Practical approaches to investigate redox regulation of heat shock protein expression and intracellular glutathione redox state.

作者: Vittorio Calabrese , Anna Signorile , Carolin Cornelius , Cesare Mancuso , Giovanni Scapagnini

DOI: 10.1016/S0076-6879(08)01206-8

关键词: Heat shock proteinNeurodegenerationCell biologyKEAP1Reactive nitrogen speciesOxidative stressHsp70MediatorCellular stress responseBiochemistryBiology

摘要: The products of vitagenes such as heat shock protein 32 (Hsp32, heme oxygenase 1) and Hsp70, the family inducible cytoprotective proteins regulated by Keap1/Nrf2/ARE pathway, small molecule antioxidants glutathione provide cell with powerful means to counteract survive various conditions stress. Among these protective systems, represent a highly conserved robust way for preservation correct conformation, recovery damaged proteins, survival. Their regulation is dependent on redox status cell, thus rapidly evolving an important metabolic modulator cellular functions, being increasingly implicated in many chronic inflammatory degenerative diseases. Protein thiols play key role sensing, state crucial mediator multiple metabolic, signalling transcriptional processes brain. Nitric oxide, reactive nitrogen species induce transcription Keap1/Nrf2/ARE-dependent genes whose functional protect against wide array subsequent challenges. Emerging interest now focusing exogenous molecules that are capable activating systems novel target minimize deleterious consequences associated free radical-induced damage, during neurodegeneration. This chapter describes methods can be used assess expression discusses their relevance mechanisms modulating onset progression neurodegenerative

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