High impact information on LEF1

• This result supports the model that SOX proteins act as architectural components in the activating complex formed on an enhancer, as indicated for another HMG domain protein, lymphoid enhancer binding factor 1 (LEF-1) [1].
• Cotransfection of beta-catenin and LEF-1 into Chinese hamster ovary cells induced transactivation of a LEF-1 reporter, which was blocked by the N-cadherin-derived molecules [2].
• The cytoplasmic tails of N- or E-cadherin colocalized with beta-catenin in the nucleus, and suppressed the constitutive LEF-1-mediated transactivation, by blocking beta-catenin-LEF-1 interaction [2].
• In somite explants, Fz1, beta-catenin and Lef1 are expressed prior to activation of myogenesis in response to Shh and Wnt signals [3].
• Predictions of roles for canonical signaling in the developing gizzard, duodenum, and large intestine in chick were tested by viral misexpression of dominant-negative (DN) forms of the downstream cofactors Tcf4 and Lef1 [4].

Anatomical context of LEF1

• Lef1 is expressed in the chick duodenum and large intestine mesoderm [4].

References