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anti-Human TEAD4 Antibodies:
anti-Mouse (Murine) TEAD4 Antibodies:
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Human Monoclonal TEAD4 Primary Antibody for IP, RNAi - ABIN563135
Benhaddou, Keime, Ye, Morlon, Michel, Jost, Mengus, Davidson: Transcription factor TEAD4 regulates expression of myogenin and the unfolded protein response genes during C2C12 cell differentiation. in Cell death and differentiation 2012
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Cow (Bovine) Polyclonal TEAD4 Primary Antibody for IF, WB - ABIN2777935
Appukuttan, McFarland, Davies, Atchaneeyasakul, Zhang, Babra, Pan, Rosenbaum, Acott, Powers, Stout: Identification of novel alternatively spliced isoforms of RTEF-1 within human ocular vascular endothelial cells and murine retina. in Investigative ophthalmology & visual science 2007
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Cow (Bovine) Polyclonal TEAD4 Primary Antibody for IHC, WB - ABIN2780491
Chen, Baty, Maeda, Brooks, Baker, Ueyama, Gursoy, Saba, Salama, London, Stewart: Transcription enhancer factor-1-related factor-transgenic mice develop cardiac conduction defects associated with altered connexin phosphorylation. in Circulation 2004
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the transcriptional regulators in the Hippo pathway, Tead4 and Yap1, are required for general vertebrate epimorphic regeneration as well as for organ size control in appendage regeneration
TEAD4 plays an important tumor-promoting role in colorectal cancer by directly targeting the YAP1.
To analyze the clinical characteristics, treatment methods and prognosis of renal cell carcinoma associated with Xp11.2 translocation/TFE3 gene fusions
LOX nuclear localization was significantly associated with poor survival in patients with Colorectal cancer (CRC). Nuclear LOX expression was correlated with synchronous or postoperative lung/hepatic metastasis. LOX may prove to be a potential target gene of YAP and TEAD4.
Hippo pathway transcription factor TEAD4 directly associates with the Wnt pathway transcription factor TCF4 via their DNA-binding domains, forming a complex on target genes. VGLL4 binds to this TEAD4-TCF4 complex to inhibit transactivation of both TCF4 and TEAD4.
TEAD4, the transcription factor that mediates Hippo-YAP signalling, undergoes alternative splicing facilitated by the tumour suppressor RBM4.
Combining single site-directed mutagenesis and double mutant analyses, the authors conduct a detailed analysis on the role of several residues located at the YAP:TEAD interface. The results provide quantitative understanding of the interactions taking place at the YAP:TEAD interface and give insights into the formation of the YAP:TEAD complex and more particularly on the interaction between TEAD and the ohm-loop found ...
Studied the effect of TEAD4 acylation on its interaction with YAP and TAZ; found YAP and TAZ bind in a similar manner to both acylated and non-acylated TEAD4. Also found TEAD4 acylation significantly enhances its stability.
High TEF3 expression is associated with cell cycle progression and angiogenesis in colon cancer.
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.
Osmotic stress promotes TEAD4 cytoplasmic translocation via p38 MAPK in a Hippo-independent manner. Stress-induced TEAD inhibition predominates YAP-activating signals and selectively suppresses YAP-driven cancer cell growth.
The transcription factor TEAD4 regulates a pro-metastasis transcription program in a YAP-independent manner in CRC, thus providing a novel mechanism of TEAD4 transcriptional regulation and its oncogenic role in CRC, independently of the Hippo pathway.
our work provides a structural basis for understanding the regulatory mechanism of TEAD4-mediated gene transcription
Our results suggest that TEAD4 plays a role in the pathophysiology of atypical teratoid/rhabdoid tumor, which represents a new insight into the biology of this aggressive tumor
It was found that the TEAD4-YAP complex in the nuclei may be related closely to transcriptions of G1 arrest-related genes.
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.
Tead4 cooperates with AP1 transcription factors to coordinate target gene transcription.
TEAD4 and KLF5, in collaboration, promoted triple negative breast cancer cell proliferation and tumor growth in part by inhibiting p27 gene transcription
potential anti-oxidation gene and can prevent H2O2-induced endothelial cell oxidative damage by activating Klotho
TEAD4 overexpression induced p16 in HAoSMCs homozygous for the nonrisk coronary disease allele, but not for the risk allele.
TAZ negatively regulate transcription of DeltaNp63 through TEAD1,2,3 and 4 transcription factors.
