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)
- Attention-Deficit/Hyperactivity Disorder (ADHD) is a highly heritable neurodevelopmental disorder; however, its genetic architecture remains poorly explored in Indigenous populations. This study aimed to analyze and characterize genetic variation in 11 genes (ADGRL3, CDH8, DCC, DUSP6, FOXP1, FOXP2, MEF2C, PCDH7, SEMA6D, SORCS3, and ST3GAL3) previously implicated in ADHD, in an indigenous sample, comparing them with reference populations from the 1000 Genomes Project. Exome data from 64 individuals representing 12 Indigenous groups from the Brazilian Amazon were analyzed. Among the identified, 99 met the inclusion criteria. Four previously unreported variants in the developed reference datasets were identified in ADGRL3, DCC, and FOXP2. Significant differences in allele frequencies were observed for 56 variants compared with continental populations. Multidimensional scaling analysis indicated genetic differentiation of the Indigenous group in relation to other populations. This study highlights the distinct genetic profile of Amazonian Indigenous populations, likely shaped by demographic and evolutionary processes such as genetic drift and founder effects. The identification of exclusive variants and marked allele frequency differences reinforces the importance of including historically underrepresented populations in genomic studies related to ADHD and neurodevelopment, contributing to a broader understanding of human genetic diversity. - Source: PubMed
Publication date: 2026/08/11
de Matos Hirlesson PaixãoMonte NatashaAguiar Kaio Evandro Cardosode Cássia Calderaro RitaSantos Aline PasquiniRodrigues Juliana Carla GomesRibeiro-Dos-Santos André MaurícioDe Souza Sandro JoséRibeiro-Dos-Santos ÂndreaGuerreiro João FariasSantos Sidney Emanuel Batista DosSantos Ney Pereira Carneiro Dos - Indigenous chickens in Eritrea are raised mainly in low-input village systems and show marked variation in body size, including reduced body size phenotype, a trait associated with reduced feed consumption, thermotolerance, disease resistance, and adaptability to resource-limited environments. This study aimed to identify genomic regions associated with reduced body size using a genome-wide association study (GWAS) in Eritrean chicken ecotypes. Blood samples from 384 ICs across 16 ecotypes (21 to 24 birds per ecotype) were genotyped using DArTseq technology. Three putative short-bodied ecotypes, Barentu (BAR), Foro (FORO), and Gogne (GOG), were compared with five heavier control ecotypes: Fshe-Mrara (FM), Adi-Tekeliezan (ADTEK), Emni-Haili (HAYL), Dekemhare (DEKE), and Adikeyh (KEIH). After filtering for individual missingness, marker call rate, and minor allele frequency, 141 birds and 42,356 SNP remained. Population structure was evaluated by principal component analysis and ADMIXTURE. Exploratory case-control GWAS were conducted for each putative reduced-body-size ecotype and for the 3 ecotypes combined. Complementary quantitative-trait GWAS used body weight, body length, back length, and shank length was carried out. Linear mixed models implemented in GEMMA included sex as a fixed effect and genomic kinship as a random effect. The first 2 principal components showed extensive ancestry sharing, although GOG was more differentiated. Ecotype-specific analyses identified significant regions near CDK6, BDNF, FOXP1, TNS3, and LGR4 in FORO; EIF2AK2, NANP, MDH1, UGP2 and FGF13 in GOG; and HMGA2, IGF2, BRSK1 and SUCNR1 in BAR. The combined analysis showed no genome-wide significant variants but revealed suggestive signals near ASAP1, EIF2AK2, and FOXP1, indicating a polygenic and ecotype-specific architecture. Overlapping candidate genes across analyses included TH (common to all) and EIF2AK2 (present in all ecotypes except FORO). Quantitative-trait analyses detected a single significant SNP within CACNB4 for back length, but none for the other traits. Overall, reduced body size in Eritrean IC appears to be a complex trait controlled by multiple loci, involving both conserved growth regulators and genes related to metabolic efficiency and environmental adaptation. These findings provide a genomic basis for future breeding strategies to improve productivity, resilience and sustainability of village poultry production systems in resource-limited regions of Eritrea. - Source: PubMed
