Ask about this productRelated genes to: CHST7 antibody
- Gene:
- CHST7 NIH gene
- Name:
- carbohydrate sulfotransferase 7
- Previous symbol:
- -
- Synonyms:
- C6ST-2, C6ST2
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-09
- Date modifiied:
- 2018-05-14
Related products to: CHST7 antibody
Related articles to: CHST7 antibody
- Differentiated cells maintain their identity through active mechanisms that suppress alternative cell fates, but disrupting these barriers can enhance direct reprogramming for organ repair. Among the regulators of cell fate stability, glycosylation-associated genes have emerged as barriers to cardiac reprogramming. Here we show that carbohydrate sulfotransferases are central fate-stabilizing regulators, with CHST7 acting through CD44 to control nuclear JUNB levels, chromatin binding, and downstream transcriptional activity. Integrated RNA-seq and ATAC-seq analyses reveal that CHST7 maintains open chromatin at JUNB- and CTCF-enriched loci while restricting accessibility at MEF2C-enriched regions, collectively reinforcing fibroblast identity and suppressing cardiac fate acquisition. We further identify PIP4K2C as a downstream effector whose inhibition enhances cardiac reprogramming efficiency and improves myocardial repair in vivo. These findings define a sulfotransferase-dependent barrier to cell fate conversion with therapeutic implications for heart regeneration. - Source: PubMed
Publication date: 2026/07/17
Romero Michaela RMurphy SeanChang Yu-LingLamba AashnaAncel SaraLlorente AliciaMarchant JamesHuang Chun-TengKumsta CarolineAndersen PeterRanade SanjeevMahmoud Ahmed IKwon ChulanFreeze Hudson HAdams Peter DSacco AlessandraRanek Mark JEmerling Brooke MWang Yu XinColas Alexandre R - Asthma is a chronic respiratory disease affecting over 230 million people worldwide, with higher prevalence in women. Environmental allergens such as house dust mite (HDM) trigger airway inflammation and hyperresponsiveness (AHR), yet the epigenetic mechanisms underlying these responses remain poorly understood. Furthermore, the role of estrogen receptors in the context of asthma is understudied. We aimed to investigate whether estrogen receptor-specific DNA methylation contributes to HDM-induced airway remodeling and hyperresponsiveness. Male and female C57BL/6J wild-type mice and estrogen receptor α and β knockout mice ( and ) were exposed to HDM or phosphate-buffered saline for 5 wk. DNA methylation and RNA sequencing data were obtained from snap-frozen whole lung tissues. HDM exposure resulted in widespread differential methylation of genes associated with inflammation and AHR, including , and . Notably, the absence of estrogen receptor β (in mice) produced the most pronounced methylation patterns, particularly in females. Pathway enrichment analysis revealed asthma-relevant processes such as extracellular matrix remodeling, leukocyte adhesion and migration, airway smooth muscle contraction, and inflammatory signaling. Integration of methylation and gene expression data confirmed significant correlations ( < 0.05) for , , and , and a marginal correlation for Chst7 ( < 0.1), implicating these genes in allergic asthma pathogenesis. Our findings demonstrate that HDM exposure induces sex-specific epigenetic changes mediated by estrogen receptor status, highlighting a potential mechanism for increased asthma susceptibility in women. These results can inform estrogen receptor-targeted treatment strategies for allergic airway diseases. Understanding estrogen receptor-mediated epigenetic regulation provides a foundation for developing sex-specific interventions for asthma, addressing the higher prevalence and severity observed in women. In this study, we demonstrate that exposure to house dust mite in the mouse lung is associated with epigenetic alterations in genes linked to airway hyperresponsiveness and lung inflammation. These alterations were dependent on the presence or absence of estrogen receptors. - Source: PubMed
Publication date: 2026/06/12
Commodore SarahEkpruke Carolyn DamilolaAlford RachelBorges-Sosa Omar ARousselle DustinBabayev MaksatIgwe ChukwudikeHemmerich Christopher MRusch Douglas BSilveyra Patricia - Sulfate is a vital nutrient for healthy brain development. More than 90 sulfate-related genes are highly conserved across mammalian species, with 16 of these genes being clinically reportable for adverse brain conditions. To determine the potential involvement of additional sulfate-related genes in human neuropathology, this study curated the spatial and temporal expression patterns of all known sulfate biology genes in the human fetal brain from 8 to 37 post conception weeks (pcw) using data from the BrainSpan database and performed network analysis to cluster sulfate-related genes with genes involved in neurodevelopmental processes. A total of 64 sulfate-related genes were abundantly or moderately expressed in 11 brain regions throughout gestation. Steady state expression was observed for some of these genes from 8 to 37 pcw, including genes that encode sulfotransferases (, ), sulfatases (, , , ), sulfatase modifying enzyme (), key enzymes in amino acid metabolism (, ), sulfate transporter (), as well as genes involved in neurodevelopmental processes (, , , , , ). Between 21-24 weeks, there were numerous clusters of sulfate biology genes with neurodevelopmental genes involved in neuronal migration ( and synaptogenesis (, , , ). At 8-13 and 17-21 pcw, fifteen sulfate genes (, , , , , , , , , , , , , , ) were expressed in the hippocampus and clustered with genes involved in neurogenesis, differentiation and synaptogenesis (, , ). Overall, this study identified 48 sulfate-related genes with moderate/abundant expression in the fetal brain that are coexpressed with genes for neurodevelopmental processes but are not considered in clinical settings. These findings provide information for future studies into the physiological roles of sulfate-related genes that are expressed in the fetal brain. - Source: PubMed
Publication date: 2026/05/08
Vijayakumar PrasidheeSummers Kim MDawson Paul A - Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by deficits in social communication, restricted interests, and repetitive behaviors. Despite considerable research efforts, the genetic complexity of ASD remains poorly understood, complicating diagnosis and treatment, especially in the Arab population, with its genetic diversity linked to migration, tribal structures, and high consanguinity. To address the scarcity of ASD genetic data in the Middle East, we conducted genome sequencing (GS) on 50 ASD subjects and their unaffected parents. Our analysis revealed 37 single-nucleotide variants from 36 candidate genes and over 200 CGG repeats in the gene in one subject. The identified variants were classified as uncertain, likely pathogenic, or pathogenic based on in-silico algorithms and ACMG criteria. Notably, 52% of the identified variants were homozygous, indicating a recessive genetic architecture to ASD in this population. This finding underscores the significant impact of high consanguinity within the Qatari population, which could be utilized in genetic counseling/screening program in Qatar. We also discovered single nucleotide variants in 13 novel genes not previously associated with ASD: , , , , , , , , , , , , and . Our investigation categorized the candidate genes into seven groups, highlighting their roles in cognitive development, including the ubiquitin pathway, transcription factors, solute carriers, kinases, glutamate receptors, chromatin remodelers, and ion channels. - Source: PubMed
Publication date: 2024/10/27
Ben-Mahmoud AfifGupta VijayAbdelaleem AliceThompson RichardAden AbdiMbarek HamdiSaad ChadiTolefat MohamedAlshaban FouadStanton Lawrence WKim Hyung-Goo - The X chromosome has remained enigmatic in Alzheimer disease (AD), yet it makes up 5% of the genome and carries a high proportion of genes expressed in the brain, making it particularly appealing as a potential source of unexplored genetic variation in AD. - Source: PubMed
Belloy Michael ELe Guen YannStewart IlariaWilliams KennedyHerz JoachimSherva RichardZhang RuiMerritt VictoriaPanizzon Matthew SHauger Richard LGaziano J MichaelLogue MarkNapolioni ValerioGreicius Michael D