TEAD4 mRNA was found to be upregulated between the 16-cell and morula stages, and nuclear localization of the TEAD4 protein was detected at the morula stage, as well as in subsequent developmental stages. TEAD4 downregulation did not affect embryonic development until the blastocyst stage, and TEAD4-downregulated embryos were capable of forming the TE under both 5% and 21% O2 conditions.
VGLL4 acted as an adaptor protein that enhanced the interaction between TEAD4 and CtBP2, and this TEAD4-VGLL4-CtBP2 ternary complex dynamically existed at the early stage of adipogenesis.
Schwann cell-specific deletion of either Hdac3 or Tead4 in mice resulted in an elevation of myelin thickness in sciatic nerves. Thus, our findings identify the HDAC3-TEAD4 network as a dual-function switch of cell-intrinsic inhibitory machinery that counters myelinogenic signals and maintains peripheral myelin homeostasis
Structural and ligand-binding analysis of the YAP-binding domain of transcription factor TEAD4.
These studies identify a novel TEAD4-dependent molecular mechanism that regulates energy metabolism in the trophectoderm lineage to ensure mammalian development.
TEAD4 mediated the interaction between YAP1 and c-JUN. YAP1 and the YAP1-TEADs complex have roles in regulating osteoclastogenesis and related gene expression.
Based on the similarity to a related family member, and in vitro transcription/translation product(s), the authors propose that translation initiates from a non-AUG (AUA or AUU) start codon.
AP-1- and TEAD4-associated cis-regulatory elements form hubs for multiple signalling-responsive transcription factors and define the cistrome that regulates vascular and hematopoietic development by extrinsic signals.
Data show that TEAD family of transcription factors Tead1 and Tead4-regulated gene expression in differentiating primary myoblasts.
Dual-luciferase reporter gene analysis showed that RTEF-1 is a direct target of mir-125a-5p, which regulates angiogenesis by repressing RTEF-1 expression and modulating eNOS and VEGF expression.
TEAD4 establishes the energy homeostasis essential for blastocoel formation.
These results show that RTEF-1-stimulated IGFBP-1 expression may be central to the mechanism by which RTEF-1 attenuates blood glucose levels.
Vgll1 interacts with TEAD4 in a manner similar to the transcription coactivators, as well as oncogenes YAP and TAZ, despite having a varied primary sequence. Vgll1 has the potential to promote cancer progression.
endothelial-specific RTEF-1 overexpressing mice had enhanced angiogenic sprouting and vascular structure remodeling, resulting in the formation of a denser and more highly interconnected superficial capillary plexus
Data suggest that altered subcellular localization of TEAD4 in blastomeres dictates first mammalian cell fate specification.
TEAD factors directly induce Myogenin, CDKN1A and Caveolin 3 expression to promote myoblast differentiation.
Gata3 and Cdx2 can act in parallel pathways downstream of Tead4 to induce the expression of common and independent targets in the trophoblast lineage, whereas Oct4 is required for continued repression of trophoblast fate in the embryonic lineage
Novel RTEF-1 transcripts are present within human ocular vascular endothelial cells and mouse neural retina during normal and retinopathy of prematurity development, and alternatively spliced products are produced under hyperoxic and hypoxic conditions
RTEF-1 regulated smooth muscle alpha-actin transcription in myofibroblasts, but not in differentiated smooth muscle
Tead4 is the earliest gene shown to be uniquely required for specification of the trophectoderm lineage
Tead4 has a distinct role from Tead1 and Tead2 in trophectoderm specification of pre-implantation embryos; it is an early transcription factor required for specification and development of the trophectoderm lineage, which includes expression of Cdx2.
This gene product is a member of the transcriptional enhancer factor (TEF) family of transcription factors, which contain the TEA/ATTS DNA-binding domain. It is preferentially expressed in the skeletal muscle, and binds to the M-CAT regulatory element found in promoters of muscle-specific genes to direct their gene expression. Alternatively spliced transcripts encoding distinct isoforms, some of which are translated through the use of a non-AUG (UUG) initiation codon, have been described for this gene.
TEA domain family member 4
, M-CAT binding factor
, M-CAT-binding factor
, transcriptional enhancer factor TEF-3
, related transcription enhancer factor 1B
, transcription factor 13-like 1
, transcription factor RTEF-1
, transcriptional enhancer factor 1-related
, transcriptional enhancer factor 3
, transcriptional enhancer factor 1-related protein
, ETF-related factor 2
, ETF-related factor-2
, FGF-regulated 19
, TEF-1-related factor 1
, TEF-1-related factor FR-19