Ask about this productRelated genes to: FOXP1 antibody
- 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
Related articles to: FOXP1 antibody
- Gene expression in regulatory T cells (Tregs) is context-dependent and maintains peripheral immune homeostasis. FOXP3 is lineage defining but not sufficient for Treg function or persistence. To define the cell-intrinsic roles of the FOXP3 paralogs FOXP1 and FOXP4, we generated and studied mice with Treg-specific deletion of and/or . FOXP1 and FOXP4 are required to maintain the peripheral Treg pool through enhancing transcription, thereby promoting sustained high-level expression of IL-2Rα and thus of the high-affinity IL-2Rαβγ complex. Integrating RNA-seq and ATAC-seq with previously published ChIA-PET and publicly available data, we propose a model of transcriptional regulation in which in which FOXP1 and FOXP4 anchor chromatin looping of the locus in mature Tregs, augment super-enhancer activity, and drive sustained CD25 expression. Our results reveal a unique role of FOXP1, and to a lesser extent FOXP4, in controlling Treg homeostasis. - Source: PubMed
Publication date: 2026/04/17
Dong DachuanHigdon Lauren EZhou JiayanLin Jian-XinPadiapu JyothiKim YeslLeonard Warren JMaltzman Jonathan S - Endometrial cancer (EC) is one of the most prevalent cancers affecting the female reproductive system and originates from the uterine epithelium, posing a significant health burden to postmenopausal women. As an E3 ubiquitin ligase, itchy E3 ubiquitin protein ligase (ITCH) plays a key role in the progression of multiple kinds of solid cancers, but its function in EC remains unclear. This work aims to explore the roles of ITCH during the carcinogenesis of EC. - Source: PubMed
Publication date: 2026/03/03
Zhang Yong-HongYu Hai-YangLi Chun-FangLi Jian-Chao - Adipose tissues exhibit a remarkable capacity to expand, regress, and remodel in response to energy status. The cellular mechanisms underlying adipose remodelling are central to metabolic health. Hypertrophic remodelling - characterised by the enlargement of existing adipocytes - is associated with insulin resistance, type 2 diabetes, and cardiovascular disease. In contrast, hyperplastic remodelling - in which new adipocytes are generated - is linked to improved metabolic outcomes. Despite its clinical importance, the regulation of hypertrophic and hyperplastic adipose morphology remains poorly understood. Here, we integrate human transcriptomic data with a quantitative CRISPR-imaging platform in zebrafish to identify regulators of adipose morphology. We developed an image-based phenotyping pipeline that captures lipid droplet size, number, and spatial patterning, and applied generalised additive modelling to quantify hyperplastic versus hypertrophic morphology signatures. Using this platform, we conducted an F0 CRISPR screen targeting 25 candidate genes and identified three that induced hypertrophic morphology (, and ) and an additional candidate that altered total adiposity (). For functional validation, we generated stable loss-of-function alleles for both zebrafish foxp1 paralogues. Spatial analysis along the anterior-posterior axis revealed that mutants display developmental hypertrophy but profoundly blunted adaptive responses to high-fat diet (~68% reduction across all spatial zones), while mutants show normal baseline morphology but disrupted spatial patterning of diet-induced hypertrophy. Together, these findings establish a scalable CRISPR-imaging platform for in vivo genetic screening of adipose morphology and reveal distinct roles for Foxp1 paralogues in developmental patterning and adaptive responses to dietary challenge in adipose tissue. - Source: PubMed
Publication date: 2026/04/22
Wafer RebeccaTandon PannaMinchin James - Genetic mutations in the transcription factor FOXP1 (forkhead box protein P1) cause an autosomal dominant neurodevelopmental disorder called FOXP1 syndrome. To understand the structural impact of pathogenic variants associated with FOXP1 syndrome, we investigated the conformational changes resulting from six distinct missense variants in FOXP1 by combining molecular dynamics simulations, molecular docking, and machine learning via self-organizing maps. Our results reveal different conformational landscapes mapped by the FOXP1 variants and reduced interactions with the DNA for mutations residing in helix H3 of the DNA-binding domain. These analyses offer a framework for assessing the structural impact of missense variants implicated in the FOXP1 syndrome, highlighting the importance of structural inferences in interpreting genetic variants. - Source: PubMed
Publication date: 2026/04/17
Motta StefanoPerta NunzioRomagnoli AliceRexha JesminaBuxbaum Joseph DDe Rubeis SilviaDi Marino Daniele - Autism spectrum disorder (ASD) is a neurodevelopmental condition that occurs in early childhood, characterized by a broad range of clinical manifestations and impairments in social communication. It represents one of the most prevalent neurodevelopmental disorders, affecting approximately 1% of the general population. The phenotypic heterogeneity of ASD arises from different genetic causes, including chromosomal abnormalities, copy number variants (CNVs), and single-nucleotide variants (SNVs), which may occur as de novo or inherited events. Moreover, the polygenic and multifactorial nature of ASD, together with epigenetic regulation and environmental influences, contributes substantially to its complex genetic architecture. Molecular diagnosis remains challenging and relies on multiple genomic approaches, such as array comparative genomic hybridization (array-CGH), whole-exome sequencing (WES), and whole-genome sequencing (WGS); however, the diagnostic yields of these methods remain limited, reflecting the complexity of ASD's genetic architecture. Notably, ASD-associated genes converge on key biological pathways, particularly those involved in transcriptional regulation, chromatin remodeling, synaptic function, and neuronal signaling. These include well-established risk genes such as , , , , , , , , and , among others. This review summarizes the current knowledge on the genetic basis of ASD, highlighting key aspects of its complex genetic architecture. By integrating evidence from major clinical and research databases, it provides a clearer understanding of the underlying mechanisms, supporting improved diagnosis and future research and therapeutic strategies. - Source: PubMed
Publication date: 2026/04/04
Treccarichi SimoneVinci MirellaVirgillito MiriamMusumeci AntoninoBruno FrancescaPapa CarlaGalati Rando RosannaMarano PietroGreco DonatellaFallea AntonioBrancato DesireeCalì SiriaGarcia GresheenFederico ConcettaSaccone SalvatoreCalì Francesco