High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal
By Michael Lotze, Kevin J. Tracey. Nature reviews. Immunology, 2005
2,608 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/c4128eb57639c4ca2a54f7a6af51e2d7f21a4418
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Clinical Biochemistry
In Immunology
In Molecular Biology
Citations in the corpus
- Induction of autophagy by spermidine promotes longevity (2009, background): “Notably, release of Nhp6A–EGFP to the extracellular space, reported for mammalian HMGB”
- The endogenous Toll–like receptor 4 agonist S100A8/S100A9 (calprotectin) as innate amplifier of infection, autoimmunity, and cancer (2009, background): “This review focuses on the recent advances in understanding the function of S100A8 and S100A9 as endogenous DAMPs.”
- Pattern recognition receptors and inflammation. (2010, background): “It has been shown that HMGB1 released from necrotic cells stimulates TLR2 and TLR4 to induce the production of proinflammatory cytokines (Lotze and Tracey, 2005).”
- HMGB1 promotes recruitment of inflammatory cells to damaged tissues by forming a complex with CXCL12 and signaling via CXCR4 (2012, background): “Several receptors have been implicated in HMGB1-mediated functions, including RAGE (receptor for advanced glycation end products) and TLR2 (Toll-like receptor 2), TLR4, and TLR9 (Lotze and Tracey, 2005; Tian et al., 2007).”
- A critical cysteine is required for HMGB1 binding to Toll-like receptor 4 and activation of macrophage cytokine release (2010, background): “Importantly, however, a large body of evidence indicates that HMGB1 is also required for the development or progression of inflammation, even in the absence of infection, as occurs during experimental autoimmunearthritis, cerebral ischemia,hemorrhagic shock, pancreatitis, sterile hepatic necrosis, a”
- Endogenous HMGB1 regulates autophagy (2010, background): “In addition to its intranuclear role, HMGB1 also functions as an extracellular signaling molecule during inflammation, cell differentiation, cell migration, and tumor metastasis (Lotze and Tracey, 2005; Tang et al., 2010a).”
- The Beclin 1 network regulates autophagy and apoptosis (2011, positive): “HMGB1 is a chromatin-associated nuclear protein and extracellular damage-associated molecular pattern molecule.(47,48) Recently, we have shown that HMGB1 is a novel Beclin 1-binding protein important in sustaining autophagy.”
- Mincle is an ITAM-coupled activating receptor that senses damaged cells (2008, background): “Another candidate Mincle ligand is the nuclear protein HMGB1 (high-mobility group box 1), which has been reported to be secreted from dead cells and to act as a signal that alerts the immune system to excessive or deregulated cell deat”