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The endothelial monocyte‐activating polypeptide II (EMAP II) is a substrate for caspase‐7
Author(s) -
Behrensdorf Heike A.,
van de Craen Marc,
Knies Ulrike E.,
Vandenabeele Peter,
Clauss Matthias
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01777-9
Subject(s) - proinflammatory cytokine , cleavage (geology) , monocyte , microbiology and biotechnology , apoptosis , caspase , chemistry , cytokine , chemotaxis , inflammation , caspase 3 , programmed cell death , biology , immunology , biochemistry , receptor , paleontology , fracture (geology)
Endothelial monocyte‐activating polypeptide II (EMAP II) is a proinflammatory cytokine and a chemoattractant for leukocytes. The mature cytokine is formed in apoptotic cells by cleavage of the precursor proEMAP II. Here we show that caspase‐7 is capable of cleaving proEMAP II in vitro. A proEMAP II mutant, in which the ASTD cleavage site was changed to the sequence ASTA, was not processed by caspase‐7. The caspase‐7‐mediated generation and release of mature EMAP II may provide a mechanism for leukocyte recruitment to sites of programmed cell death, and thus may link apoptosis to inflammation.