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抗Rat (Rattus) TFAP2B 抗体:
抗Mouse (Murine) TFAP2B 抗体:
抗Human TFAP2B 抗体:
Human Polyclonal TFAP2B Primary Antibody for ELISA, WB - ABIN563152
Bassett, Pontoriero, Feng, Marquardt, Fini, Williams, West-Mays: Conditional deletion of activating protein 2alpha (AP-2alpha) in the developing retina demonstrates non-cell-autonomous roles for AP-2alpha in optic cup development. in Molecular and cellular biology 2007
Human Polyclonal TFAP2B Primary Antibody for ICC, IF - ABIN4280859
Barzago, Kurosaki, Fratelli, Bolis, Giudice, Nordio, Cerri, Domenici, Terao, Garattini: Generation of a new mouse model of glaucoma characterized by reduced expression of the AP-2β and AP-2δ proteins. in Scientific reports 1970
LH and insulin stimulate transcription of -976/+31 bp 5'-upstream cis-acting region of porcine CYP17 gene. Maximal transcriptional responsiveness requires proximal Sp1 and AP-2-like sequences -193 to -180 bp 5' upstream of transcriptional start site.
Data demonstrates the colocalization of MARK with AP-2 and clathrin, as well as other MARK-interacting proteins such as PAK5.
tfap2b and its close relative, tfap2a, play redundant roles in the ectoderm to control skeletogenesis of neural crest cells
CVAK104 binds ATP and functions in vitro as a poly-L-lysine-stimulated kinase that is capable of autophosphorylation and phosphorylating the beta2-adaptin subunit of AP2
AP-2beta up-regulates the transcription of the CRYAB gene through stabilizing p53.
Using the Tfap2b c.435_438delCCGG homozygous mice, study verified the nature of the human c.435_438delCCGG mutation and established a new and useful animal model to explore the function of Tfap2b and the mechanisms of patent ductus arteriosus and renal formation.
these findings reveal that the AP-2 genes have a major function in mammalian neural crest development, influencing patterning of the craniofacial skeleton
AP-2beta is required in the periocular mesenchyme for normal development of the anterior segment of the eye.
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.
AP-2 beta and beta-catenin interact both in vitro through GST pull-down assays and in vivo by co-immunoprecipitation. We further identified the interaction regions to the DNA-binding domain of AP-2 beta and the 1-9 Armadillo repeats of beta-catenin.
the Tfap2a and Tfap2b transcription factors were identified as two major downstream effectors of Ptf1a.
critical roles for AP-2 activity in retinogenesis, delineating the overlapping expression patterns of Tcfap2a, Tcfap2b, and Tcfap2c in the neural retina, and revealing a redundant requirement for Tcfap2a and Tcfap2b in horizontal and amacrine cell development
Tfap2b is associated with the development and remodeling of mouse ductus arteriosus and limb patterning.
PKD is thus a common modulator of the DNA binding activity of AP-2alpha and AP-2beta through their phosphorylation for negative regulation of the ABCA1 and adiponectin genes expression, respectively.
postprandial activation of PKCmicro plays a role in disordered postprandial adipocytokine expression through AP-2beta.
Whereas AP-2alpha/beta transcription factors are in vivo not required for the onset or maintenance of noradrenergic differentiation, their essential survival functions are demonstrated for sympathetic progenitors and noradrenergic neurons.
Data suggest that AP-2beta plays critical roles in the epinephrine phenotype and maturation of adrenal chromaffin cells.
Tfap2beta, Et-1, and Hif2alpha act in a transcriptional network during ductal smooth muscle development. Disruption of this pathway may contribute to patent ductus arteriosus by affecting development of smooth muscle in the ductus arteriosus.
AP-2beta transcriptional factor is a unique regulator of IRS-1 and a candidate gene for insulin resistance.
AP-2beta is a candidate gene for producing adipocyte hypertrophy and may relate to the abnormal characteristics of adipocytes observed in obesity.
AP-2beta might modulate the expression of adiponectin by directly inhibiting its transcriptional activity
Hlxb9 and Tcfap2b were identified as genes whose expression was elevated in the ZPA compared to the rest of the developing limb bud.
The results clearly show that AP-2beta directly enhanced MCP-1 secretion by binding to its promoter. Results propose that AP-2beta positively regulates MCP-1 expression.
