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AP2a initiates neural border patterning and is sufficient to elicit a neural border-like pattern in neuralized ectoderm.
Genetic interaction between tfap2a and mitfa suggest that the factors en (Montrer MITF Kits ELISA)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 Kits ELISA), modulates Fgf and Notch (Montrer NOTCH1 Kits ELISA) signaling to control the duration, amount and speed of SAG (Montrer SAG Kits ELISA) neural development.
Prdm1a (Montrer PRDM1 Kits ELISA) directly binds and activates a tfap2a enhancer at the NPB (Montrer NPB Kits ELISA)
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 Kits ELISA) 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 Kits ELISA) 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 (Montrer MITF Kits ELISA) 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.
We identified miR (Montrer MLXIP Kits ELISA)-1254 as a negative regulator inhibiting HO-1 (Montrer HMOX1 Kits ELISA) translation by directly targeting HO-1 (Montrer HMOX1 Kits ELISA) 3'UTR (Montrer UTS2R Kits ELISA) via its seed region, and suppressing HO-1 (Montrer HMOX1 Kits ELISA) transcription via non-seed region-dependent inhibition of transcriptional factor AP-2 alpha (TFAP2A), a transcriptional activator of HO-1 (Montrer HMOX1 Kits ELISA).
dimerization-defective mutant of Nef failed to interact with either CD4 (Montrer CD4 Kits ELISA) or AP-2 (Montrer GTF3A Kits ELISA) in the BiFC assay, indicating that Nef quaternary structure is required for CD4 (Montrer CD4 Kits ELISA) and AP-2 (Montrer GTF3A Kits ELISA) recruitment as well as CD4 (Montrer CD4 Kits ELISA) down-regulation
Data show that TFAP2A binds many of the same regulatory elements as MITF (Montrer MITF Kits ELISA) in melanocytes.
the atrial fibrillation (AF)-associated SNP rs2595104 altered PITX2c (Montrer PITX2 Kits ELISA) expression via interaction with TFAP2a; such a pathway could ultimately contribute to AF susceptibility at the PITX2 (Montrer PITX2 Kits ELISA) locus associated with AF
AP-2a is an important transcription factor of DEK (Montrer DEK Kits ELISA) expression, which is correlated with the methylation level of the DEK (Montrer DEK Kits ELISA) core promoter in hepatocellular carcinoma .
AP-2alpha expression has a role in human hepatocellular cancer by regulating signaling to affect cell growth and migration
Hepatitis B virus X protein is able to elevate the expression of SPHK1 (Montrer SPHK1 Kits ELISA) in hepatoma cells by upregulating transcription factor AP2 alpha.
Results indicate that AP-2alpha activates COX-2 (Montrer COX2 Kits ELISA) expression to promote NPC (Montrer NPC1 Kits ELISA) 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.
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 Kits ELISA) are specifically expressed in post-mitotic dorsal interneurons. Subsequent functional assessment in chick embryos demonstrated that AP-2alpha and AP-2beta (Montrer TFAP2B Kits ELISA) have distinct functions in dorsal interneuron specification and differentiation.
MEX3C (Montrer MEX3C Kits ELISA) associates with the endolysosomal compartment through an endocytosis-like process. siRNA-mediated inhibition of the MEX3C (Montrer MEX3C Kits ELISA) or AP-2 complex (Montrer AP2B1 Kits ELISA) substantially decreased exosomal but not cellular microRNA miR (Montrer MLXIP Kits ELISA)-451a expression
High AP-2 alpha phosphorylation is associated with abdominal aortic aneurysm.
overexpression of Dnmt3a (Montrer DNMT3A Kits ELISA) partially rescued the impairment of adipogenesis induced by AP2alpha knockdown.
TFAP2A is a conserved component of the core network that regulates EMT (Montrer ITK Kits ELISA), acting as a repressor of many genes, including ZEB2 (Montrer ZEB2 Kits ELISA).
The AP-2beta (Montrer TFAP2B Kits ELISA) transcription factor is an important effector of PITX2 (Montrer PITX2 Kits ELISA) 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 (Montrer JUN Kits ELISA)/sigma1B (Montrer AP1S2 Kits ELISA)-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 (Montrer PTF1A Kits ELISA) 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 (Montrer FGF8 Kits ELISA) gene dosage
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 (activating enhancer binding protein 2 alpha)
, transcription factor AP-2 alpha
, AP-2 transcription factor
, transcription factor AP-2-alpha
, transcription factor AP-2
, Transcription factor AP-2 alpha
, adipocyte lipid-binding protein
, adipocyte-type fatty acid-binding protein
, fatty acid-binding protein 4
, fatty acid-binding protein, adipocyte
, activating enhancer-binding protein 2 alpha
, activating enhancer-binding protein 2-alpha
, activator protein 2
, mont blanc
, AP-2 alpha
, Ap-2 (a)