Transcriptional enhancer factor TEF-1 (TEAD1) (TEAD1)

The **Transcriptional enhancer factor TEF-1 (TEAD1)** is a transcription factor essential for development, particularly in heart, skeletal, and smooth muscle differentiation through binding to M-CAT DNA elements via its N-terminal TEA domain, which adopts a homeodomain-like three-helix bundle structure.[1][2][3] It requires coactivators such as YAP/TAZ (Hippo pathway effectors), SRC family proteins, and Vestigial-like (VGLL) proteins to activate target genes involved in proliferation and muscle-specific expression like alpha-myosin heavy chain and troponin.[1][3][8] TEAD1 is post-translationally modified by phosphorylation (e.g., by PKA and PKC) and palmitoylation, which regulate its DNA binding, stability, and activity.[1][2][4] In disease, TEAD1 promotes cancer progression by upregulating oncogenes like c-myc, survivin, CTGF, Cyr61, and Axl, especially when hyperactivated via Hippo pathway dysregulation in tumors such as glioblastoma, liver, ovarian, breast, and lung cancers.[3][5] As a therapeutic target, inhibitors like verteporfin disrupt YAP-TEAD interactions to suppress proliferation, highlighting its druggability in Hippo-related pathologies, though broader TEAD family redundancy may pose challenges.[3][9][10]

Other names

TEF-1TEA domain transcription factor 1TEAD transcription factor 1

Disruption of YAP-TEAD interaction