Anti-ENAH / Mena, clone ENAH/1988

0.2 mg/ml in 1X PBS with 0.1 mg/ml BSA (US sourced) and 0.05% sodium azide. The Wiskott-Aldrich syndrome (WAS) is characterized by thrombocytopenia, eczema, defects in cell-mediated and humoral immunity and a propensity for lymphoproliferative diseases. The syndrome is the result of a mutation in the gene encoding a proline-rich protein termed WASP. WASP is a downstream effector of Cdc42 and has been implicated in actin polymerization and cyto- skeletal organization. Distantly related proteins, VASP (vasodilator-stimulated phosphoprotein) and Mena (for mammalian enabled protein), are involved in the regulation of cytoskeletal dynamics. Both Mena and VASP accumulate at focal adhesions. Mena is highly expressed in the developing nervous system and may be involved in growth cone motility and axon guidance. Protein function: Ena/VASP proteins are actin-associated proteins involved in a range of processes dependent on cytoskeleton remodeling and cell polarity such as axon guidance and lamellipodial and filopodial dynamics in migrating cells. ENAH induces the formation of F-actin rich outgrowths in fibroblasts. Acts synergistically with BAIAP2-alpha and downstream of NTN1 to promote filipodia formation. [The UniProt Consortium]