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Human TFAP2A Protein expressed in Wheat germ - ABIN1322523
Zhang, Li, Shibahara, Takahashi: Synergistic activation of the human adrenomedullin gene promoter by Sp1 and AP-2alpha. in Peptides 2008
AP2a may regulate the osteogenic differentiation in an indirect way through competing with RUNX2 to relieve the RUNX2 activity which inhibited by YAP, and also in a direct way via inhibiting the BARX1 in mesenchymal stem cells.
In the present paper, we report that Wnt-induced lipid droplet biogenesis does not depend on the canonical TCF/LEF transcription factors. Instead, we find that TFAP2 family members mediate the pro-lipid droplet signal induced by Wnt3a, leading to the notion that the TFAP2 transcription factor may function as a 'master' regulator of lipid droplet biogenesis.
The data suggest that IRF6, TFAP2A, and GRHL3, among others, are shared in neural tube and orofacial development.
Results show that gout-associated increased NRBP1 expression is regulated through methylation-dependent TFAP2A binding to the B1 region, which might be involved in the pathogenesis of gout.
our results indicate that AP-2alpha can reverse the Multidrug resistance (MDR) of gastric cancer cells, which may be realized by inhibiting the Notch signaling pathway.
High-confidence AP2alpha-binding peaks were detected in the regulatory regions of many target genes involved in the development of facial tissues including MSX1, IRF6, TBX22, and MAFB. In addition, we uncovered multiple single-nucleotide polymorphisms (SNPs) disrupting a conserved AP2alpha consensus sequence.
We identified two SLN genes (PIGR and TFAP2A) that provided high prognostic accuracy in SLN-positive melanoma patients (AUC = 0.864). These two SLN genes, along with clinicopathological features, can differentiate the high- and low-risk groups in node-positive melanoma patients
We identified miR-1254 as a negative regulator inhibiting HO-1 translation by directly targeting HO-1 3'UTR via its seed region, and suppressing HO-1 transcription via non-seed region-dependent inhibition of transcriptional factor AP-2 alpha (TFAP2A), a transcriptional activator of HO-1.
dimerization-defective mutant of Nef failed to interact with either CD4 or AP-2 in the BiFC assay, indicating that Nef quaternary structure is required for CD4 and AP-2 recruitment as well as CD4 down-regulation
Data show that TFAP2A binds many of the same regulatory elements as MITF in melanocytes.
the atrial fibrillation (AF)-associated SNP rs2595104 altered PITX2c expression via interaction with TFAP2a; such a pathway could ultimately contribute to AF susceptibility at the PITX2 locus associated with AF
AP-2a is an important transcription factor of DEK expression, which is correlated with the methylation level of the DEK core promoter in hepatocellular carcinoma .
AP-2alpha expression has a role in human hepatocellular cancer by regulating signaling to affect cell growth and migration
role in the expression of Latent membrane protein 1
Hepatitis B virus X protein is able to elevate the expression of SPHK1 in hepatoma cells by upregulating transcription factor AP2 alpha.
Results indicate that AP-2alpha activates COX-2 expression to promote NPC growth.
The AP-2alpha transcription factor may play an important role in suppressing glioma progression.
TFAP2A might play a role in the development of Ovarian Cancer, and may be a therapeutic target in OC.
INHA gene expression is upregulated by cAMP via CRE in human trophoblasts, and TFAP2 regulates this expression by interacting with CRE.
Human melanomas display higher than normal CpG DNA methylation at the TFAP2A promoter.Aberrant CpG DNA methylation as an epigenetic mark associated with TFAP2A silencing in human melanoma.
Genetic interaction between tfap2a and mitfa suggest that the factors encoded by these genes regulate shared targets in melanocytes, possibly within single or converging pathways.
these data support a model in which Tfap2a, acting through Bmp7a, modulates Fgf and Notch signaling to control the duration, amount and speed of SAG neural development.
Prdm1a directly binds and activates a tfap2a enhancer at the NPB
Low Bmp activates expression of the transcription factor Tfap2a as part of a gene regulatory network that coordinates development of neural crest, preplacodal ectoderm and individual placodes in zebrafish.
tfap2a and foxd3 are expressed during gastrulation prior to neural crest induction in distinct, complementary, domains; tfap2a is expressed in the ventral non-neural ectoderm and foxd3 in the dorsal mesendoderm and ectoderm
These results reveal that mutations in TFAP2A are associated with a wide range of eye phenotypes and that hypomorphic tfap2a mutations can increase the risk of developmental defects arising from mutations at other loci.
These findings reveal that Tfap2 activity, mediated redundantly by Tfap2a and Tfap2e, promotes melanophore differentiation in parallel with Mitf by an effector other than Kit.
