HMGB1 Polyclonal Antibody, Invitrogen™

Description

• Positive Samples: MCF7, HL-60, SW480, Raji, mouse spleen, mouse lung; Cellular Location: Cell membrane, Chromosome, Cytoplasm, Endoplasmic reticulum-Golgi intermediate compartment, Endosome, Extracellular side, Nucleus, Peripheral membrane protein Immunogen sequence: ARYEREMKTY IPPKGETKKK FKDPNAPKRP PSAFFLFCSE YRPKIKGEHP GLSIGDVAKK LGEMWNNTAA DDKQPYEKKA AKLKEKYEKD IAAYRAKGKP HMGB1 (High-mobility group box-1) protein was originally described as a nuclear non-histone DNA binding chromosomal protein
• However, recent studies indicate that damaged, necrotic cells liberate HMGB1 into the extracellular milieu where it functions as a proinflammatory cytokine
• Mouse HMGB1 is expressed as a 215 amino acid single chain polypeptide containing three domains: two tandem-linked positively charged DNA-binding domains (HMG box A, aa 9-79; and box B, aa 89-162), and a negatively charged 30 aa C-terminal acidic tail region
• Residues 28 - 44 and 180 - 185 contain a nuclear localization signal (NLS)
• The cytokine activity of HMGB1 is contained in the B box, while the A box is associated with the helix-loop-helix domain of transcription factors
• HMGB1 acts both as an inflammatory mediator that promotes monocyte migration and cytokine secretion, as well as a mediator of T cell-dendritic cell interaction
• HMGB1 is secreted and acts to transduce cellular signals through its high affinity receptor, RAGE and possibly, TLR2 and TLR4
• HMGB1 is highly conserved and ubiquitous in the nuclei and cytoplasm of nearly all cell types, is a necessary and sufficient mediator of inflammation during sterile and infection-associated responses
• HMGB1 also act as DNA nuclear binding protein that has recently been shown to be an early trigger of sterile inflammation in animal models of trauma-hemorrhage via the activation of the Toll-like receptor 4 (TLR4) and the receptor for the advanced glycation endproducts (RAGE)
• Moreover, HMGB1 is reported that the level of HMGB1 is elevated during sterile tissue injury, infection, lethal endotoxemia or sepsis, collagen-induced arthritis, and ischemia-reperfusion induced tissue injury.