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anti-Mouse (Murine) TEAD1 Antikörper:
anti-Rat (Rattus) TEAD1 Antikörper:
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Human Monoclonal TEAD1 Primary Antibody für IF, WB - ABIN968252
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
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Human Monoclonal TEAD1 Primary Antibody für IF, WB - ABIN968251
Gupta, Amin, Gupta, Hay, Zak: Transcription enhancer factor 1 interacts with a basic helix-loop-helix zipper protein, Max, for positive regulation of cardiac alpha-myosin heavy-chain gene expression. in Molecular and cellular biology 1997
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Cow (Bovine) Polyclonal TEAD1 Primary Antibody für 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). in Human molecular genetics 2004
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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 Antikörper) and inhibits TH17 development.
We discovered that Tead1 and co-activators Yap (zeige YAP1 Antikörper) and Taz (zeige TAZ Antikörper) are required for Pmp22 (zeige PMP22 Antikörper) expression, as well as for the expression of Egr2 (zeige EGR2 Antikörper) Tead1 directly binds Pmp22 (zeige PMP22 Antikörper) and Egr2 (zeige EGR2 Antikörper) enhancers early in development and Tead1 binding is induced during myelination, correlating with Pmp22 (zeige PMP22 Antikörper) expression. The data identify Tead1 as a novel regulator of Pmp22 (zeige PMP22 Antikörper) expression during development in concert with Sox10 (zeige SOX10 Antikörper) and Egr2 (zeige EGR2 Antikörper)
YAP (zeige YAP1 Antikörper) 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 Antikörper) pathway components in reactive Muller cells under pathologic conditions.
Data show that TEAD family of transcription factors Tead1 and Tead4 (zeige TEAD4 Antikörper)-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 Antikörper) RNA expression, and cells with increased Myc (zeige MYC Antikörper) expression also became super-competitors.
The PDZ (zeige INADL Antikörper)-binding motif of YAP (zeige YAP1 Antikörper) is critical for YAP (zeige YAP1 Antikörper)-mediated oncogenesis, and that this effect is mediated by YAP's co-activation of TEAD-mediated CTGF (zeige CTGF Antikörper) transcription.
TEAD1 regulates C2C12 differentiation through negatively regulating the expression of Ccne1 (zeige CCNE1 Antikörper), 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.
TEAD1 and TEAD4 (zeige TEAD4 Antikörper) are oncogenic factors, whose aberrant activation are, in part, mediated by the silence of miR (zeige MLXIP Antikörper)-377-3p, miR (zeige MLXIP Antikörper)-1343-3p and miR (zeige MLXIP Antikörper)-4269.
adult human and mouse hearts had more Taz (zeige TAZ Antikörper) than Yap1 (zeige YAP1 Antikörper) by mRNA and protein expression and their increases in diseased hearts were proportional and did not change Yap1 (zeige YAP1 Antikörper)/Taz (zeige TAZ Antikörper) ratio. Yap1 (zeige YAP1 Antikörper), Taz (zeige TAZ Antikörper), 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 (zeige TWIST1 Antikörper)) but surprisingly without affecting muscle tissue size.
This identifies the YAP1 (zeige YAP1 Antikörper)/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 Antikörper) via a conserved PPXY motif that interacts with the YAP (zeige YAP1 Antikörper) WW domain (zeige DRP2 Antikörper). This interaction allows MRTF to recruit NcoA3 (zeige NCOA3 Antikörper) to the TEAD-YAP (zeige YAP1 Antikörper) transcriptional complex and potentiate its transcriptional activity.
MYC (zeige MYC Antikörper) 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 Antikörper) through increased levels of TEADs, highlighting the importance of the TEAD-APOBEC3B (zeige APOBEC3B Antikörper) axis in carcinogenesis.
Upregulation of transcriptional enhancer activator domain 1 was found in hepatocellular carcinoma tissues and inversely correlated with miR (zeige MLXIP Antikörper)-590-3p. Our results indicate a tumor suppressor role of miR (zeige MLXIP Antikörper)-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 Antikörper), by directly binding to its promoter.
TEAD1 mediates YAP1 (zeige YAP1 Antikörper) chromatin-binding genome-wide.
the XNTEF-1 and XDTEF-1 (zeige TEAD4 Antikörper) mRNAS are predominantly detected in eye, embryonic brain, somites and heart; in animal cap assay, the two genes are activated by bFGF (zeige FGF2 Antikörper) but are differently regulated by BMP4 (zeige BMP4 Antikörper), and the muscle regulatory factor Mef2d (zeige MEF2D Antikörper)
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