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anti-Mouse (Murine) TEAD1 Antibodies:
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Human Monoclonal TEAD1 Primary Antibody for 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
Show all 5 Pubmed References
Human Monoclonal TEAD1 Primary Antibody for 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
Show all 5 Pubmed References
Cow (Bovine) Polyclonal TEAD1 Primary Antibody for 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
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 (show TAZ Antibodies) and inhibits TH17 development.
We discovered that Tead1 and co-activators Yap (show YAP1 Antibodies) and Taz (show TAZ Antibodies) are required for Pmp22 (show PMP22 Antibodies) expression, as well as for the expression of Egr2 (show EGR2 Antibodies) Tead1 directly binds Pmp22 (show PMP22 Antibodies) and Egr2 (show EGR2 Antibodies) enhancers early in development and Tead1 binding is induced during myelination, correlating with Pmp22 (show PMP22 Antibodies) expression. The data identify Tead1 as a novel regulator of Pmp22 (show PMP22 Antibodies) expression during development in concert with Sox10 (show SOX10 Antibodies) and Egr2 (show EGR2 Antibodies)
YAP (show YAP1 Antibodies) 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 (show YAP1 Antibodies) pathway components in reactive Muller cells under pathologic conditions.
Data show that TEAD family of transcription factors Tead1 and Tead4 (show TEAD4 Antibodies)-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 (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.
TEAD1 and TEAD4 (show TEAD4 Antibodies) are oncogenic factors, whose aberrant activation are, in part, mediated by the silence of miR (show MLXIP Antibodies)-377-3p, miR (show MLXIP Antibodies)-1343-3p and miR (show MLXIP Antibodies)-4269.
adult human and mouse hearts had more Taz (show TAZ Antibodies) than Yap1 (show YAP1 Antibodies) by mRNA and protein expression and their increases in diseased hearts were proportional and did not change Yap1 (show YAP1 Antibodies)/Taz (show TAZ Antibodies) ratio. Yap1 (show YAP1 Antibodies), Taz (show TAZ Antibodies), 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 (show TWIST1 Antibodies)) but surprisingly without affecting muscle tissue size.
This identifies the YAP1 (show YAP1 Antibodies)/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 (show YAP1 Antibodies) via a conserved PPXY motif that interacts with the YAP (show YAP1 Antibodies) WW domain (show DRP2 Antibodies). This interaction allows MRTF to recruit NcoA3 (show NCOA3 Antibodies) to the TEAD-YAP (show YAP1 Antibodies) transcriptional complex and potentiate its transcriptional activity.
MYC (show MYC Antibodies) 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 (show APOBEC3B Antibodies) through increased levels of TEADs, highlighting the importance of the TEAD-APOBEC3B (show APOBEC3B Antibodies) axis in carcinogenesis.
Upregulation of transcriptional enhancer activator domain 1 was found in hepatocellular carcinoma tissues and inversely correlated with miR (show MLXIP Antibodies)-590-3p. Our results indicate a tumor suppressor role of miR (show MLXIP Antibodies)-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 (show PSG1 Antibodies), by directly binding to its promoter.
TEAD1 mediates YAP1 (show YAP1 Antibodies) chromatin-binding genome-wide.
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