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AP-2α/β Polyclonal Antibody

Product code: YP-Ab-01531
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Product introduction

Reactive species
Human;Mouse;Rat
Applications
WB;IHC;IF;ELISA
Antibody type
Polyclonal Antibody
Gene Name
TFAP2A/TFAP2B
Protein name
Transcription factor AP-2-alpha/beta
Dalton(DA)
49kD
Immunogen
The antiserum was produced against synthesized peptide derived from human AP-2. AA range:388-437
Specificity
AP-2α/β Polyclonal Antibody detects endogenous levels of AP-2α/β protein.
Constitute
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source
Polyclonal, Rabbit,IgG
Dilution rate
WB: 1/500 - 1/2000. IHC: 1/100 - 1/300. ELISA: 1/10000.. IF 1:50-200
Purification process
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration
1 mg/ml
Stockpile
-20°C/1 year
Other name
TFAP2A; AP2TF; TFAP2; Transcription factor AP-2-alpha; AP2-alpha; AP-2 transcription factor; Activating enhancer-binding protein 2-alpha; Activator protein 2; AP-2; TFAP2B; Transcription factor AP-2-beta; AP2-beta; Activating enhancer-bindi
Background
transcription factor AP-2 alpha(TFAP2A) Homo sapiens 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.[provided by RefSeq, Dec 2009],
Function
alternative products:Experimental confirmation may be lacking for some isoforms,disease:Defects in TFAP2A are the cause of branchiooculofacial syndrome (BOFS) [MIM:113620]; also known as branchial clefts with characteristic facies, growth retardation, imperforate nasolacrimal duct, and premature aging or lip pseudocleft-hemangiomatous branchial cyst syndrome. BOFS is a rare autosomal dominant cleft palate craniofacial disorder with variable expressivity. The major features include cutaneous anomalies, ocular anomalies, characteristic facial appearance (malformed pinnae, oral clefts), and, less commonly, renal and ectodermal (dental and hair) anomalies.,domain:The WW-binding motif mediates interaction with WWOX.,function:Sequence-specific DNA-binding protein that interacts with inducible viral and cellular enhancer elements to regulate transcription of selected genes. AP-2 factors bind to

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