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Cleavage of BID by Caspase 8 Mediates the Mitochondrial Damage in the Fas Pathway of Apoptosis
Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-β
It is shown that caspase-12 is localized to the ER and activated by ER stress, including disruption of ER calcium homeostasis and accumulation of excess proteins in ER, but not by membrane- or mitochondrial-targeted apoptotic signals, which may contribute to amyloid-β neurotoxicity.
Somatic mutations of the mitochondrial genome in human colorectal tumours
It is shown that mitochondria can rapidly become homogeneous in colorectal cancer cells using cell fusions and provide the first examples of homoplasmic mutations in the mtDNA of tumour cells, which have potential implications for the abnormal metabolic and apoptotic processes in cancer.
Murine Caspase-11, an ICE-Interacting Protease, Is Essential for the Activation of ICE
The PHD Finger of the Chromatin-Associated Protein ING2 Functions as a Nuclear Phosphoinositide Receptor
RIPK1 mediates axonal degeneration by promoting inflammation and necroptosis in ALS
It is found that optineurin actively suppressed receptor-interacting kinase 1 (RIPK1)–dependent signaling by regulating its turnover, and inhibiting RIPK1 kinase may provide an axonal protective strategy for the treatment of ALS and other human degenerative diseases characterized by axonal degeneration.
Small molecule regulators of autophagy identified by an image-based high-throughput screen
- Lihong Zhang, Jia Yu, Junying Yuan
- BiologyProceedings of the National Academy of Sciences
- 27 November 2007
The identification of eight compounds that can induce autophagy and promote long-lived protein degradation are identified and the possibility that some of these drugs may be useful for the treatment of Huntington's and other human diseases associated with the accumulation of misfolded proteins is suggested.
Ich-1, an Ice/ced-3-related gene, encodes both positive and negative regulators of programmed cell death
Dissecting eIF4E action in tumorigenesis.
Insight is provided into how eIF4E contributes to tumorigenesis and a level of translational control that may be suitable for therapeutic intervention is pinpointed.
Oxidative stress and redox signaling mechanisms of inflammatory bowel disease: updated experimental and clinical evidence
The sources of ROS/RNS and the redox signaling mechanism underlying oxidative stress and inflammation in IBD are discussed and the potential of using antioxidant compounds as promising therapeutic modalities of human IBD is pointed to.