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Review
. 2001 Aug 15;20(16):4337-40.
doi: 10.1093/emboj/20.16.4337.

New EMBO members' review: the double life of HMGB1 chromatin protein: architectural factor and extracellular signal

S Müller  1 , P Scaffidi, B Degryse, T Bonaldi, L Ronfani, A Agresti, M Beltrame, M E Bianchi
Affiliations
Review

New EMBO members' review: the double life of HMGB1 chromatin protein: architectural factor and extracellular signal

S Müller et al. EMBO J. .
No abstract available

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Figures

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Fig. 1. Extracellular HMGB1 mediates migration of cells, metastasis and inflammatory responses. Most types of cells (upper) passively release nuclear HMGB1 (green spheres) into their surroundings after they have died. Alternatively, HMGB1 can be actively secreted from monocytes (and a limited number of other cells, lower part of the drawing) upon stimulation with LPS, TNF-α or IL-1. Secretion does not involve passage through the endoplasmic reticulum and Golgi apparatus. Extracellular HMGB1 provokes in other cells (green) that bear a receptor for HMGB1 an appropriate response for that cell type, like cell migration or inflammation.
None
Fig. 2. Known signalling mechanisms of extracellular HMGB1. Extracellular HMGB1 (green spheres) stimulates smooth muscle cells (red) to migrate. This response is mediated through RAGE, a Gi/o protein and the MAP kinase pathway, but the exact connection between these participants in the signal transduction cascade is not known. Neurite outgrowth in neurons (yellow) is activated by HMGB1 binding to RAGE, and the signal is channelled through the Rho family of small GTPases. Signalling of HMGB1 through RAGE also activates the Ras/MAP kinase pathway, leading ultimately to activation of the transcription factor NF-κB and its nuclear translocation. Other receptors (green) might also mediate responses to extracellular HMGB1.
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