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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.
These results are consistent with two plausible models of cryptic MCAT (show MCAT Proteins) enhancer regulation by Pur alpha (show PURA Proteins), Pur beta (show PURB Proteins), and MSY1 (show YBX1 Proteins) involving either competitive single-stranded DNA binding or masking of MCAT (show MCAT Proteins)-bound transcription enhancer factor-1.
Transcription enhancer factor 1 binds multiple muscle MEF2 (show MEF2C Proteins) and A/T-rich elements during fast-to-slow skeletal (show MYL3 Proteins) muscle fiber type transitions
VITO-1 (show VGLL2 Proteins), a new scalloped interaction domain-containing protein, binds to TEF1 in vitro and strongly stimulates transcription of a reporter plasmid together with TEF-1
p38 (show CRK Proteins) MAPKs regulate TEF-1 and C/EBPbeta (show CEBPB Proteins) transcriptional activity in the absence of environmental stress.
Sveinsson's chorioretinal atrophy pathogenesis may be due to a loss-of-function of TEAD1 affecting the regulation of its target genes.
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.
Our data suggest that AIC is a genetically heterogeneous disease and is not restricted to the X chromosome, and that TEAD1 mutations may be present in male patients.
Our findings suggest that genetic variants of Hippo pathway genes, particularly YAP1 (show YAP1 Proteins) rs11225163, TEAD1 rs7944031 and TEAD4 (show TEAD4 Proteins) rs1990330, may independently or jointly modulate survival of CM patients.
Suggest central role for TEAD and YAP (show YAP1 Proteins) as signal-responsive regulators of multipotent pancreatic progenitors.
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