Linked Life Data

12110890

Source:http://linkedlifedata.com/resource/pubmed/id/12110890

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6894
pubmed:dateCreated
2002-7-11
pubmed:abstractText
High mobility group 1 (HMGB1) protein is both a nuclear factor and a secreted protein. In the cell nucleus it acts as an architectural chromatin-binding factor that bends DNA and promotes protein assembly on specific DNA targets. Outside the cell, it binds with high affinity to RAGE (the receptor for advanced glycation end products) and is a potent mediator of inflammation. HMGB1 is secreted by activated monocytes and macrophages, and is passively released by necrotic or damaged cells. Here we report that Hmgb1(-/-) necrotic cells have a greatly reduced ability to promote inflammation, which proves that the release of HMGB1 can signal the demise of a cell to its neighbours. Apoptotic cells do not release HMGB1 even after undergoing secondary necrosis and partial autolysis, and thus fail to promote inflammation even if not cleared promptly by phagocytic cells. In apoptotic cells, HMGB1 is bound firmly to chromatin because of generalized underacetylation of histone and is released in the extracellular medium (promoting inflammation) if chromatin deacetylation is prevented. Thus, cells undergoing apoptosis are programmed to withhold the signal that is broadcast by cells that have been damaged or killed by trauma.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
11
pubmed:volume
418
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
191-5
pubmed:dateRevised
2010-9-30
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation.
pubmed:affiliation
DIBIT, Istituto Scientifico San Raffaele, 20132 Milano, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't