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依赖ALPK1的cIAP1降解调节幽门螺杆菌诱导的细胞凋亡。

ALPK1-Dependent cIAP1 Degradation Regulates Helicobacter pylori-Induced Apoptosis.

作者信息

Maubach Gunter, Lim Michelle C C, Naumann Michael

机构信息

Medical Faculty, Otto von Guericke University, Institute of Experimental Internal Medicine, Magdeburg, Germany.

出版信息

FASEB J. 2025 May 31;39(10):e70593. doi: 10.1096/fj.202500764R.

Abstract

Helicobacter pylori infection poses a significant risk for disrupting the gastric epithelium by inducing inflammation and apoptosis. Here, we identify alpha kinase 1 (ALPK1) as essential in H. pylori-induced apoptosis. The absence of ALPK1 leads to the accumulation of cellular inhibitor of apoptosis 1 (cIAP1) upon H. pylori infection, which raises the threshold for the induction of apoptosis. Ablation of cIAP1 with a SMAC-mimetic restores the level of apoptosis induced by H. pylori in these cells. Our findings highlight the impact of ALPK1 on the stability of cIAP1, influencing H. pylori-induced apoptosis.

摘要

幽门螺杆菌感染通过引发炎症和细胞凋亡对胃上皮造成重大风险。在此,我们确定α激酶1(ALPK1)在幽门螺杆菌诱导的细胞凋亡中至关重要。缺乏ALPK1会导致幽门螺杆菌感染后细胞凋亡抑制蛋白1(cIAP1)积累,从而提高细胞凋亡诱导阈值。用一种SMAC模拟物消除cIAP1可恢复幽门螺杆菌在这些细胞中诱导的细胞凋亡水平。我们的研究结果突出了ALPK1对cIAP1稳定性的影响,进而影响幽门螺杆菌诱导的细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/272b/12070357/9891191bd22a/FSB2-39-e70593-g002.jpg

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