Data suggest that expression of TFAP2B in lobular carcinoma in situ and invasive lobular breast cancer is up-regulated as compared to control mammary gland epithelium; TFAP2B appear to be involved in regulation of cell proliferation in these slow-growing breast cancer subtypes.
previously, only 10 different pathogenic variants in the TFAP2B gene have been associated with the Char syndrome and patent ductus arteriosus (human gene mutation database subscription). We have thus identified the 11th mutation, namely, c.851T>C, p. Leu284Ser, which cosegregates with the phenotype.
study demonstrates that AP-2beta promotes tumor growth and predicts poor prognosis, and may represent a potential therapeutic target for breast cancer.
Reduced TFAP2B expression in EC was significantly associated with high grade (OR=2.2 for well, moderate vs. poor), stage (OR=2.5 for I vs. IV), histology (OR=1.8 for serous vs. endometrioid), distant metastasis (OR=2.4 for positive vs. negative) (all p-values<0.05).
TFAP2B mutation is associated with tooth abnormalities.
Single nucleotide polymorphisms (SNP) in angiotensin II receptor, type 1 (AGTR1), transcription factor AP-2 beta (TFAP2B), and tumor necrosis factor receptor-associated factor 1 (TRAF1) have been reported to be associated with the incidence of PDA in preterm infants.
results suggest that TFAP2B is playing a vital role in retaining retinoic acid responsiveness and mediating noradrenergic neuronal differentiation in neuroblastoma.
The presence of the nine-repeat variant of the TFAP-2beta intron 1 VNTR appears to protect girls with ADHD symptoms from the co-expression of symptoms of depression.
The expression of TFAP-2beta mRNA in tissue of patients with endometrial carcinoma was higher than that of normal endometrium. The expression of TFAP-2beta mRNA in endometrial tissue of patients with metabolism syndrome was higher than that of lean ones.
TFAP2B overexpression contributes to tumor growth and a poor prognosis of human lung adenocarcinoma through modulation of ERK and VEGF/PEDF signaling.
The AP-2beta polymorphism significantly influenced cognitive performance, whereas the MAOA and COMT polymorphisms did not.
A haploinsufficiency effect of TFAP2B could be involved in familial isolated patent ductus arteriosus.
TFAP2B rs987237 and dietary protein/carbohydrate interacted to modify weight maintenance.
genomic GATA4 and TFAP2B missense mutations may be associated with nonfamilial congenital heart disease with diverse clinical phenotypes in patients with congenital heart disease from southern China
Under energy restriction, TFAP2B may modify the effect of dietary fat intake on weight loss and waist reduction
The findings suggest the lack of involvement of known mutations of TFAP2B with syndromic or nonsyndromic CHDs in Mysore patients
TFAP2B mutation should be considered a risk factor for isolated PDA. However, the detailed genetic mechanism underlying nonsyndromic the PDA-causing TFAP2B mutation is yet to be elucidated.
This study supports a role of the SLC6A4, DRD4 and TFAP2B genes in the temperament, including a gene-gene interaction between SLC6A4 and TFAP2B. It also provides evidence about an effect of the TFAP2B polymorphism in TFAP2B gene transcription.
A novel splice-junction in TFAP-2B gene might lead to hereditary patent ductus arteriosus in a Chinese family.
Expression of TFAP2beta and TFAP2gamma genes in Xenopus laevis.
This gene encodes a member of the AP-2 family of transcription factors. AP-2 proteins form homo- or hetero-dimers with other AP-2 family members and bind specific DNA sequences. They are thought to stimulate cell proliferation and suppress terminal differentiation of specific cell types during embryonic development. Specific AP-2 family members differ in their expression patterns and binding affinity for different promoters. This protein functions as both a transcriptional activator and repressor. Mutations in this gene result in autosomal dominant Char syndrome, suggesting that this gene functions in the differentiation of neural crest cell derivatives.
transcription factor AP-2 beta (activating enhancer binding protein 2 beta)
, activating enhancer-binding protein 2 beta
, activating enhancer-binding protein 2-beta
, transcription factor AP-2-beta
, activating enhancer binding protein 2 beta
, transcription factor AP-2 beta
, AP2 transcription factor
, beta adaptin
, beta adaptin drosophila 1