Ask about this productRelated genes to: RFX3 antibody
- Gene:
- RFX3 NIH gene
- Name:
- regulatory factor X3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 9p24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-16
- Date modifiied:
- 2015-11-30
Related products to: RFX3 antibody
Related articles to: RFX3 antibody
- Chronic obstructive pulmonary disease (COPD) is associated with musculoskeletal comorbidities, including cachexia. Weight loss (WL) is the major criterion for cachexia and increases risk for mortality in COPD. Risk factors for WL in COPD are incompletely understood. We performed this whole genome sequencing (WGS) analysis to identify genetic risk variants for WL in COPD. - Source: PubMed
Chiles Joe WRocco AlisonSrinivasasainagendra VinodhRossiter Harry BCasaburi RichardThalacker-Mercer AnnaWells J MichaelWan Emily SSilverman Edwin KCho Michael HHersh Craig PPsaty Bruce MGharib Sina AGao YanO'Connor George TLange Leslie ARich Stephen SManichaikul Ani WBarr R GrahamOrtega Victor EMeyers Deborah ASmith Albert VTiwari Hemant KMcDonald Merry-Lynn N - Challenges in verbal communication are a prominent feature of autism. However, gene regulatory programs in speech-related cortical regions remain poorly characterized. In parallel, it remains unclear whether the heterogeneous genetic factors underlying autism converge on shared neurobiological mechanisms. To address these gaps, we generated paired transcriptomic and epigenomic data from post-mortem human brain tissue across 100 donors. Here, we show that transcriptional differences in the speech-related Brodmann Area 22 in individuals with neurodevelopmental conditions, including autism, are strongest among those with a known genetic diagnosis. A similar but attenuated signature is observed in those without a genetic diagnosis. These transcriptional differences are most pronounced in neurons, with glutamatergic L4/5 intratelencephalic neurons affected across multiple modalities. Finally, multimodal analysis implicates altered -dependent networks as a central hub in autism, particularly among L4/5 intratelencephalic neurons in non-verbal individuals. Together, our study identifies regulatory architecture linking chromatin state, transcriptional output, and variation in verbal ability in autism. - Source: PubMed
Publication date: 2026/04/03
Suresh VarunWigdor Emilie MHao YuhanLeonard RachelAsfouri JosephGriffiths MichaelEvans ClementsYuan GuohuaRohani NarjesWeiss JakobDema ChimmiMukthar TanzilaLassen Frederik HSchafer NicoleDong ShanPalmer Duncan SChang Edward FSanders Stephan JNowakowski Tomasz J - Innate immune and interferon-induced responses to in vivo nasal infection with rhinovirus (RV)16 in healthy subjects are accelerated by low-dose dietary supplementation with carrot-derived pectic polysaccharide rhamnogalacturonan-I (cRG-I), together with reduced duration and severity of symptoms. We aimed to further identify temporal mRNA responses by nasal epithelial cells (NEC) after RV16 infection, and to assess the effect of cRG-I supplementation. NECs were obtained prior to (day(d)-55) and after 8-weeks (d-1) of supplementation (0, 0.3, 1.5 g/d), and on d3, d6, d9 and d13 after exposure to 100 TCID50 RV16. Transcriptome data were generated and analysed with the R2: Genomics Analysis and Visualization platform (https://r2.amc.nl). RV16 infection reduced expression of genes related to oxidative phosphorylation (d3), induced gene expression by interferon (d6-9), and reduced expression of cilia-related genes (d13). cRG-I changed these responses. At low-dose, gene expression of important transcription factors and effector molecules (IRF4, IRF8, RFX3, IL-1B, CASP1) was enhanced markedly earlier (d3-6). At high-dose, cRG-I induced expression of inflammasome-related genes already after 8-weeks supplementation. cRG-I, in a dose-dependent manner, significantly affected the sequence and intensity of genes that regulate pathways involved in anti-viral responses and epithelial repair. This may underlie the reduced duration and severity of symptoms. - Source: PubMed
Mol JasperVolckmann RichardRavi AbilashRavanetti LaraCalame WimMcKay SueAlbers RuudKoster JanLutter René - - Source: PubMed
Publication date: 2025/11/27
Aldous NouraAlnesf AldanaElsayed Ahmed KAbohalawa Bushra YasinAlajez Nehad MAbdelalim Essam M - Persistent pulmonary hypertension of newborn (PPHN) occurs due to the impairment in the expected fall in pulmonary vascular resistance during the fetal to neonatal circulatory transition, with a prevalence of 1.9 per 1,000 live births and a significant mortality rate of 4-33%. We aimed to systematically review the genetic variants associated with PPHN in term and late preterm infants without a known genetic syndrome. - Source: PubMed
Publication date: 2026/03/13
Mani SrinivasanBerger Seth I