hmgb1 การใช้

• The presence of HMGB1 in the nucleus depends on posttranslational modifications.
• Activated macrophages and monocytes secrete HMGB1 as a cytokine mediator of Inflammation.
• This positions HMGB1 at the intersection of sterile and infectious inflammatory responses.
• A year later, she published a paper describing the opposing effects of H1 and HMGB1 on the nucleosome.
• HMGB1 is secreted by immune cells ( like macrophages, monocytes and dendritic cells ) through leaderless secretory pathway.
• HMGB1 is an intracellular protein that can translocate to the nucleus where it binds DNA and regulates gene expression.
• Two HMGB1 molecules bind at each side of 12-RSS and 23-RSS to stabilize the highly bent RSSs.
• The mechanism of inflammation and damage is binding to TLR4, which mediates HMGB1-dependent activation of macrophage cytokine release.
• HMGB1 can interact with TLR ligands and cytokines, and activates cells through the multiple surface receptors including TLR2, TLR4, and RAGE.
• HMGB1 has been shown to play an important role in helping the RAG endonuclease form a paired complex during V ( D ) J recombination.
• The mechanism by which pyroptosis contributes to septic shock and death is not well understood, although HMGB1 release is thought to play a role.
• Antibodies that neutralize HMGB1 confer protection against damage and tissue injury during arthritis, colitis, ischemia, sepsis, endotoxemia, and systemic lupus erythematosus.
• HMGB1-LPS complex activates TLR4, and leads to binding adapter proteins ( MyD88 and others ), which leads to signal transduction and activate signaling cascades.
• As a consequence of IRGM induced cell death, dying and necrotic cells release nuclear HMGB1, a pro-inflammatory alarmin, implicated in Crohn s disease.
• In apoptosis, HMGB1, a chromatin protein, is retained within the nucleus to result in formations of apoptotic bodies, while in paraptosis HMGB1 is released.
• In apoptosis, HMGB1, a chromatin protein, is retained within the nucleus to result in formations of apoptotic bodies, while in paraptosis HMGB1 is released.
• They found that regardless of the length of the acidic tail, it makes extensive contacts with the DNA-binding regions of the two tandem HMG-boxes in HMGB1.
• TNF amplifies and prolongs the inflammatory response by activating other cells to release interleukin-1 ( IL-1 ), high mobility group B1 ( HMGB1 ) and other cytokines.
• Interaction of HMGB1 and TLR4 results in upregulation of NF-kappa B, which leads to increased production and a release of cytokines in macrophages and in neutrophils for example stimulates release ROS via TLR-dependent activation of NADPH oxidase.
• Thomas s recent work has focused on the in-depth understanding of chromatin proteins, such as NMR mapping to better define the negative regulation of the HMGB1-DNA interaction that was suspected to be largely controlled by the acidic tail of HMGB1.