Foxj3 antibody - middle region (ARP31683_P050)
- Known as:
- Foxj3 (anti-) - middle region (ARP31683_P050)
- Catalog number:
- arp31683_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Foxj3 antibody - middle region (ARP31683_P050)
Related genes to: Foxj3 antibody - middle region (ARP31683_P050)
- Gene:
- FOXJ3 NIH gene
- Name:
- forkhead box J3
- Previous symbol:
- -
- Synonyms:
- KIAA1041
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-22
- Date modifiied:
- 2014-11-18
Related products to: Foxj3 antibody - middle region (ARP31683_P050)
Related articles to: Foxj3 antibody - middle region (ARP31683_P050)
- Focal cortical dysplasia (FCD), a major cause of drug-resistant epilepsy, involves abnormal neuronal migration and cortical architecture, yet its molecular basis remains poorly defined. Here, we identify FOXJ3 pathogenic variants in patients with autosomal dominant focal epilepsy and FCD. In the developing mouse cortex, FOXJ3 declines sharply in neural progenitors after embryonic day 15.5. In utero electroporation-mediated Foxj3 knockdown in mouse brains impairs neuronal migration, disrupts cortical lamination, and alters neuronal specification, promoting upper-layer neuron production at the expense of deeper-layer neurons. ChIP-seq and scRNA-seq analyses identify Pten as a key FOXJ3 target. Notably, Pten overexpression rescues cortical defects caused by FOXJ3 deficiency. FCD-associated variant fails to upregulate Pten, leading to dysregulated mTOR signaling and enlarged neuronal soma, a hallmark of FCD. These findings suggest that mutations in FOXJ3 may cause epilepsy and FCD and define a transcriptional program that regulates the PTEN-mTOR pathway for neuronal specification and cortical lamination. - Source: PubMed
Publication date: 2026/03/09
Cheng Haw-YuanLiu ChenNien Chiao-WenHuang Hui-ChinZhao Hong-JunNian Fang-ShinChen ChienCustodio Helena MartinsSisodiya Sanjay MLu ChienChen Hsin-HungHsu Chih-SinPi Wen-ChiehChu Chia-ChiHsu Jacob Shu-JuiChen Pei-LungChang Fu-PangTung Chien-YiChou Shen-JuAlavi ShahryarHoulden HenryChen Wei-YiLiu Yo-TsenHou Pei-ShanTsai Jin-Wu - Leukocyte traits are crucial clinical indicators for various diseases, reflecting the immunity in dairy cows and indicating production performance and elimination rate. In Southern China, diseases caused by high temperature and humidity in summer significantly impact the production of dairy cows. Conducting a genome-wide association study (GWAS) on leukocyte counts and components in healthy individuals is essential for identifying genes involved in leukocyte production, differentiation or clearance, thereby aiding in the accurate identification of genetic sources of immune variation in dairy cows. This study measured leukocyte traits in 200 healthy dairy cows and conducted GWAS. The results revealed 70 single-nucleotide polymorphisms (SNPs). Of these, 15 SNPs were within genes and all in introns. Additionally, the BEN Domain-Containing Protein 5 (BEND5) gene, which regulates white blood cell count (WBC), percentage of basophils (%BASO) and percentage of lymphocytes (%LYMPH), and the Forkhead box J3 (FOXJ3) gene, which regulates WBC and %BASO, were identified as two crucial candidate genes. This study provides new evidence on the genetic basis of immunity differences in dairy cows in Southern China, suggesting that the SNPs and candidate genes identified could be valuable for dairy cow breeding. - Source: PubMed
Liu ChenhuiYu JieZhong ZhuxiaHu XiuzhongXiang MinDu XiaoyongLatif Mohammad AbdulWang WenxuanShi LiangyuChen HongboCheng Lei - Osteoporosis involves impaired osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). The present study identified the transcription factor forkhead box (FOXJ3) as a novel regulator of this process. During in vitro osteogenic differentiation of BMSCs, FOXJ3 expression progressively increased, and was positively correlated with osteogenic markers Runt‑related transcription factor 2 (RUNX2) and osteocalcin (OCN). Functional studies confirmed the essential role of FOXJ3: Small interfering RNA‑mediated knockdown markedly impaired differentiation, as evidenced by reduced alkaline phosphatase (ALP) activity, diminished mineralized nodule formation, and downregulation of RUNX2 and OCN. Conversely, lentivirus‑induced FOXJ3 overexpression enhanced these osteogenic markers and outcomes. Mechanistically, FOXJ3 knockdown suppressed active β‑catenin expression, indicating Wnt/β‑catenin pathway involvement. Crucially, the Wnt/β‑catenin agonist SB216763 rescued the inhibitory effects of FOXJ3 knockdown on ALP activity and mineralization. Conversely, the pro‑osteogenic effects of FOXJ3 overexpression were abrogated by the Wnt inhibitor XAV939. These findings establish FOXJ3 as a positive regulator of BMSC osteogenic differentiation acting primarily through the Wnt/β‑catenin pathway, presenting a novel potential therapeutic target for osteoporosis. - Source: PubMed
Publication date: 2025/11/21
Xiao HongweiLi JianfengHuang WeiQin Yi - To explore the biological function of Forkhead box J3 (FoxJ3) in hepatocellular carcinoma (HCC). - Source: PubMed
Publication date: 2025/10/15
Li WeiWang JingChen PengyuZhao LudongNiu JixiangLiu JinghuaLiu Naiqing - We report a rare case of advanced lung adenocarcinoma harboring a novel non-canonical RET::FOXJ3 gene fusion, which has not been previously documented. A 66-year-old male was diagnosed with stage IVB non-small cell lung cancer (NSCLC). Next-generation sequencing (NGS) analysis using the Illumina NovaSeq 6000 identified a previously unreported rearrangement of RET (Rearranged During Transfection) proto-oncogene, involving a fusion of RET exon 1 to FOXJ3 (Forkhead box J3) exons 2-13. Following disease progression on first-line chemotherapy combined with PD-L1 blockage (PFS1 = 6 months), the patient was treated with the selective RET inhibitor pralsetinib (PFS2 = 2 months). However, no significant clinical response was observed, and disease progression was reassessed after 6 weeks of targeted therapy. Palliative cranial radiotherapy was subsequently administered for newly developed brain metastases (PFS3 = 5 months), resulting in an overall survival of 18 months (OS = 18 months). This case expands the current understanding of RET fusion partners and raises important questions regarding the functional and therapeutic implications of non-canonical fusions. It underscores the necessity of corroborating DNA-level findings with RNA and/or protein expression data and highlights the limitations of existing RET-targeted therapies for atypical RET fusions that may lack an intact kinase domain. - Source: PubMed
Publication date: 2025/11/05
Wang PingTang Hao Xi LucasSong JiaqinYang YuyanYao YaoXia Lei