HMGB proteins function as universal sentinels for nucleic-acid-mediated innate immune responses
By H. Yanai, T. Ban, Zhichao Wang, M. Choi, T. Kawamura, Hideo Negishi, M. Nakasato, Yan Lu, S. Hangai, Ryuji Koshiba and 8 more. Nature, 2009
719 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology
View Paper: https://www.semanticscholar.org/paper/ca042d3d31704fffc447fd5b6ada1eb1e672b1d2
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- Shizuo Akira
- D. Tang
- R. Kang
- O. Takeuchi
- Katherine A. Fitzgerald
- G. Barber
- Oliver Soehnlein
- Taro Kawai
In Immunology
- Shizuo Akira
- O. Takeuchi
- Katherine A. Fitzgerald
- Jacques Banchereau
- G. Barber
- Kevin J. Tracey
- Michael Lotze
- C. Reis e Sousa
Citations in the corpus
- HMGB1 Is a Therapeutic Target for Sterile Inflammation and Infection (2011, background): “It has been known for decades that HMGB1 can facilitate cellular uptake of DNA, and recent evidence has placed this mechanism into the context of inflammation (28).”
- Netting Neutrophils Are Major Inducers of Type I IFN Production in Pediatric Systemic Lupus Erythematosus (2011, background): “3A), a protein that functions as a universal sentinel for nucleic acids and leads to type I IFN and inflammatory cytokine secretion by targeting DNA or RNA to cytosolic nucleic acid–sensing receptors (26).”
- PAMPs and DAMPs: Signal 0s that Spur Autophagy and Immunity (2012, background): “Indeed, HMGB family members function as universal sentinels for nucleic acids in innate immune signaling (79).”
- Sepsis: current dogma and new perspectives. (2014, background): “As a universal sentinel for infection or injury, HMGB1 appears as a delayed mediator after the onset of infection and serum concentrations might remain elevated in survivors—for up to 30 days in mice, and even longer in humans (Chavan et al., 2012; Yanai et al., 2012; Yanai et al., 2009).”
- The role of defective clearance of apoptotic cells in systemic autoimmunity (2010, background): “In this regard, highly conserved molecules that bind to nucleic acids, such as HMGB1, are potentially important in modulating the ability of nucleic acids to activate innat”
- Phagocyte partnership during the onset and resolution of inflammation (2010, background): “We now know that complexes between HMGB1 and DAMPs (such as single-stranded DNA, LPS or nucleosomes) interact with the canonical HMGB1 receptor RAGE (receptor for advanced glycation end products) as well as TLR2 , TLR4, TLR9 and IL-1R to induce cytokine productio”
- STING-Dependent Cytosolic DNA Sensing Mediates Innate Immune Recognition of Immunogenic Tumors (2014, background): “Chaperoning of tumor-derived DNA by high-mobility group box 1 (HMGB1) is another potential mechanism (Yanai et al., 2009), which based on our results would likely be via a TLR-independent fashion.”
- Cytosolic Sensing of Viruses (2013, background): “LRRFIP1, HMGB proteins, and ABCF1 (ATP-binding cassette, subfamily F member 1) have also been shown to bind DNA directly and positively regulate IFN responses (Lee et al., 2013; Yanai et al., 2009; Yang et al., 2010).”
- Endogenous HMGB1 regulates autophagy (2010, background): “, 2008), and its critical role as a universal DNA sensor (Yanai et al., 2009; Sims et al., 2010), we propose a more nuanced conceptual model involving HMGB1 and cell death.”