MLKL polymerization-induced lysosomal membrane …
2023年11月23日 · Our study demonstrates that upon induction of necroptosis, activated MLKL translocates to and polymerizes on the lysosomal membrane. MLKL polymerization-induced …
【小优细节君】坏死性凋亡之MLKL检测经验分享 - 知乎
mlkl是tnf（肿瘤坏死因子）诱导的坏死性凋亡过程中的关键靶标，它作为ripk1和ripk3下游的效应蛋白发挥作用。 RIPK3在Ser227位点被磷酸化，此磷酸化为MLKL激活所必需。
MLKL Requires the Inositol Phosphate Code to Execute Necroptosis
2018年6月7日 · Here, using an unbiased, genome-scale screening approach, we identified an essential role for the kinase-dependent inositol phosphate (IP) messenger pathway in …
Direct Activation of Human MLKL by a Select Repertoire of Inositol ...
2019年6月20日 · We propose that the combined effects of IP 4, IP 5, and IP 6 are essential for necroptotic induction by human MLKL and genetically implicate inositol pentakisphosphate 2 …
phosphate (IP) messenger pathway in execution of necroptosis by MLKL. We show that IP kinases are critical for necroptosis induced by cytokine-dependent death receptor activation …
MLKL: Functions beyond serving as the Executioner of Necroptosis
2022年3月1日 · This process requires several inositol phosphate (IP) (e.g., IP 4, IP 5 and IP 6) and inositol pentakisphosphate 2-kinase, which transforms IP 5 into IP 6 31. Conversely, …
Sequential Engagement of Distinct MLKL ... - Cell Press
2016年2月18日 · Plasma membrane recruitment involves engagement of low-affinity phosphatidylinositol phosphate (PIP)-binding sites followed by a higher-affinity PIP-binding site …
A toolbox for imaging RIPK1, RIPK3, and MLKL in mouse and ... - Nature
2021年2月15日 · Here, we describe a toolbox of antibodies for immunofluorescent detection of the core necroptosis effectors, RIPK1, RIPK3, and MLKL, and their phosphorylated forms, in …
重组MLKL磷酸化抗体pS345[EPR9515(2)](ab196436)|Abcam
IP: L929 whole cell lysate treated with TNF alpha (ab9642) + Smac mimetic + z-VAD (ab120382) compound for 8h. This antibody was developed through collaboration with the lab of Xiaodong …
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CNS前沿文献追踪 – 追踪程序性坏死过程中MLKL行为|pMLKL|程序 …
2020年6月29日 · 用mb37封住mlkl和膜互作的位点后，tsi诱导的mlkl、pmlkl聚集、膜损伤现象消失 作者又用NSA封住MLKL和膜互作的位点，发现NSA抑制了MLKL的寡聚、膜转位、pMLKL聚 …