TEAD1

Official Full Name

TEA domain transcription factor 1

Organism

Homo sapiens

GeneID

7003

Background

This gene encodes a ubiquitous transcriptional enhancer factor that is a member of the TEA/ATTS domain family. This protein directs the transactivation of a wide variety of genes and, in placental cells, also acts as a transcriptional repressor. Mutations in this gene cause Sveinsson's chorioretinal atrophy. Additional transcript variants have been described but their full-length natures have not been experimentally verified. [provided by RefSeq, May 2010]

Synonyms

AA; REF1; TCF13; TEF-1; NTEF-1; TCF-13; TEAD-1;

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Detailed Information

The TEAD1 gene, also known as Transcriptional Enhancer Factor TEF-1, is located on human chromosome 11p15.3-p15.1. It encodes a highly evolutionarily conserved transcription factor belonging to the TEA/ATTS domain family. The protein's defining feature is an N-terminal TEA domain of approximately 70 amino acids, which binds DNA in a sequence-specific manner. TEAD1 specifically recognizes enhancer sequences in the genome, most notably the 5'-GTGGAATGT-3' motif, found in the promoters or enhancers of numerous genes. TEAD1 itself possesses limited intrinsic transcriptional activation capability; its function largely depends on interactions with coactivators. TEAD1 is broadly expressed across tissues, with particularly critical roles in the heart, skeletal muscle, and placenta.

Biological Significance

TEAD1's biological importance is most prominently demonstrated in the Hippo signaling pathway, where it serves as an indispensable downstream transcriptional effector. The Hippo pathway is a highly conserved network central to organ size control, tissue homeostasis, tumor suppression, and regeneration. Its kinase cascade relies on activated LATS1/2 kinases to phosphorylate and inhibit downstream effectors YAP and TAZ. When the pathway is inactive, unphosphorylated YAP/TAZ translocate to the nucleus and bind TEAD1, forming functional transcriptional complexes. Assembly of this complex is a prerequisite for the transcription of target genes involved in cell proliferation, migration, anti-apoptotic responses, and epithelial–mesenchymal transition. Thus, TEAD1 functions as a molecular bridge linking Hippo pathway activity to cell fate decisions.

Beyond its Hippo-dependent roles, TEAD1 is crucial during embryogenesis, particularly in cardiac development. By binding M-CAT motifs in cardiomyocyte-specific genes, TEAD1 directly regulates their expression, influencing cardiac morphogenesis and functional maturation. Loss of TEAD1 function leads to severe cardiac developmental defects. In adult tissues, TEAD1 continues to maintain homeostasis and mediate tissue repair, while its hyperactivation is a key driver of proliferation and invasiveness in many solid tumors.

Clinical Relevance

TEAD1's clinical significance is evident in two domains: rare genetic eye disorders and various cancers. Loss-of-function mutations in TEAD1 have been identified as the cause of Sveinsson's chorioretinal atrophy, an autosomal dominant disease characterized by progressive chorioretinal degeneration leading to vision loss. This disorder underscores TEAD1's essential role in maintaining ocular tissue, particularly the retinal pigment epithelium and choroid.

In oncology, TEAD1 acts as a critical oncogenic signaling hub. Dysregulation of the Hippo pathway in multiple cancers results in abnormal YAP/TAZ activation and nuclear translocation. The oncogenic activity of YAP/TAZ is largely dependent on interaction with TEAD transcription factors. Consequently, targeting the TEAD1-YAP/TAZ interface has emerged as a promising anticancer strategy. Current research focuses on developing inhibitors that either directly block YAP/TAZ-TEAD1 binding (small molecules or peptides), disrupt TEAD1 function, or target TEAD1 palmitoylation sites. TEAD1 palmitoylation is critical for its stability and complex formation with YAP/TAZ; inhibitors of this process effectively suppress TEAD1 transcriptional activity, thereby inhibiting Hippo pathway-driven tumor growth. Beyond cancer, modulating TEAD1 activity to promote tissue repair and regeneration is a developing area in regenerative medicine.

In summary, TEAD1 is a key transcriptional effector whose loss causes genetic disease, while its aberrant activation drives tumorigenesis, making it a pivotal molecule linking developmental biology and cancer biology, as well as a promising therapeutic target.

References

Zhao B, Ye X, Yu J, et al. TEAD mediates YAP-dependent gene induction and growth control. Genes Dev. 2008;22(14):1962-1971.
Fossdal R, Jonasson F, Kristjansdottir GT, et al. A novel TEAD1 mutation is the causative allele in Sveinsson's chorioretinal atrophy (helicoid peripapillary chorioretinal degeneration). Hum Mol Genet. 2004;13(9):975-981.
Pobbati AV, Hong W. Emerging roles of TEAD transcription factors and its coactivators in cancers. Cancer Biol Ther. 2013;14(5):390-398.
Landin-Malt A, Benhaddou A, Zider A, et al. An evolutionary, structural, and functional overview of the mammalian TEAD1 and TEAD2 transcription factors. Gene. 2016 Oct 10;591(1):292-303.

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