title: S-nitrosylation/denitrosylation and apoptosis of immune cells.
abstract: Nitric oxide (NO) as an immunoregulatory molecule, predominantly depending on S-nitrosylation, acts as a versatile player that executes its regulation and signal transduction for exerting its multi-functions and pleiotropy. Apoptosis of immune cells is an intricate process coupled with positive/negative selection depending on integrated diverse endogenous and exogenous signals and functions to sustain homeostasis in the immune system. Here, the dual roles of NO depending on its concentration in apoptosis are reviewed, breeding up a switch mode in the apoptotic process. Following comments of different switches from apoptosis-death, a new finding of checkpoint (early fluorescence point) of GSNO-initiated thymocyte apoptosis and NOS-GSNOR double control are highlighted. Moreover, S-nitrosylation/denitrosylation, being as a redox switch, logically approaches to networks of metabolism itself and further accesses the neuroendicrine-immune-free radical network as a whole. Moreover, the host defense mediated by NO on pathogens, via protein S-nitrosylation are also discussed.
authors.affiliation: Guang An Men Hospital, China Academy of Chinese Medical Sciences, Beijing 10053, China. shaojduan@yahoo.com
authors.forename: Shaojin
authors.initials: S
authors.lastname: Duan
authors.forename: Chang
authors.initials: C
authors.lastname: Chen
mesh_terms: D000445:Aldehyde Oxidoreductases / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D010084:Oxidation-Reduction; D011506:Proteins / Q000378:metabolism; D026422:S-Nitrosoglutathione / Q000378:metabolism*; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism*
chemical_list: D011506:Proteins; D009569:Nitric Oxide; D026422:S-Nitrosoglutathione; D019001:Nitric Oxide Synthase; D000445:Aldehyde Oxidoreductases; C087006:formaldehyde dehydrogenase, glutathione-independent