생화학분자생물학회입니다.
The mechanism of HMGB1 secretion and release
작성자
Daolin Tang작성일자
2022-03-24조회수
407Daolin 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/