Early B-cell factor 3 (EBF3)

Early B-cell factor 3 (EBF3) is a member of the EBF family of DNA-binding transcription factors with a critical role in development and differentiation. It contains an N-terminal DNA-binding domain, an IPT/TIG domain for protein interaction, and a helix-loop-helix domain for dimerization[1]. EBF3 regulates gene networks involved in the terminal differentiation of muscle (notably in the diaphragm), neuronal development, and suppression of cell proliferation. It directly activates genes like p21, p27, and p57 (cyclin-dependent kinase inhibitors) to induce cell cycle arrest and apoptosis, as well as negatively regulates survival genes such as Mcl-1—indicative of a tumor suppressor function[2][3]. In cancer, EBF3 is frequently inactivated by deletion or methylation at its locus on chromosome 10q26.3, particularly in high-grade gliomas and other tumors, where its re-expression can induce growth arrest and apoptosis. In addition to tumorigenesis, germline mutations in EBF3 are associated with HADDS, a neurodevelopmental disorder[4][3][5]. EBF3 has not been established as a direct pharmacological target, and there are currently no drugs known to interact with it.

Other names

Transcription factor COE3COE3EBF-3O/E-2OE-2DKFZp667B0210Early B-cell factor 3Olf-1/EBF-like 2HADDS