High mobility group box 1 protein interacts with multiple Toll-like receptors.

By Jong Sung Park, F. Gamboni‐Robertson, Q. He, D. Svetkauskaite, Jae-Yeol Kim, D. Strassheim, J. Sohn, S. Yamada, I. Maruyama, A. Banerjee and 2 more. American Journal of Physiology - Cell Physiology, 2006

994 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Immunology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/daefd55eb2bc202066bf8e07b31a5d1c22f6a7a0

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In Clinical Biochemistry

1. H. Kono
2. DM Mosser
3. X. Zhang
4. K. Rock
5. R. Dhupar
6. Jon S. Cardinal
7. J. Klune
8. R. Medzhitov

In Immunology

1. Shizuo Akira
2. R. Medzhitov
3. L. Zitvogel
4. F. Barrat
5. Oliver Kepp
6. H. Kono
7. D. Golenbock
8. K. Rock

In Pathology and Forensic Medicine

1. J. Gensel
2. P. Saftig
3. R. Medzhitov
4. David J. Loane
5. Alok Kumar

Citations in the corpus

• Para-inflammation in the aging retina. (2009, background): “HMGB1 can bind to TLRs (TLR2, TLR4, and TLR9) (Park et al., 2006) and the receptor of advanced glycation end products (RAGEs) (Dumitriu et al.”
• Immunogenic cell death and DAMPs in cancer therapy (2012, background): “These authors showed that a recombinant N-terminal fragment of CRT (39-272) is a potent inducer of activation and maturation of B cells and macrophages and can trigger Ig class switching in B cells without T cell help in vitro and in vivo72.”
• Identification of a key pathway required for the sterile inflammatory response triggered by dying cells (2007, background): “There is evidence that some mammalian cellular components can stimulate TLR”
• Immunogenic death of colon cancer cells treated with oxaliplatin (2010, background): “Surface CRT serves as an engulfment signal (Obeid et al., 2007a, b) and similarly targets apoptotic cells for interaction with DCs and subsequent cross-presentation of tumor antigens (Zeng et al., 2006).”
• Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord (2009, background): “M1 macrophages, activated via toll-like receptors (TLRs) and IFN , produce proinflammatory cytokines and oxidative metabolites that facilitate their role as indiscriminate killers of microbes and tumor cells (Gordon, 2003; Mantovani et al., 2004).”
• Blood-brain barrier pathophysiology in traumatic brain injury (2011, background): “In addition to LPS, TLR4 has been shown to be activated by a number of endogenous factors released in response to injury, the so-called damageassociated molecular patterns (DAMPs), such as, for instance, high mobility group box 1 (HMGB1) protein, a DNA-binding protein [19].”
• Toll-like receptor 4–dependent contribution of the immune system to anticancer chemotherapy and radiotherapy (2007, background): “22 ) and the alarmin high-mobility-group box 1 protein (HMGB1”
• Macrophage activation by endogenous danger signals (2008, background): “HMGB1 is synthesized relatively late in sepsis by LPS-activated macrophages.”
• Origin and physiological roles of inflammation (2008, background): “HMGB1 and S100A12 engage the receptor RAGE (advanced glycation end-product-specific receptor; also known as AGER), which (at least in the case of HMGB1) cooperates with TLRs to induce an inflammatory respons”
• HMGB1: Endogenous Danger Signaling (2008, background): “HMGB1 binding of TLR2 and TLR4 results in NF-κB upregulation (61) (62) (63) , thus making it likely that HMGB1 stimulation of these receptors can lead to cytokine release.”