Characterization of RAGE, HMGB1, and S100beta in inflammation-induced preterm birth and fetal tissue injury.

@article{Buhimschi2009CharacterizationOR,
  title={Characterization of RAGE, HMGB1, and S100beta in inflammation-induced preterm birth and fetal tissue injury.},
  author={Catalin Sorin Buhimschi and Margaret Ann Baumbusch and Antonette T. Dulay and Emily A. Oliver and Sarah Y Lee and Guomao Zhao and Vineet Bhandari and Richard A. Ehrenkranz and Carl P. Weiner and Joseph A. Madri and Irina Alexandra Buhimschi},
  journal={The American journal of pathology},
  year={2009},
  volume={175 3},
  pages={958-75}
}
Immune activation represents an adaptive reaction triggered by both noxious exogenous (microbes) and endogenous [high mobility group box-1 protein (HMGB1), S100 calcium binding proteins] inducers of inflammation. Cell stress or necrosis lead the release of HMGB1 and S100 proteins in the extracellular compartment where they act as damage-associated molecular pattern molecules (or alarmins) by engaging the receptor for advanced glycation end-products (RAGE). Although the biology of RAGE is… CONTINUE READING
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