Anti-Vpr Activities of Heat Shock Protein 27

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منابع مشابه

High Levels of Anti-Heat Shock Protein 27 Antibody in Pemphigus Vulgaris

266 Ann Dermatol Received March 13, 2012, Revised September 2, 2012, Accepted for publication September 9, 2012 Corresponding author: Majid Ghayour-Mobarhan, Biochemistry of Nutrition Research Center, Faculty of Medicine, Mashhad University of Medical Science, Mashhad, Iran. Tel: 98-511-8829261, Fax: 98-511-8827040, E-mail: [email protected] This is an Open Access article distributed under th...

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Retinal preconditioning and the induction of heat-shock protein 27.

PURPOSE Brief periods of ischemia have been shown to protect the retina from potentially damaging periods of ischemia. This phenomenon has been termed ischemic preconditioning or ischemic tolerance. In the present study the cellular changes in levels of heat shock protein (Hsp)27, -70, and -90 mRNA and expression of Hsp in the rat retina associated with ischemic preconditioning were evaluated. ...

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Anti–Heat Shock Protein 27 Antibody Levels and Diabetes Complications in the EURODIAB Study

OBJECTIVE To assess whether serum anti-heat shock protein 27 (HSP27) antibody levels are associated with micro- and macrovascular complications of type 1 diabetes. RESEARCH DESIGN AND METHODS Anti-HSP27 IgG antibody levels were measured in 531 type 1 diabetic subjects recruited as part of the cross-sectional analysis of the EURODIAB Prospective Complications Study. Case subjects (n = 363) wer...

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Heat shock protein 27 controls apoptosis by regulating Akt activation.

Activation of the serine-threonine kinase Akt by cytokines, chemokines, and bacterial products delays constitutive neutrophil apoptosis, resulting in a prolonged inflammatory response. We showed previously that Akt exists in a signaling complex with p38 MAPK, MAPK-activated protein kinase-2 (MAPKAPK-2), and heat shock protein-27 (Hsp27); and Hsp27 dissociates from the complex upon neutrophil ac...

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Reductive stress: linking heat shock protein 27, glutathione, and cardiomyopathy?

Normal cellular functions essentially depend on a balanced redox environment. Free radicals and nonradical oxidants can shift the redox balance toward a more “oxidized” state, which is counteracted by the intracellular antioxidant defense systems. These include the enzymes superoxide dismutase and catalase, as well as the thiol-reducing systems (glutathione, glutaredoxin, and thioredoxin). Glut...

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ژورنال

عنوان ژورنال: Molecular Medicine

سال: 2007

ISSN: 1076-1551,1528-3658

DOI: 10.2119/2007-00004.liang