FOXP1 antibody - N-terminal region (ARP32564_T100)
- Known as:
- FOXP1 (anti-) - N-terminal region (ARP32564_T100)
- Catalog number:
- arp32564_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FOXP1 antibody - N-terminal region (ARP32564_T100)
Related genes to: FOXP1 antibody - N-terminal region (ARP32564_T100)
- Gene:
- FOXP1 NIH gene
- Name:
- forkhead box P1
- Previous symbol:
- -
- Synonyms:
- QRF1, 12CC4, HSPC215, hFKH1B
- Chromosome:
- 3p13
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-07
- Date modifiied:
- 2016-06-10
Related products to: FOXP1 antibody - N-terminal region (ARP32564_T100)
Related articles to: FOXP1 antibody - N-terminal region (ARP32564_T100)
- Antigen-loss variants (ALVs) are a major cause of relapse following chimeric antigen receptor (CAR) T cell therapy, particularly in solid tumors where antigen heterogeneity and immune suppression prevail. By integrating public single-cell RNA sequencing analysis with experimental validation, we identify the transcription factor FOXP1 as a critical brake limiting Th9 CAR-T cell differentiation and effector programming. FOXP1 knockdown reprograms Th9 CAR-T but not Tc9 cells toward a metabolically active, cytotoxic, and exhaustion-resistant phenotype, thereby enhancing their persistence and antitumor activity. CUT&Tag and transcriptomic profiling reveal that FOXP1 binds regulatory regions of Il9, Spi1, and Runx1, as well as effector loci such as Tnf and Gzmb, repressing both Th9-lineage and TCR-downstream transcriptional programs. Its depletion releases this repression, broadly activating MAPK, PI3K-Akt/mTOR, and NF-κB pathways that sustain cytokine production and memory formation. Functionally, FOXP1-deficient Th9 CAR-T cells eradicate both antigen-positive and antigen-loss tumor populations by recruiting dendritic cells and promoting endogenous CD8 T cell clonal expansion via the CD6-Flt3L axis. Our findings establish FOXP1 as a transcriptional checkpoint integrating cytokine and signaling networks to control Th9 CAR-T cell function and provide a mechanistic rationale for engineering CAR-T therapies capable of overcoming antigen escape. - Source: PubMed
Publication date: 2026/09/16
Zhu YihanXie XingweiWu XiaohuanOuyang SuidongZhou YangWen KangZhong YutongChen YuyangWang HanduoGao YuanJiang LingLi HuiZhao WenliXu AbaiBi Enguang - Kidney cystic epithelium primarily comprises proliferating A-intercalated (A-IC) cells in humans and mouse models of TSC. These studies explored the expression of transcription factors (TF) that drive the development of A-IC cells and the downregulation of B-intercalated (B-IC) cells, as well as the status and localization of and in epithelial cells lining the cysts. Transcriptome studies indicated enhanced expression of the following TFs: DMRT2, FOXI1, and FOXP1 in young TSC mice, and DMRT2 and FOXI1 in aged mice. The expression of decreased in TSC mice of all ages. Our studies further demonstrated: (1) distinct and predominant DMRT2 and FOXP1 localization in the cystic epithelium of in TSC mouse models; and (2) expression of , , and in epithelial cells lining the kidney cysts. Expression of DMRT2, FOXI1, and FOXP1 is enhanced in the A-IC cells lining the kidney cysts of TSC mouse models. In the same models, the expression of mRNA is decreased and is accompanied by the loss of B-IC cells in cyst epithelia. Both DMRT2 and FOXP1 localized to the nucleus of A-IC cells of the renal cysts, suggesting that TSC kidney cystogenesis is driven by factors that exclusively promote A-IC expansion. - Source: PubMed
Publication date: 2026/08/22
Soleimani ManoocherZahedi KamyarBrooks MarybethIn Julie GBarone Sharon - Growing evidence implicates prenatal exposure to di-(2-ethylhexyl) phthalate (DEHP), a common endocrine-disrupting plasticizer, in the development of autism and attention-deficit/hyperactivity disorder (ADHD). Yet underlying mechanisms remain unclear. - Source: PubMed
Publication date: 2026/09/11
