Ask about this productRelated genes to: RUNX3 antibody
- Gene:
- RUNX3 NIH gene
- Name:
- RUNX family transcription factor 3
- Previous symbol:
- CBFA3
- Synonyms:
- AML2, PEBP2A3
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-02
- Date modifiied:
- 2019-04-04
Related products to: RUNX3 antibody
Related articles to: RUNX3 antibody
- Natural killer (NK) cells are core components of innate antitumor immunity, the dysfunction of NK cells in the tumor microenvironment is a major obstacle to the antitumor efficacy. Runt-related transcription factor 3 (RUNX3) acts as a critical tumor suppressor and regulates immune cell function, while its biological role in NK cells remains largely unexplored. Herein, we investigated the interaction between RUNX3 and NK cells in tumor microenvironment. - Source: PubMed
Publication date: 2026/04/07
Lin GuofuLin LanlanZhang JincanChen LeiyuanHu Weitao - [This retracts the article DOI: 10.1016/j.omtn.2017.12.020.]. - Source: PubMed
Publication date: 2026/04/15
Shen ShuyuanYu HaiLiu XiaobaiLiu YunhuiZheng JianWang PingGong WeiChen JiajiaZhao LiniXue Yixue - Neural crest cells are a transient, multipotent population that gives rise to diverse structures during vertebrate embryonic development, including craniofacial cartilage and pigment cells. Although the transcriptional regulation of neural crest development is well characterized, the role of microRNAs remains less understood. Using a double-transgenic zebrafish model expressing fluorescent reporters under the promoter, combined with fluorescence-activated cell sorting and RNA sequencing, we identified microRNAs enriched in neural crest cells. We focused on miR-133a-3p and miR-338-3p, previously linked to tumor suppression, to explore their developmental roles. The overexpression of either microRNA led to craniofacial cartilage malformations and reduced melanophore number, accompanied by decreased expression of key regulators including , , and Reporter assays confirmed direct targeting of the 3'untranslated region. In addition, miR-338-3p overexpression increased neural crest cell numbers, suggesting a role in proliferation. These findings uncover novel functions for miR-133a-3p and miR-338-3p in vertebrate craniofacial and pigment cell development, highlighting shared regulatory features between embryogenesis and tumorigenesis. - Source: PubMed
Publication date: 2026/04/17
Steeman Tomás JTorres MercedesWeiner Andrea MjRubiolo Juan ASánchez Laura ECoux GabrielaCalcaterra Nora B - A major technical challenge in single-cell transcriptomics is the absence of an integrative analytic pipeline that can simultaneously leverage gene regulatory network (GRN) architecture, AI-assisted gene panel discovery, and functional relevance analyses to generate coherent biological insights. Existing approaches often treat these components independently, focusing on clusters, marker genes, or predictive features without integrating them into a mechanistically grounded framework. Consequently, comprehensive screening that links regulatory association, gene signature screening, and functional interpretation within single-cell datasets remains limited, underscoring the need for an integrated strategy. - Source: PubMed
Publication date: 2026/04/06
Borra SantoshiYan DaWelner Robert SYue Zongliang - Objectives CD4+ T cells play key roles in regulating immune responses during pregnancy, therefore we aimed to understand the CD4+ T cell surface proteome and transcriptome during pregnancy. Methods CD4+ T cells were analysed in blood and decidua from term-pregnancies (>37 weeks), and non-pregnant blood. >350 surface proteins were screened via flow cytometry, and transcriptomes were analysed using single-cell RNA sequencing with >130 CITE-seq barcoded antibodies. Results Surface protein screening identified changes to ILT4/CD85d, CD9, IFN-γ receptor β-chain, CX3CR1 and CCR5 in the pregnant blood and decidual CD4+ T cells. CX3CR1 and CCR5 had the highest expression on the effector-memory T cell (TEM) subset in the blood, with expression consistent across subsets in decidua. CD126/IL-6R was lower in pregnant blood and decidual CD4+ T cells, while scRNAseq identified enrichment in the IL-6R signalling pathway in naive CD4+ T cells in pregnant blood. Both sIL-6R and IL-6 concentrations were increased in plasma during pregnancy, suggesting perturbations to the IL-6/IL-6R signalling axis. Meanwhile, decidual CD4+ T cells had increased expression of transcription factor RUNX3 in the CD69+ tissue-resident-like subset. Conclusions Our findings demonstrate altered molecular expression in CD4+ T cells during pregnancy. This provides important mechanistic insight of their adaptation and regulation during placental development, which may drive placental dysfunction or pregnancy complications including preeclampsia, fetal growth restriction and stillbirth. These new data may inform future studies that focus on determining the significance of differentially-expressed immune features in pregnancy to identify potential targets for immune modulation to treat pregnancy complications and infections. Keywords: CD4+ T cell, pregnancy, human, IL-6R. - Source: PubMed
Publication date: 2026/03/30
Habel JenniferNguyen Thi H Ode Alwis NatashaAllen E KaitlynnLi ShihanJuno Jennifer AKent Stephen JBond KatherineWilliamson DeborahLappas MarthaHannan NatalieWalker SusanSchroeder JanCrawford Jeremy ChaseThomas PaulKedzierska KatherineRowntree Louise