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Dual roles of NF-κB in cell survival and implications of NF-κB inhibitors in neuroprotective therapy

  
@article{APS3710,
	author = {Zheng-hong Qin and Lu-yang Tao and Xin Chen},
	title = {Dual roles of NF-κB in cell survival and implications of NF-κB inhibitors in neuroprotective therapy},
	journal = {Acta Pharmacologica Sinica},
	volume = {28},
	number = {12},
	year = {2016},
	keywords = {},
	abstract = {NF-κB is a well-characterized transcription factor with multiple physiological and pathological functions. NF-κB plays important roles in the development and maturation of lymphoids, regulation of immune and inflammatory response, and cell death and survival. The influence of NF-κB on cell survival could be protective or destructive, depending on types, developmental stages of cells, and pathological conditions. The complexity of NF-κB in cell death and survival derives from its multiple roles in regulating the expression of a broad array of genes involved in promoting cell death and survival. The activation of NF-κB has been found in many neurological disorders, but its actual roles in pathogenesis are still being debated. Many compounds with neuroprotective actions are strongly associated with the inhibition of NF-κB, leading to speculation that blocking the pathological activation of NF-κB could offer neuroprotective effects in certain neurodegenerative conditions. This paper reviews the recent developments in understanding the dual roles of NF-κB in cell death and survival and explores its possible usefulness in treating neurological diseases. This paper will summarize the genes regulated by NF-κB that are involved in cell death and survival to elucidate why NF-κB promotes cell survival in some conditions while facilitating cell death in other conditions. This paper will also focus on the effects of various NF-κB inhibitors on neuroprotection in certain pathological conditions to speculate if NF-κB is a potential target for neuroprotective therapy.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/3710}
}