Tanner SamuelEisner AlexNovakovic BorisHolland LadaMansell TobyEngland-Mason GillianMerrill SarahDewey DeborahO'Hely MartinSymeonides ChristosSaffery RichardTang Mimi L KSly Peter DVuillermin PeterJung Chol-HeePark DanielPonsonby Anne-Louise - We report a 9-year-old female with FOXP1 syndrome due to a de novo in-frame deletion in the FOXP1 gene. The child has a severe neurodevelopmental disorder including global developmental delay and autism spectrum disorder. At age 2, she developed severe headbanging, which was progressive and did not respond to multidisciplinary, behavioral management strategies or to multiple medication treatments. Although repetitive behaviors are frequent in patients with FOXP1 variants, severe and intractable headbanging has not been reported to date. Levodopa/carbidopa was prescribed at age 7 due to progressive foot dystonia and contracture development. This treatment was not clearly beneficial for the dystonia and foot position, but immediate improvement in headbanging was observed and the response sustained for over 19 months. The FOXP1 gene codes for a transcriptional regulator protein that has been shown to regulate the development of brain and spinal motor neurons, and some evidence has linked FOXP1 to the differentiation of midbrain dopaminergic neurons via the homeobox protein PITX3, thus providing a potential mechanism for the observed benefit. This case report may provide expansion of the behavioral phenotype associated with FOXP1 variants and suggests avenues for further animal research and/or clinical trial of levodopa in individuals with FOXP1 variants. - Source: PubMed
Publication date: 2026/09/08
Veale PamelaTiessen ChristopherGnanakumar Vithya - Gallbladder cancer (GBC) is a highly aggressive and insidious malignancy with a poor prognosis, primarily due to the lack of specific therapeutic targets and early diagnostic biomarkers. Therefore, identifying novel oncogenes involved in GBC and exploring targeted therapeutic strategies against them are of particular importance. STK31 is a cancer/testis antigen, but its biological function and mechanistic role in GBC remain unclear. This study investigates how STK31 influences GBC. STK31 expression in GBC and gastrointestinal tumors were analyzed using collected clinical samples and TCGA database respectively. Its pro-tumorigenic functions were then confirmed by in vivo and in vitro assays, while downstream regulatory mechanisms were uncovered via multi-platform proteomic strategies. Molecular docking was employed to screen 1,008 ChEMBL small molecules post STK31 functional validation. Significant upregulation of STK31 expression was observed in both GBC and gastrointestinal malignancies through our comprehensive analysis. STK31 depletion decreased GBC cell proliferation, migration and induced G1/S phase arrest and cellular polyploidization. Gene Set Enrichment Analysis (GSEA) demonstrated that STK31 functionally correlates with core biological processes including DNA Replication, Cell Cycle and Extracellular Matrix (ECM) Receptor Interaction. STK31 directly binds to both c-Myc and FOXP1, thereby regulating MCM and ITG family proteins to exert its biological function. In addition, STK31 influences the phosphorylation of c-Myc through its kinase activity. Atovaquone identified through molecular docking screening, binds STK31 and reduces its expression and kinase activity, demonstrating anti-tumor effects against GBC both in vitro and in vivo. We demonstrate that STK31 facilitates GBC progression through c-Myc/FOXP1-mediated DNA replication dysregulation. Its inhibition triggers lethal polyploidization, with ATO identified as a potential STK31-targeting drug candidate. - Source: PubMed
Publication date: 2026/09/08
Zhang BinPeng Hai-YingLin Zhu-YingZhu Wei-YuLi Shuang-XinYang Song-LinYe Qiu WenZhao Yi-YiGao HuiHe ShanLiu YuanWang Xiao-DanGuo Yang-FanWang Wen-JuLiao Li-WeiHou Zong-LiuMeng Ming-YaoLi Lin