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The mechanism of HMGB1 secretion and release

  • 작성자

    Daolin Tang
  • 작성일자

    2022-03-24
  • 조회수

    322
Daolin Tang( Daolin.tang@utsouthwestern.edu )
2018-present Associate Professor, Department of Surgery, UT Southwestern Medical Center, USA
2016-2018 Associate Professor, Department of Surgery, University of Pittsburgh, USA
2012-2015 Assistant Professor, Department of Surgery, University of Pittsburgh, USA
2010-2012 Research Assistant Professor, Department of Surgery, University of Pittsburgh, USA
2007-2009 Postdoctoral Fellow, Department of Surgery, University of Pittsburgh, USA
2002-2007 PhD, Department of Pathophysiology, Xiangya School of Medicine, Central South University, China
2000-2002 Teaching Assistant, Department of Pathophysiology, Xiangya School of Medicine, Central South University, China
1995-2000 MD, Norman Bethune College of Medicine, Jilin University, China

The mechanism of HMGB1 secretion and release

High mobility group box 1 (HMGB1) is a nonhistone nuclear protein that has multiple functions according to its subcellular location. In the nucleus, HMGB1 is a DNA chaperone that maintains the structure and function of chromosomes. In the cytoplasm, HMGB1 can promote autophagy by binding to BECN1 protein. After its active secretion or passive release, extracellular HMGB1 usually acts as a damage-associated molecular pattern (DAMP) molecule, regulating inflammation and immune responses through different receptors or direct uptake. The secretion and release of HMGB1 is fine-tuned by a variety of factors, including its posttranslational modification (e.g., acetylation, ADP-ribosylation, phosphorylation, and methylation) and the molecular machinery of cell death (e.g., apoptosis, pyroptosis, necroptosis, alkaliptosis, and ferroptosis). In this minireview, we introduce the basic structure and function of HMGB1 and focus on the regulatory mechanism of HMGB1 secretion and release. Understanding these topics may help us develop new HMGB1-targeted drugs for various conditions, especially inflammatory diseases and tissue damage.

Exp Mol Med. 2022 Feb 25. doi: 10.1038/s12276-022-00736-w.
https://pubmed.ncbi.nlm.nih.gov/35217834/