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)
- 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 - Some organisms exhibit a remarkable ability to adapt their life history strategies within a single lifespan in response to dynamic biotic and abiotic cues, such as Caenorhabditis elegans larval facultative diapause. However, the molecular basis of how conspecific and prey cues are processed to conditionally alter the time to reproductive maturation remains largely unexplored. Here we discover that the longest transcript of the forkhead transcription factor FKH-7/FOXP is expressed and acts in C. elegans pheromone and bacteria-sensing neurons to promote larval development into growth-arrested diapause under resource-scarce conditions. We further demonstrate that human FOXP1 can functionally substitute for FKH-7 in these chemosensory neurons and that incorporating a hypomorphic missense mutation associated with a human neurodevelopmental disorder characterized by social interaction deficits reduces frequency of the adaptive response in nematode populations. In the fkh-7/FOXP1 missense variant, single-cell transcriptomics of chemosensory neurons identifies the set of candidate genes for deeper characterization of variant-specific molecular pathology at single neuron resolution in the context of an adaptive developmental decision. - Source: PubMed
Publication date: 2026/04/14
Chai Cynthia MTaylor Seth RTischbirek Carsten HWong Wan-RongWolf Trevor JCai LongMiller Iii David MSternberg Paul W - Ventral midbrain dopaminergic neurons are a key cell type for schizophrenia pathophysiology but information about cell type-specific genomic dysregulation in diseased brains is missing. We generated a unique midbrain functional genomics resource with 97 RNA-seq and 34 Hi-C chromosomal contact libraries for Nurr1 + /NeuN+ dopaminergic and their surrounding Nurr1-/NeuN- nuclei, collected from donors diagnosed with schizophrenia (SCZ), bipolar disorder (BD) and compared to neurotypical controls. Among the 954 dopamine neuron genes specifically dysregulated in SCZ, 331 were downregulated, with selective enrichment for risk-associated synaptic plasticity and neuronal connectivity pathways and embedded within dopamine neuron-specific topologically associated chromosomal domains (TAD). Transcript-resolved analysis revealed 2,350 transcripts with altered expression in SCZ dopamine neurons, affecting key susceptibility genes such as the FOXP1, MAPK10, PCM1 and NRXN1. Therefore, genomic dysregulation in the ventral midbrain of subjects diagnosed with SCZ selectively affects dopaminergic neurons, and includes a unilateral association of genetic risk with down-, but not upregulated transcription at the sites of highly organized chromosomal domains harboring neuron-specific genes with complex transcriptional architectures. - Source: PubMed
Publication date: 2026/04/06
Singh SwadhaIskhakova MarinaLambert Tova YValada AditiShokrian NedaEvans VivianaBendl JaroslavAuluck Pavan KMarenco StefanoWang MinghuiZhang BinHoffman Gabriel EGirdhar KiranRoussos PanosAkbarian Schahram - Sleep disturbances are among the most prevalent clinical features of FOXP1 syndrome, yet their nature and underlying mechanisms remain unclear. Here, we report that individuals with FOXP1 syndrome suffer from insomnia with sleep maintenance problems and early waking. Consistently, common variants in FOXP genes were associated with insomnia symptoms and short sleep. These sleep disturbances were recapitulated in Drosophila FoxP mutants, which exhibit severely fragmented and reduced sleep. FoxP loss also led to circadian arrhythmicity and impaired the plasticity of neuropeptide pigment dispersing factor-secreting (PDF-secreting) neurons in a non-cell-autonomous manner. FoxP was required during development for adult sleep integrity, particularly in peptidergic neurons. Transcriptomic analyses revealed a dysregulation of genes involved in peptidergic signaling, including hugin. FoxP was expressed in hugin+ neurons (afferent to PDF-secreting neurons) during development, and its knockdown in these cells was sufficient to induce sleep fragmentation. Our findings establish an evolutionarily conserved role for FOXP proteins in the peptidergic regulation of sleep. - Source: PubMed
Publication date: 2026/04/01
Coll-Tané MireiaEidhof IlseHan JieRaun Nicholasvan Renssen Lara VFisher Simon EKayser Matthew SKleefstra TjitskePillen SigridHudac Caitlin MMayneris-Perxachs JordiKlein MariekeKoene SaskiaCastells-Nobau AnnaSchenck Annette