Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher tous les synonymes
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
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 (Montrer TAZ Anticorps) and inhibits TH17 development.
We discovered that Tead1 and co-activators Yap (Montrer YAP1 Anticorps) and Taz (Montrer TAZ Anticorps) are required for Pmp22 (Montrer PMP22 Anticorps) expression, as well as for the expression of Egr2 (Montrer EGR2 Anticorps) Tead1 directly binds Pmp22 (Montrer PMP22 Anticorps) and Egr2 (Montrer EGR2 Anticorps) enhancers early in development and Tead1 binding is induced during myelination, correlating with Pmp22 (Montrer PMP22 Anticorps) expression. The data identify Tead1 as a novel regulator of Pmp22 (Montrer PMP22 Anticorps) expression during development in concert with Sox10 (Montrer SOX10 Anticorps) and Egr2 (Montrer EGR2 Anticorps)
YAP (Montrer YAP1 Anticorps) 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 (Montrer YAP1 Anticorps) pathway components in reactive Muller cells under pathologic conditions.
Data show that TEAD family of transcription factors Tead1 and Tead4 (Montrer TEAD4 Anticorps)-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 (Montrer MYC Anticorps) RNA expression, and cells with increased Myc (Montrer MYC Anticorps) expression also became super-competitors.
The PDZ (Montrer INADL Anticorps)-binding motif of YAP (Montrer YAP1 Anticorps) is critical for YAP (Montrer YAP1 Anticorps)-mediated oncogenesis, and that this effect is mediated by YAP's co-activation of TEAD-mediated CTGF (Montrer CTGF Anticorps) transcription.
TEAD1 regulates C2C12 differentiation through negatively regulating the expression of Ccne1 (Montrer CCNE1 Anticorps), 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.
YAP1 (Montrer YAP1 Anticorps) interacted with TEAD1, exerted their transcriptional control of the functional target, glucose transporter 1 (Glut1 (Montrer SLC2A1 Anticorps)).
Yap1 (Montrer YAP1 Anticorps) post-translational modifications favoring its ubiquitination and apoptosis characterize hepatocellular carcinoma (HCC (Montrer FAM126A Anticorps)) with better prognosis, whereas conditions favoring the formation of YAP1 (Montrer YAP1 Anticorps)-TEAD complexes are associated with aggressiveness and acquisition of stemness features by HCC (Montrer FAM126A Anticorps) cells
TEAD1 and TEAD4 (Montrer TEAD4 Anticorps) are oncogenic factors, whose aberrant activation are, in part, mediated by the silence of miR (Montrer MLXIP Anticorps)-377-3p, miR (Montrer MLXIP Anticorps)-1343-3p and miR (Montrer MLXIP Anticorps)-4269.
adult human and mouse hearts had more Taz (Montrer TAZ Anticorps) than Yap1 (Montrer YAP1 Anticorps) by mRNA and protein expression and their increases in diseased hearts were proportional and did not change Yap1 (Montrer YAP1 Anticorps)/Taz (Montrer TAZ Anticorps) ratio. Yap1 (Montrer YAP1 Anticorps), Taz (Montrer TAZ Anticorps), 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 (Montrer TWIST1 Anticorps)) but surprisingly without affecting muscle tissue size.
This identifies the YAP1 (Montrer YAP1 Anticorps)/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 (Montrer YAP1 Anticorps) via a conserved PPXY motif that interacts with the YAP (Montrer YAP1 Anticorps) WW domain (Montrer DRP2 Anticorps). This interaction allows MRTF to recruit NcoA3 (Montrer NCOA3 Anticorps) to the TEAD-YAP (Montrer YAP1 Anticorps) transcriptional complex and potentiate its transcriptional activity.
MYC (Montrer MYC Anticorps) 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 (Montrer APOBEC3B Anticorps) through increased levels of TEADs, highlighting the importance of the TEAD-APOBEC3B (Montrer APOBEC3B Anticorps) axis in carcinogenesis.
Upregulation of transcriptional enhancer activator domain 1 was found in hepatocellular carcinoma tissues and inversely correlated with miR (Montrer MLXIP Anticorps)-590-3p. Our results indicate a tumor suppressor role of miR (Montrer MLXIP Anticorps)-590-3p in hepatocellular carcinoma through targeting transcriptional enhancer activator domain 1 and suggest its use in the diagnosis and prognosis of liver cancer.
the XNTEF-1 and XDTEF-1 (Montrer TEAD4 Anticorps) mRNAS are predominantly detected in eye, embryonic brain, somites and heart; in animal cap assay, the two genes are activated by bFGF (Montrer FGF2 Anticorps) but are differently regulated by BMP4 (Montrer BMP4 Anticorps), and the muscle regulatory factor Mef2d (Montrer MEF2D Anticorps)
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