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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 (zeige TAZ Proteine) and inhibits TH17 development.
We discovered that Tead1 and co-activators Yap (zeige YAP1 Proteine) and Taz (zeige TAZ Proteine) are required for Pmp22 (zeige PMP22 Proteine) expression, as well as for the expression of Egr2 (zeige EGR2 Proteine) Tead1 directly binds Pmp22 (zeige PMP22 Proteine) and Egr2 (zeige EGR2 Proteine) enhancers early in development and Tead1 binding is induced during myelination, correlating with Pmp22 (zeige PMP22 Proteine) expression. The data identify Tead1 as a novel regulator of Pmp22 (zeige PMP22 Proteine) expression during development in concert with Sox10 (zeige SOX10 Proteine) and Egr2 (zeige EGR2 Proteine)
YAP (zeige YAP1 Proteine) 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 (zeige YAP1 Proteine) pathway components in reactive Muller cells under pathologic conditions.
Data show that TEAD family of transcription factors Tead1 and Tead4 (zeige TEAD4 Proteine)-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 (zeige MYC Proteine) RNA expression, and cells with increased Myc (zeige MYC Proteine) expression also became super-competitors.
The PDZ-binding motif of YAP (zeige YAP1 Proteine) is critical for YAP (zeige YAP1 Proteine)-mediated oncogenesis, and that this effect is mediated by YAP's co-activation of TEAD-mediated CTGF (zeige CTGF Proteine) transcription.
TEAD1 regulates C2C12 differentiation through negatively regulating the expression of Ccne1 (zeige CCNE1 Proteine), 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.
This identifies the YAP1 (zeige YAP1 Proteine)/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 (zeige YAP1 Proteine) via a conserved PPXY motif that interacts with the YAP (zeige YAP1 Proteine) WW domain. This interaction allows MRTF to recruit NcoA3 (zeige NCOA3 Proteine) to the TEAD-YAP (zeige YAP1 Proteine) transcriptional complex and potentiate its transcriptional activity.
MYC (zeige MYC Proteine) 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 (zeige APOBEC3B Proteine) through increased levels of TEADs, highlighting the importance of the TEAD-APOBEC3B (zeige APOBEC3B Proteine) axis in carcinogenesis.
Upregulation of transcriptional enhancer activator domain 1 was found in hepatocellular carcinoma tissues and inversely correlated with miR (zeige MLXIP Proteine)-590-3p. Our results indicate a tumor suppressor role of miR (zeige MLXIP Proteine)-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 (zeige PSG1 Proteine), by directly binding to its promoter.
TEAD1 mediates YAP1 (zeige YAP1 Proteine) chromatin-binding genome-wide.
show that the proangiogenic microfibrillar-associated protein 5 (MFAP5 (zeige MFAP5 Proteine)) is a direct transcriptional target of YAP (zeige YAP1 Proteine)/TEAD in cholangiocarcinoma cells transcription factors.
Melanoma reprogramming involves thousands of genomic regulatory regions underlying the proliferative and invasive states, identifying SOX10 (zeige SOX10 Proteine)/MITF (zeige MITF Proteine) and AP-1 (zeige FOSB Proteine)/TEAD as regulators, respectively.
TAZ (zeige TAZ Proteine) negatively regulate transcription of DeltaNp63 through TEAD1,2,3 and 4 transcription factors.
the XNTEF-1 and XDTEF-1 (zeige TEAD4 Proteine) mRNAS are predominantly detected in eye, embryonic brain, somites and heart; in animal cap assay, the two genes are activated by bFGF (zeige FGF2 Proteine) but are differently regulated by BMP4 (zeige BMP4 Proteine), and the muscle regulatory factor Mef2d (zeige MEF2D Proteine)
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