Ask about this productRelated genes to: ZFP42 antibody
- Gene:
- ZFP42 NIH gene
- Name:
- ZFP42 zinc finger protein
- Previous symbol:
- -
- Synonyms:
- REX1, ZNF754
- Chromosome:
- 4q35.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-09
- Date modifiied:
- 2014-11-19
Related products to: ZFP42 antibody
Related articles to: ZFP42 antibody
- Rett syndrome arises from loss-of-function mutations in the X-linked chromatin regulator MECP2, yet the earliest molecular derailments in development are poorly defined. Using isogenic human embryonic stem cell (hESC) models carrying three patient-derived MECP2 mutations, we followed the transcriptome from pluripotency through neuroectoderm, neural stem/progenitor stages. Developmental stage dominated transcriptional variance, but mutants shared a secondary program enriched for synaptic-membrane and extracellular matrix genes. Single-cell/bulk profiling at the embryonic stem cell (ESC) stage revealed partial naïve-like drift, marked by the up-regulation of the naïve-enriched factor ZFP42/REX1 and related markers in MECP2-mutant lines. Among convergently dysregulated genes, the cortical determinant EMX1 showed an abnormal developmental trajectory, early repression followed by overshoot, and was consistently altered across independent Rett PSC models. Single-nucleus RNA-seq of cerebral organoids uncovered allele-specific yet convergent disturbances in cortical lineage allocation. These data chart a continuous developmental trajectory for MECP2-mutant cells and nominate naïve-like drift and mis-timed EMX1 expression as tractable entry points for dissecting Rett pathogenesis. - Source: PubMed
Publication date: 2026/04/23
Guillon MarionBrin MargauxGabet ElodieGromaire JustineBernard MathéaLaurent LaetitiaRabin ThéoBianchin LisaVeziano MarieKloda JulieBernard AlexiaAsali LailaLiu YiFlamier Anthony - Aging and stress-related factors affect sperm DNA methylation in regions associated with genes responsible for embryonic development. The stochastic epigenetic variation hypothesis holds potential to explain these patterns, proposing that, in response to stressors, naturally variable methylation regions (VMRs) associated with morphogenetic genes exhibit increased methylation variation to diversify phenotypes and improve the chances of survival of the genetic lineage. Here, we test predictions from this hypothesis using mouse and rat sperm DNA methylation data from publicly available sources. Specifically, we identify VMRs and analyze their overlap with regions differentially methylated (DMRs) in response to aging, stressors, and with various genomic elements. We demonstrate that the nature of the DNA regions, rather than the nature of the stressor, determines the response of the sperm methylome to aging and stress, and propose a model that explains shifts in methylation within VMRs through stochastic changes, whereby initially hypermethylated regions lose methylation and initially hypomethylated regions gain methylation. VMRs are depleted of open chromatin regions and histones in male germ cells and are enriched for a binding motif for ZFP42, an epigenetic remodeler. This knowledge may open opportunities for the development of interventions to control epigenetic information transfer via germ cells. - Source: PubMed
Publication date: 2026/03/21
Arowolo OlatunbosunZhu JiahuiNowak KarolinaPilsner J RichardSuvorov Alexander - The role of circadian rhythm in regulating stemness in adult stem cells remains unclear. We investigated this in human epidermal stem and progenitor cells (EPSCs), finding that ~10% of expressed genes exhibit rhythmicity, with shared genes between fetal and adult EPSCs enriched in critical biological processes including the cell cycle, senescence, and apoptosis. Promoter motif analysis revealed ZFP42, a pluripotent stem cell marker, enriched in fetal rhythmic genes. ZFP42 knockdown led to the loss of stemness in human EPSCs and reduced expression of Cryptochrome Circadian Regulator 1 (CRY1), a core component of the molecular circadian clock that functions as a transcriptional repressor within the CLOCK-BMAL1 feedback loop, resulting in decreased cell proliferation and increased differentiation gene expression. These results highlight the critical role of ZFP42 in the circadian regulation of epidermal homeostasis, linking stemness maintenance to circadian mechanisms. Our findings deepen the understanding of how circadian rhythms govern epidermal stem cell functions. - Source: PubMed
Publication date: 2026/01/21
Gao ShuiyingTan HaoXu ShuqiaZhang ZhaoyuSun YushuangLi YaqiongJian DanQi XiaowenTang QingChen RunWang DongyuZhen MiaoWang PengShu BinLi Jingting - Human genetic analyses have identified numerous single-nucleotide polymorphism (SNP) loci in noncoding regions associated with obesity-related traits; however, the functional contributions of such SNP loci to obesity are largely unknown. The noncoding variant rs713586, with its risk allele C, is linked to two candidate genes, DNAJC27 and ADCY3, potentially implicated in obesity. However, whether rs713586 primary targets ADCY3 or DNAJC27 gene to regulate body weight and what molecular mechanisms underlie this process remain unclear. - Source: PubMed
Publication date: 2026/01/05
Wang WeinaLiu YuweiDong ShengWu XiaomanZhang FeiWang XizhiZhang XueyingHu XiaoyuWang Zhenshan - The crosstalk between translation and metabolism is fundamental for cellular plasticity. While most studies focus on translation within canonical coding regions, the roles of non-canonical open reading frames (ORFs) in metabolic regulation and early development remain unclear. Here, we show that selective translation of an upstream ORF in the 5' untranslated region (UTR) of Lin28b produces an 85-amino acid microprotein, PLUM (pluripotency-associated Lin28b uORF-encoded microprotein). Depletion of PLUM leads to deterministic and synchronized (near 100%) induction of naïve pluripotency and causes embryo implantation defects in vivo. Mechanistically, PLUM depletion dissolves L1td1 condensates and enhances L1td1 binding to pluripotency mRNAs such as Tfcp2l1 and Zfp42, stabilizing them and promoting coordinated gene activation. Concurrently, PLUM loss disrupts P-bodies enriched with a subset of nuclear-encoded mitochondrial mRNA, potentially preventing their degradation. Together, these alterations trigger an early burst of mitochondrial oxidative phosphorylation and synchronized naïve gene expression, accelerating acquisition of the naïve state. Our study identifies the novel uORF-encoded microprotein PLUM as a pluripotency determinant integrating RNA regulation and metabolic remodeling. - Source: PubMed
Publication date: 2025/11/26
Hao ZhihongWu YiHuang YileZhang MaoleiLiu YangLi YueqiaoLi WenxinRuan ZifengZhang JianDing YingzheLi LinpengXing GuangsuoLiu ZichaoZhou YanshuangWang QiChen KeshiWang WumingLu GangQin DajiangChan Wai-YeeLiu Xingguo