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anti-Mouse (Murine) TEAD1 Anticorps:
anti-Rat (Rattus) TEAD1 Anticorps:
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Cow (Bovine) Polyclonal TEAD1 Primary Antibody pour IHC, 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). dans Human molecular genetics 2004
Show all 2 Pubmed References
VGLL4 inhibits cardiomyocyte proliferation by inhibiting TEAD1-YAP interaction and by targeting TEAD1 for degradation. [Hippo]
Studies in human provide evidence for the exclusive use of a non-AUG (AUU) start codon for translation initiation in vivo. This AUU codon is highly conserved among vertebrates.
The YAP/TEAD1 complex binds to DNA element and regulates the expression of genes involved in cell growth..our data demonstrate an important role of TEAD1 in early development in mice, and the floxed TEAD1 mouse model will be a valuable genetic tool to determine the temporal and tissue-specific functions of TEAD1.
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 and inhibits TH17 development.
We discovered that Tead1 and co-activators Yap and Taz are required for Pmp22 expression, as well as for the expression of Egr2 Tead1 directly binds Pmp22 and Egr2 enhancers early in development and Tead1 binding is induced during myelination, correlating with Pmp22 expression. The data identify Tead1 as a novel regulator of Pmp22 expression during development in concert with Sox10 and Egr2
YAP 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 pathway components in reactive Muller cells under pathologic conditions.
Data show that TEAD family of transcription factors Tead1 and Tead4-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 RNA expression, and cells with increased Myc expression also became super-competitors.
The PDZ-binding motif of YAP is critical for YAP-mediated oncogenesis, and that this effect is mediated by YAP's co-activation of TEAD-mediated CTGF transcription.
TEAD1 regulates C2C12 differentiation through negatively regulating the expression of Ccne1, 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 and A/T-rich elements during fast-to-slow skeletal muscle fiber type transitions
VITO-1, 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 MAPKs regulate TEF-1 and C/EBPbeta 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.
RTEF-1 bound to the element-containing region within the smooth muscle alpha-actin promoter in myofibroblasts, whereas TEF-1 was bound to the same region in differentiated smooth muscle cells
Tead1 and Tead2 are functionally redundant, use YAP as a major coactivator, and support notochord maintenance as well as cell proliferation and survival in development.
YAP1-TEAD1 signaling induces mitochondrial biogenesis in endothelial cells and stimulates angiogenesis through PGC1alpha.
TEA domain transcription factor1 (TEAD1) trans occupies at accessibility sites within AQP4, EGFR, and CDH4. TEAD1 knockout in patient-derived glioblastoma (GBM) lines diminishes migration, in vitro and in vivo, and alters migratory and epithelial-to-mesenchymal transition (EMT) transcriptome signatures with downregulation of its target AQP4.
YAP1 interacted with TEAD1, exerted their transcriptional control of the functional target, glucose transporter 1 (Glut1).
Yap1 post-translational modifications favoring its ubiquitination and apoptosis characterize hepatocellular carcinoma (HCC) with better prognosis, whereas conditions favoring the formation of YAP1-TEAD complexes are associated with aggressiveness and acquisition of stemness features by HCC cells
TEAD1 and TEAD4 are oncogenic factors, whose aberrant activation are, in part, mediated by the silence of miR-377-3p, miR-1343-3p and miR-4269.
adult human and mouse hearts had more Taz than Yap1 by mRNA and protein expression and their increases in diseased hearts were proportional and did not change Yap1/Taz ratio. Yap1, Taz, and Tead1 were accumulated in the nuclear fraction and cardiomyocyte nuclei of diseased hearts
Here, the authors show that TEAD1-expressing skeletal muscle of transgenic mice features a dramatic hyperplasia of muscle stem cells (i.e. satellite cells, SCs) but surprisingly without affecting muscle tissue size.
This identifies the YAP1/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 via a conserved PPXY motif that interacts with the YAP WW domain. This interaction allows MRTF to recruit NcoA3 to the TEAD-YAP transcriptional complex and potentiate its transcriptional activity.
MYC 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 through increased levels of TEADs, highlighting the importance of the TEAD-APOBEC3B axis in carcinogenesis.
Upregulation of transcriptional enhancer activator domain 1 was found in hepatocellular carcinoma tissues and inversely correlated with miR-590-3p. Our results indicate a tumor suppressor role of miR-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, by directly binding to its promoter.
TEAD1 mediates YAP1 chromatin-binding genome-wide.
show that the proangiogenic microfibrillar-associated protein 5 (MFAP5) is a direct transcriptional target of YAP/TEAD in cholangiocarcinoma cells transcription factors.
Melanoma reprogramming involves thousands of genomic regulatory regions underlying the proliferative and invasive states, identifying SOX10/MITF and AP-1/TEAD as regulators, respectively.
TAZ 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 rs11225163, TEAD1 rs7944031 and TEAD4 rs1990330, may independently or jointly modulate survival of CM patients.
Suggest central role for TEAD and YAP as signal-responsive regulators of multipotent pancreatic progenitors.
the XNTEF-1 and XDTEF-1 mRNAS are predominantly detected in eye, embryonic brain, somites and heart; in animal cap assay, the two genes are activated by bFGF but are differently regulated by BMP4, and the muscle regulatory factor Mef2d
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