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Wnt/beta-catenin signaling via Axin2 is required for myogenesis and, together with YAP/Taz and Tead1, active in IIa/IIx muscle fibers
Overexpression of TEAD1 induced Treg cell differentiation. TEAD sequesters TAZ (show TAZ Proteins) and inhibits TH17 development.
We discovered that Tead1 and co-activators Yap (show YAP1 Proteins) and Taz (show TAZ Proteins) are required for Pmp22 (show PMP22 Proteins) expression, as well as for the expression of Egr2 (show EGR2 Proteins) Tead1 directly binds Pmp22 (show PMP22 Proteins) and Egr2 (show EGR2 Proteins) enhancers early in development and Tead1 binding is induced during myelination, correlating with Pmp22 (show PMP22 Proteins) expression. The data identify Tead1 as a novel regulator of Pmp22 (show PMP22 Proteins) expression during development in concert with Sox10 (show SOX10 Proteins) and Egr2 (show EGR2 Proteins)
YAP (show YAP1 Proteins) and TEAD1, key downstream effectors of the Hippo pathway, are specifically expressed in Muller cells. We also uncovered a deregulation of the expression and activity of Hippo/YAP (show YAP1 Proteins) pathway components in reactive Muller cells under pathologic conditions.
Data show that TEAD family of transcription factors Tead1 and Tead4 (show TEAD4 Proteins)-regulated gene expression in differentiating primary myoblasts.
Cells with reduced Tead activity became losers, whereas cells with increased Tead activity became super-competitors. Tead directly regulated Myc (show MYC Proteins) RNA expression, and cells with increased Myc (show MYC Proteins) expression also became super-competitors.
The PDZ-binding motif of YAP (show YAP1 Proteins) is critical for YAP (show YAP1 Proteins)-mediated oncogenesis, and that this effect is mediated by YAP's co-activation of TEAD-mediated CTGF (show CTGF Proteins) transcription.
TEAD1 regulates C2C12 differentiation through negatively regulating the expression of Ccne1 (show CCNE1 Proteins), which can explain the transition between proliferation and differentiation.
TEAD1 is shown to be a mediator of skeletal muscle development.
increased TEAD-1 can induce characteristics of cardiac remodeling associated with cardiomyopathy and heart failure.
This identifies the YAP1 (show YAP1 Proteins)/TEAD1 complex as the representative dysregulated profile of Hippo signaling in OS and provides proof-of-principle that targeting TEAD1 may be a therapeutic strategy of osteosarcoma.
The authors show MRTF family proteins bind YAP (show YAP1 Proteins) via a conserved PPXY motif that interacts with the YAP (show YAP1 Proteins) WW domain. This interaction allows MRTF to recruit NcoA3 (show NCOA3 Proteins) to the TEAD-YAP (show YAP1 Proteins) transcriptional complex and potentiate its transcriptional activity.
MYC (show MYC Proteins) and TEAD activity is able to stratify different breast cancer subtypes in large panels of breast cancer patients.
Collectively, these results indicate that human papillomavirus 16 E6 induces upregulation of APOBEC3B (show APOBEC3B Proteins) through increased levels of TEADs, highlighting the importance of the TEAD-APOBEC3B (show APOBEC3B Proteins) axis in carcinogenesis.
Upregulation of transcriptional enhancer activator domain 1 was found in hepatocellular carcinoma tissues and inversely correlated with miR (show MLXIP Proteins)-590-3p. Our results indicate a tumor suppressor role of miR (show MLXIP Proteins)-590-3p in hepatocellular carcinoma through targeting transcriptional enhancer activator domain 1 and suggest its use in the diagnosis and prognosis of liver cancer.
TEAD1 could enhance the expression levels of SP1 (show PSG1 Proteins), by directly binding to its promoter.
TEAD1 mediates YAP1 (show YAP1 Proteins) chromatin-binding genome-wide.
show that the proangiogenic microfibrillar-associated protein 5 (MFAP5 (show MFAP5 Proteins)) is a direct transcriptional target of YAP (show YAP1 Proteins)/TEAD in cholangiocarcinoma cells transcription factors.
Melanoma reprogramming involves thousands of genomic regulatory regions underlying the proliferative and invasive states, identifying SOX10 (show SOX10 Proteins)/MITF (show MITF Proteins) and AP-1 (show FOSB Proteins)/TEAD as regulators, respectively.
TAZ (show TAZ Proteins) negatively regulate transcription of DeltaNp63 through TEAD1,2,3 and 4 transcription factors.
the XNTEF-1 and XDTEF-1 (show TEAD4 Proteins) mRNAS are predominantly detected in eye, embryonic brain, somites and heart; in animal cap assay, the two genes are activated by bFGF (show FGF2 Proteins) but are differently regulated by BMP4 (show BMP4 Proteins), and the muscle regulatory factor Mef2d (show MEF2D Proteins)
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.
TEA domain family member 1
, TEA domain family member 1 (SV40 transcriptional enhancer factor)
, TEA domain family member 1-like
, transcriptional enhancer factor TEF-1-like
, transcription factor 13
, transcriptional enhancer factor TEF-1
, protein GT-IIC
, transcriptional enhancer factor 1