AES Antibody

Adhesion to extracellular matrix regulates cell survival through both integrin engagement and appropriate cell spreading. Anoikis is the molecular mechanism of apop-tosis induced by integrin detachment. Amino-terminal enhancer of split (AES) is a member of the Groucho/ transducin-like enhancer of split (TLE) family of transcriptional regulators, a group of transcriptional co-repressors that play important roles in neurogenesis, segmentation, and sex determination. AES forms a complex with Bit1 (Bcl-2 inhibitor of transcription 1), a mitochondrial protein that is released into the cytoplasm upon onset of apoptosis. It has been suggested that this complex turns off a survival-promoting gene transcription program controlled by the TLE protein family. Interestingly, apoptosis of cells transfected with AES and Bit1 could be inhibited if the cells were allowed to attach to fibronectin through the alpha5beta1 integrin suggesting that the Bit1-AES pathway contributing to anoikis is regulated by integrins, and in particular, the alpha5beta1 integrin.