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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 Proteins (3) and TEAD1 Kits (1) and many more products for this protein.
Showing 10 out of 36 products:
Human Monoclonal TEAD1 Primary Antibody for IF, WB - ABIN968251
Deshpande, Chopra, Rangarajan, Shashidhara, Rodrigues, Krishna: The human transcription enhancer factor-1, TEF-1, can substitute for Drosophila scalloped during wingblade development. in The Journal of biological chemistry 1997
Show all 5 references for ABIN968251
Human Polyclonal TEAD1 Primary Antibody for WB - ABIN2781167
Fossdal, Jonasson, Kristjansdottir, Kong, Stefansson, Gosh, Gulcher, Stefansson: A novel TEAD1 mutation is the causative allele in Sveinsson's chorioretinal atrophy (helicoid peripapillary chorioretinal degeneration). in Human molecular genetics 2004
Show all 2 references for ABIN2781167
Chicken Polyclonal TEAD1 Primary Antibody for WB - ABIN2777238
Cuddapah, Cui, Zhao: Transcriptional enhancer factor 1 (TEF-1/TEAD1) mediates activation of IFITM3 gene by BRGl. in FEBS letters 2008
Cells with reduced Tead activity became losers, whereas cells with increased Tead activity became super-competitors. Tead directly regulated Myc (show MYC Antibodies) RNA expression, and cells with increased Myc (show MYC Antibodies) expression also became super-competitors.
The PDZ (show INADL Antibodies)-binding motif of YAP (show YAP1 Antibodies) is critical for YAP (show YAP1 Antibodies)-mediated oncogenesis, and that this effect is mediated by YAP's co-activation of TEAD-mediated CTGF (show CTGF Antibodies) transcription.
TEAD1 regulates C2C12 differentiation through negatively regulating the expression of Ccne1 (show CCNE1 Antibodies), 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 Antibodies) enhancer regulation by Pur alpha (show PURA Antibodies), Pur beta (show PURB Antibodies), and MSY1 (show YBX1 Antibodies) involving either competitive single-stranded DNA binding or masking of MCAT (show MCAT Antibodies)-bound transcription enhancer factor-1.
Transcription enhancer factor 1 binds multiple muscle MEF2 (show MEF2C Antibodies) and A/T-rich elements during fast-to-slow skeletal (show MYL3 Antibodies) muscle fiber type transitions
VITO-1 (show VGLL2 Antibodies), 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 Antibodies) MAPKs regulate TEF-1 and C/EBPbeta (show CEBPB Antibodies) 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 mediates YAP1 (show YAP1 Antibodies) chromatin-binding genome-wide.
show that the proangiogenic microfibrillar-associated protein 5 (MFAP5 (show MFAP5 Antibodies)) is a direct transcriptional target of YAP (show YAP1 Antibodies)/TEAD in cholangiocarcinoma cells transcription factors.
Melanoma reprogramming involves thousands of genomic regulatory regions underlying the proliferative and invasive states, identifying SOX10 (show SOX10 Antibodies)/MITF (show MITF Antibodies) and AP-1 (show FOSB Antibodies)/TEAD as regulators, respectively.
TAZ (show TAZ Antibodies) 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 Antibodies) rs11225163, TEAD1 rs7944031 and TEAD4 (show TEAD4 Antibodies) rs1990330, may independently or jointly modulate survival of CM patients.
Suggest central role for TEAD and YAP (show YAP1 Antibodies) as signal-responsive regulators of multipotent pancreatic progenitors.
the YAP (show YAP1 Antibodies)-TEAD interaction can be disrupted using cyclic YAP (show YAP1 Antibodies)-like peptides, which targets the HIPPO pathway
TEAD1 causes the nuclear sequestration of p65 (show GORASP1 Antibodies) leading to a novel TEAD1/p65 (show GORASP1 Antibodies) complex that associates with the intronic enhancer and is necessary for cytokine induction of MnSOD (show SOD2 Antibodies).
the first evidence demonstrating that TEAD1 is a novel general repressor of smooth muscle-specific gene expression through interfering with myocardin binding to SRF.
the XNTEF-1 and XDTEF-1 (show TEAD4 Antibodies) mRNAS are predominantly detected in eye, embryonic brain, somites and heart; in animal cap assay, the two genes are activated by bFGF (show FGF2 Antibodies) but are differently regulated by BMP4 (show BMP4 Antibodies), and the muscle regulatory factor Mef2d (show MEF2D Antibodies)
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