Publication date: 2026/07/27
Habteslasie Hortuma APerini FrancescoNgeno KiplangatColombi DanieleLasagna EmilianoDessie TadelleKahi Alexander - De novo variants in the ubiquitin-proteasome pathway are linked to autism spectrum disorder (ASD), yet their functional impact on neurodevelopment remains poorly understood. We investigated USP15, a deubiquitinating enzyme with rare damaging variants identified in individuals with ASD, using isogenic human iPSC-derived brain organoids and single-cell transcriptomics. USP15 mutant organoids showed genotype-dependent, progenitor-centered alterations during corticogenesis. Heterozygous organoids modeling haploinsufficiency displayed a shift toward later pseudotime states together with altered maturation and synaptic organization of deep-layer neurons. In contrast, homozygous organoids showed broader phenotypes, including mitotic suppression, aberrant HOX gene expression, and stress-response activation. Regulon analysis showed reduced activity of progenitor-associated regulons, including SOX2, NR2F1, and NR2F2, in heterozygous organoids, whereas homozygous organoids exhibited broader changes in transcriptional regulatory networks. Furthermore, USP15 mutant-associated gene expression patterns were significantly enriched for established ASD risk genes. Comparison with the mouse brain perturbation atlas showed that the transcriptional signature of the USP15 mutant showed notable overlap with those of Fezf2 and Foxp1 mutants, key regulators of deep-layer projection neuron identity. These findings characterize genotype-dependent neurodevelopmental phenotypes associated with reduced USP15 dosage and provide a human neural framework for investigating ASD-relevant developmental mechanisms in the context of a rare ubiquitin-pathway variant. - Source: PubMed
Publication date: 2026/07/29
Park Tae-HwanKoh In GyeongSung SeoyoungPark HayoonKim JieunLee SebinLee Yun JinKo HyunsooHan Jae HyunBong GuiyoungYoo Hee JeongKim JaesangAn Joon-YongLee Ji Yeoun - The progression of acute coronary syndrome (ACS) is primarily determined by the transition from stable to vulnerable atherosclerotic plaque. The primary objective of this study was to investigate the mechanism of SLC25A25 antisense RNA 1 (SLC25A25-AS1) in ACS. The level of SLC25A25-AS1 was determined using reverse transcription quantitative real-time PCR (RT-qPCR) in serum samples from healthy controls (n = 81) and ACS patients (n = 162). The clinical relevance of SLC25A25-AS1 in ACS was evaluated through correlation, receiver operating characteristic (ROC), and logistic regression analyses. SLC25A25-AS1 was significantly downregulated in ACS patients. Overexpression of SLC25A25-AS1 protected oxidized low-density lipoprotein (ox-LDL) treated human coronary artery smooth muscle cells (HCASMCs) from damage in an atherosclerosis model. Specifically, these protective effects were against abnormal cell proliferation, inflammatory responses, cell migration, and maintenance of the contractile phenotype in HCASMCs. Both bioinformatics analyses and experimental validation confirmed the existence of the SLC25A25-AS1/ microRNA‑34a‑5p (miR-34a-5p)/Forkhead box P1 (FOXP1) regulatory axis. Collectively, SLC25A25-AS1 modulated ox-LDL-induced atherosclerotic responses in HCASMCs through the miR-34a-5p/FOXP1 pathway. These findings suggested that SLC25A25-AS1 may play a protective role in ACS by alleviating ox-LDL-induced HCASMC dysfunction and inflammation via the miR-34a-5p/FOXP1 axis. - Source: PubMed
Publication date: 2026/07/29
Wang QiupingChen DongshengLi Ting - Immunometabolism plays a vital role in the immunopathogenesis of people living with human immunodeficiency virus type 1 (HIV-1) (PLWH). However, the precise relationship between metabolic profiles and T-cell dysfunction in this population remains unclear. This study aimed to investigate the metabolic reprogramming and underlying mechanisms contributing to T-cell dysfunction in PLWH, highlighting potential pathogenic mechanisms during chronic HIV-1 infection. - Source: PubMed
Publication date: 2025/10/27
Zhao Jin-FangZhen ChengWang You-YuanZhou Ming-JuSun Yong-BingHuang Hui-HuangJiao Yan-MeiSong Jin-WenFan XingZhang XinJiang Tian-JunZhang ChaoWang Fu-Sheng