Bruhn et al. (1997) demonstrated that ALY is a ubiquitously expressed nuclear protein that specifically associates with the activation domains of LEF1 (153245) and AML1 (CBFA2; 151385). In addition, ALY can increase DNA binding by both LEF1 and AML proteins. Overexpression of ALY stimulated the activity of the TCR-alpha (see 186880) enhancer complex reconstituted in transfected nonlymphoid HeLa cells, whereas downregulation of ALY by antisense oligonucleotides virtually eliminated TCR-alpha enhancer activity in T cells. Similar to LEF1, ALY can stimulate transcription in the context of the TCR-alpha enhancer but apparently not when tethered to DNA through a heterologous DNA-binding domain. Bruhn et al. (1997) proposed that ALY mediates context-dependent transcriptional activation by facilitating the functional collaboration of multiple proteins in the TCR-alpha enhancer complex.