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1: J Biol Chem. 1998 Dec 18;273(51):33897-900.
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The death effector domain of PEA-15 is involved in its regulation of integrin activation.

Ramos JW, Kojima TK, Hughes PE, Fenczik CA, Ginsberg MH.

Department of Vascular Biology, The Scripps Research Institute, La Jolla, California 92037, USA.

Increased integrin ligand binding affinity (activation) is triggered by intracellular signaling events. A Ras-initiated mitogen-activated protein kinase pathway suppresses integrin activation in fibroblasts. We used expression cloning to isolate cDNAs that prevent Ras suppression of integrin activation. Here, we report that PEA-15, a small death effector domain (DED)-containing protein, blocks Ras suppression. PEA-15 does not block the capacity of Ras to activate the ERK mitogen-activated protein kinase pathway. Instead, it inhibits suppression via a pathway blocked by a dominant-negative form of the distinct small GTPase, R-Ras. Heretofore, all known DEDs functioned in the regulation of apoptosis. In contrast, the DED of PEA-15 is essential for its capacity to reverse suppression of integrin activation. Thus, certain DED-containing proteins can regulate integrin activation as opposed to apoptotic protease cascades.

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PMID: 9852038 [PubMed - indexed for MEDLINE]