Ask about this productRelated genes to: NR4A2 antibody
- Gene:
- NR4A2 NIH gene
- Name:
- nuclear receptor subfamily 4 group A member 2
- Previous symbol:
- NURR1
- Synonyms:
- TINUR, NOT, RNR1, HZF-3
- Chromosome:
- 2q22-q23
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-11
- Date modifiied:
- 2015-11-18
Related products to: NR4A2 antibody
Related articles to: NR4A2 antibody
- The Cavβ4 subunit of voltage-gated Cav1.2 channels regulates gene expression in neurons and cardiac cells. It increases the expression of interferon-β-related genes in H9c2 cardiomyocytes derived from rat ventricular tissue, but the possibility that it also regulates the expression of microRNAs (miRs) remains unexplored. Furthermore, its role in cardiac hypertrophy is unknown. Although the mechanisms underlying cardiac hypertrophy have been studied extensively, the antihypertrophic response is poorly understood. We conducted quantitative reverse-transcriptase polymerase chain reaction, western blot, and immunofluorescence experiments with H9c2 cardiomyocytes to examine the effects of Cavβ4 overexpression on isoproterenol-induced hypertrophy; the protein abundance of the transcription factors nuclear receptor 4A2 (NR4A2) and forkhead box O1 (FOXO1), which counter agonist-induced hypertrophic growth; and the expression of miR-183-5p, which targets NR4A2 and FOXO1 mRNAs. We found that the Cavβ4 subunit prevented the development of H9c2 cardiomyocyte hypertrophy, down-regulating miR-183-5p expression and increasing the protein abundance of NR4A2 and FOXO1. We also observed a transient decrease in Cavβ4 mRNA expression in rat ventricles at 6 h after isoproterenol injection. These results suggest that the Cavβ4 subunit plays a channel-independent role in the antihypertrophic response in cardiac muscle cells. - Source: PubMed
Carrillo Elba DGalicia ErickGarcía María CSánchez Jorge A - [This corrects the article DOI: 10.3389/fimmu.2026.1861669.]. - Source: PubMed
Publication date: 2026/07/13
Faisal ShahUllah IbadKambey Piniel AlphayoMalik AbdulEjaz Muhammad AdeelShah Sajjad AliLi Yin-Xiong - As a transcription factor, nuclear receptor subfamily 4 group A member 2 (NR4A2) regulates target gene transcription by directly binding to response elements within gene promoters. However, the exact role and molecular mechanism of NR4A2 in fracture healing have not been fully elucidated. Here, we identified NR4A2 as a key functional molecular cargo enriched in exosomes secreted by aged bone marrow stromal cells (BMSCs). Upon uptake by recipient cells, exosomal NR4A2 functioned as a transcriptional repressor that specifically bound to the promoter region of the Neural EGFL-like 2 (NELL2) gene, thereby suppressing its transcription. We further demonstrated that NELL2 acted as a critical adaptor protein that enhanced the binding affinity between fibronectin 1 (Fn1) and integrin β1, thereby licensing FAK/AKT cascade activation essential for osteogenic differentiation. Mechanistically, NR4A2-mediated suppression of NELL2 impaired the assembly of the NELL2/Fn1/integrin β1 complex and attenuated FAK/AKT phosphorylation, thereby inhibiting osteogenesis and culminating in delayed fracture healing. Collectively, our findings delineate a novel exosome-dependent regulatory axis, through which aged BMSCs deteriorated the bone repair microenvironment via the NR4A2/NELL2/FAK-AKT signaling cascade. This study reveals a previously unrecognized molecular mechanism underlying age-associated fracture healing impairment. - Source: PubMed
Publication date: 2026/07/27
Ye PengBai RuiDing XiaoliChen HongboBai ZhenyuWu Long - To determine lactate metabolism-associated biomarkers for non-alcoholic fatty liver disease (NAFLD). Based on NAFLD datasets from the gene expression omnibus database and lactate metabolism-related genes from GeneCards database, NAFLD-lactate metabolism hub genes (NAFLD-LM HGs) were screened via differential analysis, weighted gene co-expression network analysis and four machine learning algorithms. Their diagnostic efficacy was evaluated; molecular subtyping was performed; single-cell RNA sequencing (scRNA-seq) was subsequently conducted; and validation was finally conducted in NAFLD mouse models. We finally screened out eight NAFLD-LM HGs, namely CCAAT/enhancer-binding protein alpha (CEBPA), flavin containing dimethylaniline monooxygenase 1 (FMO1), insulin-like growth factor-binding protein 1 (IGFBP1), krüppel-like factor 4 (KLF4), low-density lipoprotein receptor (LDLR), myelocytomatosis oncogene (MYC), nuclear receptor subfamily 4 group A member 2 (NR4A2), and thymidylate synthase (TYMS), with a diagnostic rate of 0.798 and an area under the curve of 0.948. These genes drove the molecular heterogeneity in NAFLD patients by modulating of metabolism and immune microenvironment. The results of scRNA-seq clarified that Th17 cells were identified as the most abundant annotated cell subset. Through animal experiments, five genes (LDLR, MYC, IGFBP1, NR4A2, and KLF4) were established to have potential protective effects against NAFLD. Five genes (LDLR, MYC, IGFBP1, NR4A2, KLF4) are identified as "protective factors", and their downregulation is associated with NAFLD progression. The remaining three genes (CEBPA, FMO1, TYMS) exhibit inconsistent expression patterns, suggesting bidirectional regulation. - Source: PubMed
Publication date: 2026/07/21
Wang XiaocuiWang XinhanZhao LiangSong Li - Subplate neurons (SpNs) are among the earliest-born and maturing neurons in the developing cerebral cortex. They arise from multiple origins and can be classified into several subgroups based on morphology, connectivity, and gene expression. These neurons play essential roles in cortical circuit formation, yet their cellular diversity and transcriptional dynamics remain incompletely understood. Here, we characterized transcriptomic profiles of SpN subpopulations in embryonic mouse cortex using Lpar1-EGFP and NeuroD1/Cre-ERT2 (D1B) reporter lines. We applied complementary approaches of gene expression profiling, including bulk microarray analysis, single-cell RNA sequencing (scRNA-seq), and Visium spatial transcriptomics. At embryonic day 17 (E17), scRNA-seq identified 10 distinct Lpar1-EGFP-positive SpN clusters, which spatial transcriptomics mapped to specific cortical regions. While many markers showed enrichment within the subplate region, others extended into the hippocampus and ventral pallium (including the amygdala, claustrum, and endopiriform nucleus). Integrated analysis of Lpar1-EGFP and D1B lines revealed both overlapping and unique gene expression signatures, highlighting dynamic markers of subplate identity. Comparisons between E15 and E17 datasets showed substantial transcriptional shifts, suggesting rapid developmental changes in SpN subgroups. Validation with in situ hybridization and RNAscope confirmed the selectivity of key markers, including Cryab, Cdh13, Nr4a2, and Lmo3. Together, these findings provide a molecular framework for further classifying SpN subtypes and identifying candidate markers for transient versus persistent populations, thereby advancing our understanding of early cortical development. - Source: PubMed
Publication date: 2026/07/16
Achiwa HitomiHara YuichiroKawaji HideyaOshima MinoriKaneko NoeMorioka AyumuHoerder-Suabedissen AnnaMolnár ZoltánOhtaka-Maruyama Chiaki