)表达的影响.方法 30只APP/PS1双转基因雄性小鼠称重后... 马春林,吴红彦,兰美华,... - 《中国中医药信息杂志》 被引量: 0发表: 2019年 黑逍遥散对APP/PS1双转基因小鼠海马CREB1蛋白及其磷...
Interestingly, Di Virgilio and colleagues reported that amyloidβ peptide (Aβ25–35) triggered increases in intracellular Ca2+, IL-1β release, and plasma membrane permeabilization in microglia derived from wild-type but not P2X7R-deficient mice [2]. However, the results of this study, although...