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anti-Human TFAP2A Anticorps:
anti-Mouse (Murine) TFAP2A Anticorps:
anti-Rat (Rattus) TFAP2A Anticorps:
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Human Polyclonal TFAP2A Primary Antibody pour WB - ABIN3434032
Mitchell, Abdelrahim, Weng, Stafford, Safe, Bar-Eli, Liu: Regulation of KiSS-1 metastasis suppressor gene expression in breast cancer cells by direct interaction of transcription factors activator protein-2alpha and specificity protein-1. dans The Journal of biological chemistry 2006
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Mouse (Murine) Polyclonal TFAP2A Primary Antibody pour WB - ABIN1945094
Moser, Pscherer, Bauer, Imhof, Seegers, Kerscher, Buettner: The complete murine cDNA sequence of the transcription factor AP-2. dans Nucleic acids research 1993
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Human Polyclonal TFAP2A Primary Antibody pour WB - ABIN1882156
Semenza: Oxygen-dependent regulation of mitochondrial respiration by hypoxia-inducible factor 1. dans The Biochemical journal 2007
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Chicken Monoclonal TFAP2A Primary Antibody pour ICC, IF - ABIN261468
Milgrom-Hoffman, Michailovici, Ferrara, Zelzer, Tzahor: Endothelial cells regulate neural crest and second heart field morphogenesis. dans Biology open 2014
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Human Polyclonal TFAP2A Primary Antibody pour ELISA, ICC - ABIN6259961
Yang, Wei, Song, Cai, Zhou, Peng, Jiang, Peng: E4BP4 mediates glucocorticoid-regulated adipogenesis through COX2. dans Molecular and cellular endocrinology 2018
The data suggest that IRF6 (Montrer IRF6 Anticorps), TFAP2A, and GRHL3 (Montrer GRHL3 Anticorps), among others, are shared in neural tube and orofacial development.
Results show that gout-associated increased NRBP1 (Montrer NRBP1 Anticorps) 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 (Montrer NOTCH1 Anticorps) signaling pathway.
High-confidence AP2alpha (Montrer AP2A1 Anticorps)-binding peaks were detected in the regulatory regions of many target genes involved in the development of facial tissues including MSX1 (Montrer MSX1 Anticorps), IRF6 (Montrer IRF6 Anticorps), TBX22 (Montrer TBX22 Anticorps), and MAFB (Montrer MAFB Anticorps). In addition, we uncovered multiple single-nucleotide polymorphisms (SNPs) disrupting a conserved AP2alpha (Montrer AP2A1 Anticorps) consensus sequence.
We identified two SLN (Montrer SLN Anticorps) genes (PIGR (Montrer PIGR Anticorps) and TFAP2A) that provided high prognostic accuracy in SLN (Montrer SLN Anticorps)-positive melanoma patients (AUC = 0.864). These two SLN (Montrer SLN Anticorps) genes, along with clinicopathological features, can differentiate the high- and low-risk groups in node-positive melanoma patients
We identified miR (Montrer MLXIP Anticorps)-1254 as a negative regulator inhibiting HO-1 (Montrer HMOX1 Anticorps) translation by directly targeting HO-1 (Montrer HMOX1 Anticorps) 3'UTR (Montrer UTS2R Anticorps) via its seed region, and suppressing HO-1 (Montrer HMOX1 Anticorps) transcription via non-seed region-dependent inhibition of transcriptional factor AP-2 alpha (TFAP2A), a transcriptional activator of HO-1 (Montrer HMOX1 Anticorps).
dimerization-defective mutant of Nef failed to interact with either CD4 (Montrer CD4 Anticorps) or AP-2 (Montrer GTF3A Anticorps) in the BiFC assay, indicating that Nef quaternary structure is required for CD4 (Montrer CD4 Anticorps) and AP-2 (Montrer GTF3A Anticorps) recruitment as well as CD4 (Montrer CD4 Anticorps) down-regulation
Data show that TFAP2A binds many of the same regulatory elements as MITF (Montrer MITF Anticorps) in melanocytes.
the atrial fibrillation (AF)-associated SNP rs2595104 altered PITX2c (Montrer PITX2 Anticorps) expression via interaction with TFAP2a; such a pathway could ultimately contribute to AF susceptibility at the PITX2 (Montrer PITX2 Anticorps) locus associated with AF
AP-2a is an important transcription factor of DEK (Montrer DEK Anticorps) expression, which is correlated with the methylation level of the DEK (Montrer DEK Anticorps) core promoter in hepatocellular carcinoma .
Genetic interaction between tfap2a and mitfa suggest that the factors en (Montrer MITF Anticorps)coded 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 (Montrer BMP7 Anticorps), modulates Fgf and Notch (Montrer NOTCH1 Anticorps) signaling to control the duration, amount and speed of SAG (Montrer SAG Anticorps) neural development.
Prdm1a (Montrer PRDM1 Anticorps) directly binds and activates a tfap2a enhancer at the NPB (Montrer NPB Anticorps)
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 (Montrer FOXD3 Anticorps) are expressed during gastrulation prior to neural crest induction in distinct, complementary, domains; tfap2a is expressed in the ventral non-neural ectoderm and foxd3 (Montrer FOXD3 Anticorps) 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 (Montrer TFAP2E Anticorps), promotes melanophore differentiation in parallel with Mitf (Montrer MITF Anticorps) 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.
Here, the authors show that adam13 (Montrer ADAM33 Anticorps) interacts with the arid3a/dril1 (Montrer ARID3A Anticorps)/Bright transcription factor. This interaction promotes a proteolytic cleavage of arid3a (Montrer ARID3A Anticorps) 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.
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 (Montrer APOE Anticorps)-/- 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 (Montrer TFAP2B Anticorps) are specifically expressed in post-mitotic dorsal interneurons. Subsequent functional assessment in chick embryos demonstrated that AP-2alpha and AP-2beta (Montrer TFAP2B Anticorps) have distinct functions in dorsal interneuron specification and differentiation.
MEX3C (Montrer MEX3C Anticorps) associates with the endolysosomal compartment through an endocytosis-like process. siRNA-mediated inhibition of the MEX3C (Montrer MEX3C Anticorps) or AP-2 complex (Montrer AP2B1 Anticorps) substantially decreased exosomal but not cellular microRNA miR (Montrer MLXIP Anticorps)-451a expression
High AP-2 alpha phosphorylation is associated with abdominal aortic aneurysm.
overexpression of Dnmt3a (Montrer DNMT3A Anticorps) partially rescued the impairment of adipogenesis induced by AP2alpha knockdown.
TFAP2A is a conserved component of the core network that regulates EMT (Montrer ITK Anticorps), acting as a repressor of many genes, including ZEB2 (Montrer ZEB2 Anticorps).
The AP-2beta (Montrer TFAP2B Anticorps) transcription factor is an important effector of PITX2 (Montrer PITX2 Anticorps) function during corneal development, required for differentiation of corneal endothelium and establishment of angiogenic privilege.
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)