TFAP2B

Last update 08 May 2025

Basic Info

Synonyms

Activating enhancer-binding protein 2-beta, AP-2beta, AP2-B

+ [4]

Introduction

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 the consensus sequence 5'-GCCNNNGGC-3' and activate genes involved in a large spectrum of important biological functions including proper eye, face, body wall, limb and neural tube development. They also suppress a number of genes including MCAM/MUC18, C/EBP alpha and MYC. AP-2-beta appears to be required for normal face and limb development and for proper terminal differentiation and function of renal tubular epithelia.

100 Clinical Results associated with TFAP2B

100 Translational Medicine associated with TFAP2B

0 Patents (Medical) associated with TFAP2B

267

Literatures (Medical) associated with TFAP2B

01 Apr 2025·Experimental Neurology

Transcription factor AP-2 Beta, a potential target of repetitive Transspinal magnetic stimulation in spinal cord injury treatment, reduced inflammation and alleviated spinal cord injury

Article

Author: Yang, Yang ; Xu, Aihua ; Zhang, Yuxi ; Shao, Yang ; Sun, Yongxin ; Wang, Kunpeng ; Dai, Qi

Spinal cord injury (SCI) is a neurodegenerative disease, with a high disability rate. According to the results of mRNA-seq, transcription factor AP-2 Beta (TFAP2B) is a potential target of repetitive Transspinal Magnetic Stimulation (rTSMS) in SCI treatment. Our results demonstrated that rTSMS significantly improved motor function and promoted neuronal survival post-SCI. The result showed that TFAP2B was downregulated following SCI, while significant upregulation after rTSMS treatment, suggesting its pivotal role in neuronal repair. Overexpression of TFAP2B improved Basso Beattie and Bresnahan (BBB) score and athletic ability, and decreased cell apoptosis in SCI rats. Additionally, overexpression of TFAP2B reduced the expression of Iba1 and GFAP in spinal cord, and the expression of PDGFrβ was also reduced in SCI rats after TFAP2B overexpression. Knockdown of TFAP2B reverses the effect of rTSMS treatment in SCI. We found that rTSMS alleviate osteoporosis caused by SCI, resulting in increased BMD, BV/TV, and Tb.Th. rTSMS treatment lowered the RANKL/OPG ratio. In all, our study illustrated TFAP2B is a downstream target of rTSMS for the treatment of SCI, and overexpression of TFAP2B enhanced the therapeutic effect of rTSMS.

06 Mar 2025·Genome Biology and Evolution

Genome-Wide Selection Scans in Mexican Indigenous Populations Reveal Recent Signatures of Pathogen and Diet Adaptation

Article

Author: Morett, Enrique ; Reynolds, Austin W ; Miron-Toruno, Maria Fernanda ; Aguilar-Ordonez, Israel

AbstractWhole-genome scans for natural selection signatures across Mexican indigenous populations remain underrepresented in the literature. Here, we conducted the first comparative analysis of genetic adaptation in Mexican indigenous populations using whole-genome sequencing data from 76 individuals representing 27 different ethnic groups in Mexico. We divided the cohort into northern, central, and southern populations and identified signals of natural selection within and across populations. We find evidence of adaptation to pathogenic environments in all our populations, including significant signatures in the Duffy blood group gene in central Mexican indigenous populations. Despite each region exhibiting unique local adaptation profiles, selection signatures on ARHGAP15, VGLL4, LINGO2, SYNDIG1, and TFAP2B were common to all populations. Our results also suggest that selection signatures falling within enhancers or promoters are usually connected to noncoding features, with notable exceptions like ARHGAP15 and GTDC1. This paper provides new evidence on the selection landscape of Mexican indigenous populations and lays the foundation for additional work on Mexican phenotypic characterization.

01 Mar 2025·Biochemical and Biophysical Research Communications

TFAP2B governs the regulation of SIRT1 to inhibit osteoclast-induced bone destruction

Article

Author: Chen, Peixiong ; Lin, Zengping ; Zeng, Xiaoxia ; Zhao, Dapeng ; Zeng, Xianhai ; Wen, Liting

BACKGROUNDCholesteatoma is a benign epithelial lesion that affects the middle ear or mastoid process, causing otorrhea and hearing impairment. Currently, the pathogenesis of temporal bone injury in middle ear cholesteatoma remains elusive, hindering the development of effective treatment strategies.METHODS AND RESULTSWe examined the expression of transcription factor AP-2-beta (TFAP2B) and its downstream factor silent mating type information regulation 2 homolog 1 (SIRT1) in clinical samples from patients with middle ear cholesteatoma and analyzed the potential correlation between TFAP2B expression and clinical conditions. The findings revealed a significant down-regulation of TFAP2B and SIRT1 in patients diagnosed with middle ear cholesteatoma (p < 0.01), and TFAP2B expression was negatively correlated with the clinical manifestations of hearing impairment and bone destruction. We further explored the role of TFAP2B in the differentiation of RAW 264.7 cells into osteoclasts induced by receptor activator of nuclear factor kappa B ligand (RANKL) in vitro. TFAP2B overexpression significantly inhibited, while TFAP2B knockdown promoted osteoclast differentiation of RAW264.7 cells. Further investigation suggested that TFAP2B positively regulated SIRT1 (p < 0.01) and negatively regulated NF-κB activation. Finally, we demonstrated that TFAP2B transcriptionally regulated SIRT, which inhibited the activation of the NF-κB signaling pathway by reducing the acetylation level of the p65 subunit, thereby suppressing osteoclast differentiation.CONCLUSIONSTFAP2B/SIRT1 plays a crucial role in regulating osteoclast differentiation in middle ear cholesteatoma. The downregulation of TFAP2B/SIRT1 triggers enhanced osteoclast differentiation, which may contribute to one of the mechanisms underlying bone destruction in middle ear cholesteatoma.

Analysis

Perform a panoramic analysis of this field.

view full example data

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

TFAP2B

Basic Info

Related

Analysis