Results demonstrate that tfap2a is required for early steps in neural crest development and for the survival of a subset of neural crest derivatives.
data show that hindbrain noradrenergic neurons of the locus coeruleus and the posterior groups both require Tfap2a to establish their noradrenergic identity
Ap-2alpha regulates multiple steps of melanophore development, and is required for development of other neuronal and non-neuronal neural crest derivatives.
function in the neural crest in specification of subpopulations of pigment cells and segmental patterning of the pharyngeal skeleton through the regulation of Hox genes
Data suggest that tfap2a does not appear to be involved in early specification and cell proliferation of neural crest, but it is a key regulator of an early differentiation phase and is required for cell survival in neural crest derived cell lineages.
tfap2a and its close relative, tfap2b, play redundant roles in the ectoderm to control skeletogenesis of neural crest cells
Redundant activities of Tfap2a and Tfap2c are required for neural crest induction and development of other non-neural ectoderm derivatives in zebrafish embryos.
Here, the authors show that adam13 interacts with the arid3a/dril1/Bright transcription factor. This interaction promotes a proteolytic cleavage of arid3a and its translocation to the nucleus where it regulates another transcription factor: tfap2alpha. Tfap2alpha in turn activates multiple genes including the protocadherin pcdh8l (PCNS).
AP2a initiates neural border patterning and is sufficient to elicit a neural border-like pattern in neuralized ectoderm.
Electroporating siRNA into bovine trophoblast cells could be an efficient method to manipulate binucleate trophoblast giant cells function and to study the regulation mechanism of specific gene transcription.
Together these findings demonstrate the requirement for both AP-2alpha and AP-2beta in proper amacrine mosaic patterning and a normal functional light response in the retina.
AP2gamma is present in a sub-population of hippocampal transient amplifying progenitors. There, it is found to act as a positive regulator of the cell fate determinants Tbr2 and NeuroD, promoting proliferation and differentiation of new glutamatergic granular neurons. Conditional ablation of AP2gamma in adult brain reduced hippocampal neurogenesis and disrupted coherence between ventral hippocampus and medial prefronta...
these findings reveal that the AP-2 genes have a major function in mammalian neural crest development, influencing patterning of the craniofacial skeleton
RNA interference of transcriptional factor activator protein 2alpha (AP-2alpha) reversed the inhibitory effects of aspirin on atherosclerosis in Apoe-/- mice.
Study systematically examined the expression profile of AP-2 family in the developing mouse and chick spinal cord and found that AP-2alpha and AP-2beta are specifically expressed in post-mitotic dorsal interneurons. Subsequent functional assessment in chick embryos demonstrated that AP-2alpha and AP-2beta have distinct functions in dorsal interneuron specification and differentiation.
MEX3C associates with the endolysosomal compartment through an endocytosis-like process. siRNA-mediated inhibition of the MEX3C or AP-2 complex substantially decreased exosomal but not cellular microRNA miR-451a expression
High AP-2 alpha phosphorylation is associated with abdominal aortic aneurysm.
overexpression of Dnmt3a partially rescued the impairment of adipogenesis induced by AP2alpha knockdown.
TFAP2A is a conserved component of the core network that regulates EMT, acting as a repressor of many genes, including ZEB2.
The AP-2beta transcription factor is an important effector of PITX2 function during corneal development, required for differentiation of corneal endothelium and establishment of angiogenic privilege.
the regulation of synaptic-vesicle (SV) recycling via early endosomes by the interdependent regulation of AP-2-mediated endocytosis and AP-1/sigma1B-mediated SV reformation, is reported.
By gain-of function and loss-of-function approaches, ap2a and 2b were identified to be the major downstream targets of Ptf1a to specify the amacrine cell fate.
Tfap2a-dependent changes in mouse facial morphology result in clefting that can be ameliorated by a reduction in Fgf8 gene dosage
results suggested that RNF20 may play roles in adipocyte differentiation by stimulating ubiquitin-proteasome-dependent degradation of AP-2alpha.
These findings indicate that Suv39h1 enhances AP-2alpha-mediated transcriptional repression of C/EBPalpha in an epigenetic manner and further inhibits adipocyte differentiation.
N-terminal peptide sequencing indicates use of a downstream start codon in the human ortholog of AP-2.
A conserved N-terminus is observed for alpha, beta, gamma, and epsilon members of this gene family.
AP-2alpha defines epididymis-specific androgen receptor recruitment. It is constitutively bound to chromatin and guides AR to specific genomic loci upon hormone exposure.
The protein encoded by this gene is a transcription factor that binds the consensus sequence 5'-GCCNNNGGC-3'. The encoded protein functions as either a homodimer or as a heterodimer with similar family members. This protein activates the transcription of some genes while inhibiting the transcription of others. Defects in this gene are a cause of branchiooculofacial syndrome (BOFS). Three transcript variants encoding different isoforms have been found for this gene.
transcription factor AP-2 alpha
, transcription factor AP-2
, AP-2 transcription factor
, activating enhancer-binding protein 2-alpha
, activator protein 2
, transcription factor AP-2-alpha
, transcription factor AP-2 alpha (activating enhancer binding protein 2 alpha)
, mont blanc
, activating enhancer-binding protein 2 alpha
, Transcription factor AP-2 alpha
, AP-2 alpha
, Ap-2 (a)