Ask about this productRelated genes to: PHF21B antibody
- Gene:
- PHF21B NIH gene
- Name:
- PHD finger protein 21B
- Previous symbol:
- PHF4
- Synonyms:
- BHC80L, FLJ34161
- Chromosome:
- 22q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-07
- Date modifiied:
- 2019-03-01
Related products to: PHF21B antibody
Related articles to: PHF21B antibody
- Complex neural activity in the mammalian central nervous system are achieved through the coordinated function of diverse neuronal subtypes. The sequential generation of distinct types of neurons from neural progenitor cells during development is a key process in establishing this complexity. However, how this temporal specification of neuronal identities is regulated across different brain regions during development remains only partially understood. Here, we identify PHF21B, ZFP7, and ZFP57 as critical regulators that control the transition from the generation of early-born to late-born neurons by neural progenitor cells in the developing mouse cortex and ganglionic eminence. Combinatorial overexpression of these factors in developmentally advanced progenitors that normally generate late-born neurons led to a prolonged generation of early-born neuronal subtypes. Conversely, simultaneous knockdown of these genes markedly reduced generation of early-born neurons. Because these factors are predicted to function as transcriptional regulators involved in heterochromatin formation at their target genomic loci, our findings suggest the presence of a shared epigenetic mechanism that governs the temporal specification of neurons across multiple regions of the developing brain. - Source: PubMed
Publication date: 2026/04/16
Hisamatsu DaisukeHasegawa HiroyukiNaka-Kaneda HayatoNakajima KazunoriOkano HideyukiShimazaki Takuya - Most women experience hot flashes (hot flushes) during the menopause transition. Menopausal hot flashes typically persist for years, and for a sizeable minority of women, are substantially impairing. Genetic investigations can improve understanding of hot flash etiology. - Source: PubMed
Publication date: 2026/01/06
Werwath Kathryn ELawn Rebecca BSalem Madeleine TLi TaydenMitchell Brittany LShen HanyangGordon Scott DKung BensonStafford CieraVemuri MytileeRatanatharathorn AndrewMeijsen JoeriShadyab Aladdin HKooperberg CharlesKoenen Karestan CCrandall Carolyn JMartin Nicholas GDuncan Laramie E - Given the intricate and multifactorial molecular mechanisms underlying cardiac hypertrophy (CH), conventional pharmacological treatments often face significant challenges in achieving disease reversal. This review presents an innovative approach to treating CH by combining natural products with artificial intelligence (AI) and multi-omics technologies. We provide detailed analysis of the molecular pathways that drive pathological hypertrophy, with a particular emphasis on impaired calcium signaling and the pro-inflammatory-oxidative feedback loop involving ferroptosis and pyroptosis. Advanced AI-driven methodologies, such as single-cell spatial transcriptomics and machine learning algorithms, facilitate a more nuanced understanding of cellular heterogeneity and the identification of key pharmacological targets, including Sirtuin 3 (SIRT3) and Toll-Like Receptor 4 (TLR4). Natural products like ginsenoside Rb1 and baicalin exhibit superior multitarget pharmacological effects compared to conventional single-target drugs, effectively modulating critical pathways like AMP-activated protein kinase (AMPK) activation and Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) inhibition. Moreover, metabolites derived from the gut microbiota, including trimethylamine N-oxide (TMAO) and short-chain fatty acids, emerge as novel modulators of cardiac remodeling, influencing epigenetic regulation through pathways such as the Histone Deacetylases (HDACs)-PHD Finger Protein 21B (PHF21B) axis. By integrating cutting-edge technologies with pharmacological insights, this review outlines a comprehensive strategy for precision pharmacotherapy, ranging from early-stage signaling modulation to systemic network reprogramming, thus shifting the focus of treatment from symptom management to potential disease reversal. - Source: PubMed
Publication date: 2025/08/06
Wang JinhuiPan JiaojiaoLuan FeiShi HuanxianXie YundongZhao ChongboZou JunboShi YajunGuo DongyanSun JingZhang Xiaofei - Pathological cardiac hypertrophy is a hallmark of various cardiovascular diseases, unfortunately, effective targeted therapies are still lacking. This study aims to verify the role of plant-homeodomain finger protein21b (PHF21B) in pathological cardiac hypertrophy. - Source: PubMed
Publication date: 2025/02/01
Sheng SiqiLiu GuannanLv PengchengLiu JialiangLv LinYuan MengLuo DankunXiong JieDong PengweiZhang JingyueXie BaodongDong ZengxiangShi Yuanqi - The carcinogenesis and progression of colon adenocarcinoma (COAD) are intensively related to the abnormal expression of the zinc finger (ZNF) protein genes. We aimed to employ these genes to provide a reliable prognosis and treatment stratification tool for COAD patients. - Source: PubMed
Publication date: 2024/04/25
Xu FanSun JiahuiGu XinyueZhou Qingxin