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TEAD1 encodes a ubiquitous transcriptional enhancer factor that is a member of the TEA/ATTS domain family. Additionally we are shipping TEAD1 Antibodies (36) and TEAD1 Proteins (3) and many more products for this protein.
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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 ELISA Kits) RNA expression, and cells with increased Myc (show MYC ELISA Kits) expression also became super-competitors.
The PDZ (show INADL ELISA Kits)-binding motif of YAP (show YAP1 ELISA Kits) is critical for YAP (show YAP1 ELISA Kits)-mediated oncogenesis, and that this effect is mediated by YAP's co-activation of TEAD-mediated CTGF (show CTGF ELISA Kits) transcription.
TEAD1 regulates C2C12 differentiation through negatively regulating the expression of Ccne1 (show CCNE1 ELISA Kits), 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 enhancer regulation by Pur alpha, Pur beta, and MSY1 involving either competitive single-stranded DNA binding or masking of MCAT-bound transcription enhancer factor-1.
Transcription enhancer factor 1 binds multiple muscle MEF2 (show MEF2C ELISA Kits) and A/T-rich elements during fast-to-slow skeletal (show MYL3 ELISA Kits) muscle fiber type transitions
VITO-1 (show VGLL2 ELISA Kits), 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 ELISA Kits) MAPKs regulate TEF-1 and C/EBPbeta (show CEBPB ELISA Kits) 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.
TEAD1 could enhance the expression levels of SP1 (show PSG1 ELISA Kits), by directly binding to its promoter.
TEAD1 mediates YAP1 (show YAP1 ELISA Kits) chromatin-binding genome-wide.
show that the proangiogenic microfibrillar-associated protein 5 (MFAP5 (show MFAP5 ELISA Kits)) is a direct transcriptional target of YAP (show YAP1 ELISA Kits)/TEAD in cholangiocarcinoma cells transcription factors.
Melanoma reprogramming involves thousands of genomic regulatory regions underlying the proliferative and invasive states, identifying SOX10 (show SOX10 ELISA Kits)/MITF (show MITF ELISA Kits) and AP-1 (show FOSB ELISA Kits)/TEAD as regulators, respectively.
TAZ (show TAZ ELISA Kits) 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 ELISA Kits) rs11225163, TEAD1 rs7944031 and TEAD4 (show TEAD4 ELISA Kits) rs1990330, may independently or jointly modulate survival of CM patients.
Suggest central role for TEAD and YAP (show YAP1 ELISA Kits) as signal-responsive regulators of multipotent pancreatic progenitors.
the YAP (show YAP1 ELISA Kits)-TEAD interaction can be disrupted using cyclic YAP (show YAP1 ELISA Kits)-like peptides, which targets the HIPPO pathway
TEAD1 causes the nuclear sequestration of p65 (show GORASP1 ELISA Kits) leading to a novel TEAD1/p65 (show GORASP1 ELISA Kits) complex that associates with the intronic enhancer and is necessary for cytokine induction of MnSOD (show SOD2 ELISA Kits).
the XNTEF-1 and XDTEF-1 (show TEAD4 ELISA Kits) mRNAS are predominantly detected in eye, embryonic brain, somites and heart; in animal cap assay, the two genes are activated by bFGF (show FGF2 ELISA Kits) but are differently regulated by BMP4 (show BMP4 ELISA Kits), and the muscle regulatory factor Mef2d (show MEF2D ELISA Kits)
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