Karolinska Institutet

About: Karolinska Institutet is a education organization based out in Stockholm, Sweden. It is known for research contribution in the topics: Population & Poison control. The organization has 46212 authors who have published 121142 publications receiving 6008130 citations.

Thioredoxin and thioredoxin reductase.

Abstract: Publisher Summary This chapter summarizes current methods to determine Trx and thioredoxin reductase (TR). Thioredoxin (Trx) is a small (Mr 12,000) multifunctional and ubiquitous protein characterized by having a redox-active disulfide/dithiol within the conserved active site sequence: -Trp-Cys-Gly-Pro-Cys-. Oxidized thioredoxin (Trx-S 2 ) has a disulfide, and reduced thioredoxin [Trx-(SH) 2 ] has a dithiol. Thioredoxin reductase specifically reduces Trx-S 2 to Trx-(SH) 2 using NADPH. The Trx-(SH) 2 form is a powerful protein disulfide reductase. Thus, Trx, TR, and NADPH, collectively called the thioredoxin system, operate as a powerful NADPH-dependent protein disulfide reductase system. Thioredoxin has been isolated and characterized from a wide variety of prokaryotic and eukaryotic species. Mammalian thioredoxins show about 25% sequence identity to the well-characterized E. coli protein with 108 residues. One classic function of the thioredoxin system is to act as a hydrogen donor for ribonucleotide reductase, which is essential for DNA synthesis. Redox control processes involve changes in the activity of an enzyme, a receptor, or a transcription factor via dithiol/disulfide interchange reactions. Mammalian thioredoxin reductase, with its broader substrate specificity, is likely to be involved in multiple signaling systems for redox control of cellular processes.

Inflammation and atherosclerosis

Abstract: Atherosclerosis, the cause of myocardial infarction, stroke, and ischemic gangrene, is an inflammatory disease. The atherosclerotic process is initiated when cholesterol-containing low-density lipoproteins accumulate in the intima and activate the endothelium. Leukocyte adhesion molecules and chemokines promote recruitment of monocytes and T cells. Monocytes differentiate into macrophages and upregulate pattern recognition receptors, including scavenger receptors and toll-like receptors. Scavenger receptors mediate lipoprotein internalization, which leads to foam-cell formation. Toll-like receptors transmit activating signals that lead to the release of cytokines, proteases, and vasoactive molecules. T cells in lesions recognize local antigens and mount T helper-1 responses with secretion of pro-inflammatory cytokines that contribute to local inflammation and growth of the plaque. Intensified inflammatory activation may lead to local proteolysis, plaque rupture, and thrombus formation, which causes ischemia and infarction. Inflammatory markers are already used to monitor the disease process and anti-inflammatory therapy may be useful to control disease activity.

A new classification for HIV-1

Abstract: The phenotype of HIV-1 isolates is defined by the cells in which they replicate in vitro, but these phenotypes can change in vivo with profound implications for viral transmission, pathogenesis and disease progression. Here we propose a new classification system based on co-receptor use, providing a more accurate description of viral phenotype than the present imprecise and often misleading classification schemes.