DNA damage triggers tubular endoplasmic reticulum extension to promote apoptosis by facilitating ER-mitochondria signaling
نویسندگان
چکیده
منابع مشابه
Effects of targeted Bcl-2 expression in mitochondria or endoplasmic reticulum on renal tubular cell apoptosis.
Bcl-2 family proteins are central regulators of apoptosis. As the prototypic member, Bcl-2 protects various types of cells against apoptotic insults. In mammalian cells, Bcl-2 has a dual subcellular localization, in mitochondria and endoplasmic reticulum (ER). The respective roles played by mitochondrial and ER-localized Bcl-2 in apoptotic inhibition are unclear. Using Bcl-2 constructs for targ...
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BACKGROUND Both endoplasmic reticulum (ER) stress, a fundamental cell response associated with stress-initiated unfolded protein response (UPR), and loss of Klotho, an anti-aging hormone linked to NF-κB-induced inflammation, occur in chronic metabolic diseases such as obesity and type 2 diabetes. We investigated if the loss of Klotho is causally linked to increased ER stress. METHODS We treat...
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OBJECTIVES Manganese chloride (MnCl(2)) is one of heavy metals for causing neurogenerative dysfunction like Manganism. The purpose of this study was to determine the acute toxicity of MnCl(2) using different times and various concentrations including whether manganese toxicity may involve in two intrinsic pathways, endoplasmic reticulum (ER) stress and mitochondria dysfunction and lead to neuro...
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The endoplasmic reticulum (ER) is a central organelle entrusted with lipid synthesis, protein folding and protein maturation. It is endowed with a quality control system that facilitates the recognition and targeting of aberrant proteins for degradation. When the capacity of this quality control system is exceeded, a stress response (ER stress) is switched on. Prolonged stress leads to apoptosi...
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Hepatic insulin resistance is a key feature of type 2 diabetes, and the consequent dysregulation of glucose and lipid output from the liver are important contributors to the observed hyperglycemia and hyperlipidemia. While excessive lipid accumulation (1) and defective signaling by protein kinase C (2) have been implicated in the past, the full panoply of molecular mechanisms involved is still ...
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ژورنال
عنوان ژورنال: Cell Research
سال: 2018
ISSN: 1001-0602,1748-7838
DOI: 10.1038/s41422-018-0065-z