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S-Nitrosylated protein-disulphide isomerase links protein misfolding to neurodegeneration
TLDR
It is shown that PDI is S-nitrosylated, a reaction transferring a nitric oxide group to a critical cysteine thiol to affect protein function, which prevents neurotoxicity associated with ER stress and protein misfolding in neurodegenerative disorders.
Activation signal of nuclear factor-kappa B in response to endoplasmic reticulum stress is transduced via IRE1 and tumor necrosis factor receptor-associated factor 2.
TLDR
Results suggest that ER stress-induced NF-kappaB activation is also mediated by the IRE1-TRAF2 pathway, as well as JNK activation.
Loss of HRD1-Mediated Protein Degradation Causes Amyloid Precursor Protein Accumulation and Amyloid-β Generation
TLDR
The results suggest that the breakdown of HRD1-mediated ERAD causes Aβ generation and ER stress, possibly linked to AD.
Microglial activation and amyloid-beta clearance induced by exogenous heat-shock proteins.
TLDR
It is shown that heat-shock proteins, such as HSP90, HSP70, and HSP32, induce the production of interleukin 6 and tumor necrosis factor alpha and increase the phagocytosis and clearance of Abeta peptides, suggesting that HSP-induced microglial activation may serve a neuroprotective role by facilitating Abeta clearance and cytokine production.
Brain stem is a direct target for leptin's action in the central nervous system.
TLDR
It is reported here that peripherally applied leptin increased STAT3 phosphorylation not only in the hypothalamus but also in the brain stem as assessed by Western blotting, and suggested that circulating leptin may directly act in thebrain stem to elicit autonomic and neuroendocrine control of food intake and energy expenditure.
Sodium 4-Phenylbutyrate Protects against Cerebral Ischemic Injury
TLDR
The results indicate that 4-PBA could protect against cerebral ischemia through inhibition of ER stress-mediated apoptosis and inflammation, and its use as a chemical chaperone would provide a novel approach for the treatment of stroke.
Protective effects of the antiparkinsonian drugs talipexole and pramipexole against 1-methyl-4-phenylpyridinium-induced apoptotic death in human neuroblastoma SH-SY5Y cells.
TLDR
Talipexole has dual actions: (1) it directly scavenges ROS, affording slight protection against MPP+-induced apoptosis, and (2) it induces Bcl-2 expression, thereby affording more potent protection, if it is administrated before MPP+.
Suppressive effects of 4‐phenylbutyrate on the aggregation of Pael receptors and endoplasmic reticulum stress
TLDR
Results suggest that 4‐PBA suppresses ER stress by directly reducing the amount of misfolded protein, including Pael‐R accumulated in the ER.
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