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Damage-associated molecular pattern;; cytokine;; pathogen-associated;; molecular pattern;; innate immunity;; therapy;; MOBILITY GROUP BOX-1;; INFLAMMASOME ACTIVATION;; STERILE INFLAMMATION;; NLRP3 INFLAMMASOME;; IMMUNE-RESPONSES;; CYTOKINE RELEASE;; GENE-EXPRESSION;; PROTEIN HMGB1;; RECEPTOR 4;; CELLS;; Multidisciplinary Sciences
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Full-Text Articles in Medicine and Health Sciences
Jak/Stat1 Signaling Promotes Hmgb1 Hyperacetylation And Nuclear Translocation, B. Lu, K. Kwan, M. Robinson, M. A. D. Van Zoelen, H. Yang, J. Li, S. S. Chavan, H. Wang, U. Andersson, K. J. Tracey, +5 Additional Authors
Jak/Stat1 Signaling Promotes Hmgb1 Hyperacetylation And Nuclear Translocation, B. Lu, K. Kwan, M. Robinson, M. A. D. Van Zoelen, H. Yang, J. Li, S. S. Chavan, H. Wang, U. Andersson, K. J. Tracey, +5 Additional Authors
Journal Articles
Extracellular high-mobility group box (HMGB)1 mediates inflammation during sterile and infectious injury and contributes importantly to disease pathogenesis. The first critical step in the release of HMGB1 from activated immune cells is mobilization from the nucleus to the cytoplasm, a process dependent upon hyperacetylation within two HMGB1 nuclear localization sequence (NLS) sites. The inflammasomes mediate the release of cytoplasmic HMGB1 in activated immune cells, but the mechanism of HMGB1 translocation from nucleus to cytoplasm was previously unknown. Here, we show that pharmacological inhibition of JAK/STAT1 inhibits LPS-induced HMGB1 nuclear translocation. Conversely, activation of JAK/STAT1 by type 1 interferon (IFN) stimulation …