(Q93003125)

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PACS2 is required for ox-LDL-induced endothelial cell apoptosis by regulating mitochondria-associated ER membrane formation and mitochondrial Ca2+ elevation

scientific article published on 07 April 2019

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3 May 2020

PACS2 is required for ox-LDL-induced endothelial cell apoptosis by regulating mitochondria-associated ER membrane formation and mitochondrial Ca2+ elevation (English)

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3 May 2020

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Sanjiu Yu

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3 May 2020

Laiping Zhang

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Chuan Liu

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Jie Yang

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Jihang Zhang

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Lan Huang

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7 April 2019

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3 May 2020

Experimental Cell Research

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191-202

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3 May 2020

Epidemiology of Atherosclerosis and the Potential to Reduce the Global Burden of Atherothrombotic Disease.

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Oxidized LDL-induced injury and apoptosis in atherosclerosis. Potential roles for oxysterols

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Store-operated calcium entry-activated autophagy protects EPC proliferation via the CAMKK2-MTOR pathway in ox-LDL exposure

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Ca2+ hot spots on the mitochondrial surface are generated by Ca2+ mobilization from stores, but not by activation of store-operated Ca2+ channels.

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Structural and functional features and significance of the physical linkage between ER and mitochondria.

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Chronic enrichment of hepatic endoplasmic reticulum-mitochondria contact leads to mitochondrial dysfunction in obesity

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FTY720 inhibits the activation of pancreatic stellate cells by promoting apoptosis and suppressing autophagy via the AMPK/mTOR pathway.

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α-Synuclein binds to the ER-mitochondria tethering protein VAPB to disrupt Ca2+ homeostasis and mitochondrial ATP production

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mTORC1 inhibitor rapamycin and ER stressor tunicamycin induce differential patterns of ER-mitochondria coupling

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Mitochondrial calcium signalling and cell death: approaches for assessing the role of mitochondrial Ca2+ uptake in apoptosis

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Calcium elevation in mitochondria is the main Ca2+ requirement for mitochondrial permeability transition pore (mPTP) opening.

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Mitochondrial Ca2+ transport in the endothelium: regulation by ions, redox signalling and mechanical forces.

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PACS-2 controls endoplasmic reticulum-mitochondria communication and Bid-mediated apoptosis

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Endothelial cell apoptosis: biochemical characteristics and potential implications for atherosclerosis

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Redox Nanodomains Are Induced by and Control Calcium Signaling at the ER-Mitochondrial Interface

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Fis1 and Bap31 bridge the mitochondria-ER interface to establish a platform for apoptosis induction

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Trafficking of TRPP2 by PACS proteins represents a novel mechanism of ion channel regulation

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Akt and 14-3-3 control a PACS-2 homeostatic switch that integrates membrane traffic with TRAIL-induced apoptosis

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Oxidized low-density lipoprotein elicits an intracellular calcium rise and increases the binding activity of the transcription factor NFAT.

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Cellular inhibitor of apoptosis (cIAP)-mediated ubiquitination of phosphofurin acidic cluster sorting protein 2 (PACS-2) negatively regulates tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) cytotoxicity

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Identifiers

10.1016/J.YEXCR.2019.04.002

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Europe PubMed Central

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3 May 2020

1 reference

Europe PubMed Central

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3 May 2020

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