AEBP2
- Known as:
- AEBP2
- Catalog number:
- 001256A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AEBP2
Related genes to: AEBP2
- Gene:
- AEBP2 NIH gene
- Name:
- AE binding protein 2
- Previous symbol:
- -
- Synonyms:
- MGC17922
- Chromosome:
- 12p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-18
- Date modifiied:
- 2012-10-02
Related products to: AEBP2
Related articles to: AEBP2
- Polycomb Repressive Complex 2 (PRC2) is an essential chromatin regulator responsible for mono-, di- and tri-methylating H3K27. Control of PRC2 activity is a critical process in development and disease, yet no inhibitory cofactor has been identified in somatic cells. Here, we show that the alternative isoforms of its accessory subunit AEBP2, namely AEBP2 (short) and AEBP2 (long), perform opposite functions in modulating PRC2 activity. Contrary to prior assumptions that AEBP2 enhances PRC2 function, we find that the widely expressed AEBP2 isoform inhibits it. AEBP2 is expressed throughout embryogenesis and adulthood and inhibits PRC2 DNA binding, histone methyltransferase activity, and binding to target genes. In contrast, AEBP2, expressed during early embryogenesis, promotes PRC2 DNA-binding activity and is essential for de novo repression of target genes during the transition from naïve to primed pluripotency. Mechanistically, through high-resolution cryo-EM and mutagenesis, we show that the recently evolved, negatively charged N-terminal region of AEBP2 inhibits PRC2. We propose a scenario in which the N-terminus of AEBP2 arose in vertebrates to restrain PRC2 activity in somatic cells. - Source: PubMed
Publication date: 2025/10/30
Mucha MarlenaLai ZhihaoMcKenzie Nicholas JMatrà FrancescaBoudes MarionFlanigan Sarena FAlejo-Vinogradova Maria TeresaMonger CraigZhang QiNimmo DarraghHealy EvanSilva Ademar JAngelov DanielReck David MHolland GráinneAtmaca Zeynep EdaKing Helen EHamilton MaeveGlancy EleanorNolan JamesWeatheritt Robert JBell OliverVermeulen MichielDavidovich ChenBracken Adrian P - Triple-negative breast cancer (TNBC) is an aggressive, heterogeneous subtype of breast cancer. miRNAs play an essential role in TNBC pathogenesis and prognosis. Obesity is linked with an increased risk for several cancers, including breast cancer. Obesity is also related to the dysregulation of miRNA expression in adipose tissues. However, there is limited knowledge about race- and obesity-specific differential miRNA expression in TNBC. We performed miRNA sequencing of 48 samples (24 tumor and 24 adjacent non-tumor tissues) and RNA sequencing of 24 tumors samples from Black (AA) and White (EA) TNBC patients with or without obesity. We identified 55 miRNAs exclusively associated with tumors in obese EA patients and 33 miRNAs in obese AA patients, each capable of distinguishing tumor tissues from obese from lean individuals within their respective racial groups. In EA, we detected 41 significant miRNA-mRNA correlations. Notably, miR-181b-5p and miR-877-5p acted as negative regulators of tumor-suppressor genes (e.g., , , ), while miR-204-5p and miR-143-3p appeared to indirectly target oncogenes (e.g., , , , ). Among AA patients, we found 28 significant miRNA-mRNA interactions. miR-195-5p, miR-130a-3p, miR-130a-5p, miR-424-5p, miR-148a-3p, miR-374-5p, and miR-30a-5p each potentially downregulated two or more genes (e.g., , , , , ). Pathway enrichment analysis highlighted , , , , , and as the most commonly differentially expressed in EA, whereas , , and were most frequently in AA. These findings highlight the importance of considering race-specific miRNA-mRNA signatures in understanding TNBC in the context of obesity, offering insights into biomarker-driven patient stratification for targeted therapeutic strategies. - Source: PubMed
Publication date: 2025/09/18
Hossain FokhrulGonzalez-Ramirez Martha IGarai JonePolania-Villanueva DianaLi LiNafees FarzeenManirujjaman MdLiu BolinMajumder SamarpanWu Xiao-ChengHicks ChindoDel Valle LuisDanos DeniseOchoa AugustoMiele LucioZabaleta Jovanny - Acute kidney injury (AKI) is a common renal condition associated with various factors, including pre-renal, post-renal, and renal causes, with ischemia- reperfusion being a frequent contributor leading to tubular injury. Early identification of AKI is crucial but remains challenging. - Source: PubMed
Zhu HengyueYang XuejiaYuan ZiweiHu ZujianGuo YangyangBai YonghengZhou Jingzong - Acute kidney injury (AKI) is a severe condition with high morbidity and mortality. Innovative biomarkers and treatments are essential for improving patient outcomes. This study aims to investigate the role of ferroptosis-related genes (FRGs) in AKI for identifying potential biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2024/07/23
Luo GangGao YiZheng ZiyuGao BaobaoWang LiniTang XuemiaoLei Chong - Recurrent spontaneous abortion (RSA) affects approximately 1 % of women striving for conception, posing a significant clinical challenge. This study aimed to identify a prognostic signature in RSA and elucidate its molecular mechanisms. Prognostic gene impacts were further assessed in HTR-8/SVneo and human primary extravillous trophoblast (EVT) cells in vitro experiments. A total of 6168 differentially expressed genes (DEGs) were identified, including 3035 upregulated and 3133 downregulated genes. WGCNA pinpointed 8 significant modules and 31 ferroptosis-related DEGs in RSA. Optimal clustering classified RSA patients into three distinct subgroups, showing notable differences in immune cell composition. Six feature genes (AEBP2, CISD2, PML, RGS4, SRSF9, STK11) were identified. The diagnostic model showed high predictive capabilities (AUC: 0.966). Mendelian randomization indicated a significant association between CISD2 levels and RSA (OR: 1.069, P-value: 0.049). Furthermore, the downregulation of CISD2 promotes ferroptosis in HTR-8/SVneo and human primary EVT cells. CISD2 emerged as a pivotal gene in RSA, serving as a ferroptosis-related therapeutic target. The diagnostic model based on gene expression and Mendelian randomization provides novel insights into the pathogenesis of RSA. - Source: PubMed
Publication date: 2024/04/14
Shangguan MengyuanZheng JingyingLiu NingZhao JingWang Qiang