ATXN1 ELISA kit
- Known as:
- ATXN1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ATXN1-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ATXN1 ELISA kit
Related genes to: ATXN1 ELISA kit
- Gene:
- ATXN1 NIH gene
- Name:
- ataxin 1
- Previous symbol:
- SCA1
- Synonyms:
- D6S504E, ATX1
- Chromosome:
- 6p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
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- Source: PubMed
- Cerebral malaria (CM) is associated with disruption of the blood-brain barrier (BBB), neurovascular injury, and high mortality. Although mesenchymal stem cells (MSCs) have demonstrated therapeutic efficacy in experimental cerebral malaria (ECM), the molecular mechanisms underlying these effects remain insufficiently defined. In this study, we investigated how MSC treatment modulates host miRNA networks during ECM using a Plasmodium berghei ANKA infection in C57BL/6 mice. MSC treatment significantly reduced clinical severity, improved survival, and preserved BBB integrity, as indicated by decreased Evans blue extravasation and reduced microvascular sequestration within brain. RNA sequencing identified 64 differentially expressed miRNAs associated with MSC treatment. Pathway enrichment using DIANA-miRPath v4.0 identified 23 miRNAs associated to CM-relevant pathways. Eleven miRNAs with highest pathway interactions were subsequently validated by RT-qPCR, confirming consistent down-regulation of eight miRNAs following MSC treatment. miRNA-mRNA network construction revealed several hub genes, including Rora, Nfia, Nfib, Slc1a2, Tcf4, Pura, and Atxn1, linked to neurological phenotypes relevant to CM pathology. Collectively, these findings suggest that MSCs mitigate ECM pathology by reprogramming miRNA-mRNA regulatory networks governing cerebral and neuronal stability. The identified miRNA-mRNA hubs represent promising candidates for future biomarker studies and may provide a foundation for the development of adjunctive therapeutic strategies against cerebral malaria. - Source: PubMed
Publication date: 2026/07/07
Chaudhary AmrendraSharma InduThakur Reva SharanRanjha RiteshDas Jyoti - Expanded short tandem repeats contribute to a broad spectrum of neurodegenerative diseases, yet their roles in Parkinson's disease (PD) and parkinsonism remain incompletely characterized, especially across diverse ancestries. We analyzed short-read whole-genome (WGS) and clinical exome sequencing (CES) data from 38,365 individuals (28,861 WGS; 9,504 CES), encompassing 23,242 patients with PD, 4,729 patients with atypical parkinsonism and 10,394 healthy controls from 11 genetic ancestries. To determine carrier frequencies and characterize repeat structures across diverse ancestries, we genotyped 12 established pathogenic loci where normal, intermediate, and pathogenic alleles can be reliably differentiated using short-read sequencing data. Additionally, we conducted threshold-based associations to determine the minimum threshold associated with increased PD risk in 15,995 individuals (8,591 PD, 7,404 controls) of European ancestry. Pathogenic repeat expansions were detected in 62 patients (56 PD and 6 atypical parkinsonism) and 5 controls across seven loci ( , , , , , and ), spanning seven ancestries. Among these, expansions were the most frequently observed in PD and were present in African, East Asian, European and Middle Eastern ancestries. Additionally, intermediate repeat expansions exhibited a strong, length-dependent association with PD risk in the European population, with individuals with ≥32 repeats having a more than four-fold increased risk (odds ratio 4.25, 95% confidence interval 1.80-12.05). Overall, >92% of expanded alleles harbor CAA interruptions within the CAG tract. Pathogenic expansions at other loci, such as and , showed more ancestry-specific distributions. Clinically, individuals with pathogenic and expansions most often presented with typical PD features but frequently showed earlier disease onset and a strong family history of PD. This large-scale, multi-ancestry study comprehensively maps the genetic landscape of pathogenic and intermediate repeat expansions in PD. Our findings confirm a length- and structure-dependent risk association for with PD in the European population and highlight the pleiotropic effects of repeat expansions across the parkinsonian spectrum. - Source: PubMed
Publication date: 2026/06/22
Lange Lara MCerquera-Cleves CatalinaTan Ai HueyLim Shen-YangOkubadejo Njideka ULin Chin-HsienChen Pin-ShiuanShin Jung HwanAhmad-Annuar AzlinaScreven Laurel AChelban VioricaDilliot Allison AFienemann AndréGhosh Galvelis KamaliniHoulden HenryIwaki HirotakaJaunmuktane ZaneCullinane Patrick WWarner ThomasJunker JohannaKanana YuliiaKeller Sarmiento Ignacio JKlein ChristineKung Pin-JuiLeonard Hampton LMencacci Niccoló ENalls Mike AReal RaquelBen Sassi SamiaTrinh JoanneVitale DanWestenberger AnaWu Lesley YSingleton Andrew BMorris Huw RLohmann KatjaBlauwendraat CornelisHeutink PeterFang Zih-Hua - Recent evidence from genome-wide association studies has linked the ataxin-1 gene (ATXN1) to an increased risk of developing the autoimmune demyelinating disorder multiple sclerosis. From a mechanistic standpoint, our previous work explained this genetic association by defining an immunomodulatory function for ataxin-1 in controlling specific genetic programs underlying B cell proliferation, activation, immunoglobulin production, and antigen presentation. Here, we employed a high-resolution multiomics analytical pipeline to further dissect the role of ataxin-1 in distinct B cell subsets upon encephalitogenic stress. By combining single-nuclei RNA-seq and ATAC-seq, along with mass-spectrometry proteomics, we documented that ataxin-1 is significantly enriched in B1 cells, marginal zone B cells, memory B cells, and precursor B cells. Pathway analysis highlighted that ataxin-1 is implicated in RNA splicing and translation processes. Conversely, no major effects were implicated for ataxin-1 in chromatin remodeling in the B cell population. Our findings expand the current knowledge of the cellular functions controlled by ataxin-1 outside of the central nervous system, and further describe a key regulator of B cell biology in health and disease. - Source: PubMed
Carver Jonathan JDenbrock Rachael RLau Kristy MZeczycki Tonya NYin ChanghongHuang WeihuaDidonna Alessandro - Acute myeloid leukemia (AML), a heterogeneous hematopoietic malignancy, continues to present significant challenges in clinical management due to its unfavorable prognosis despite advances in therapy. The identification of novel molecular markers remains essential for improving prognostic stratification and guiding therapeutic decision-making. - Source: PubMed
Publication date: 2026/07/01
Liu An-QiShao Yang-LiuWang Ke-TaoWang NanYang Zhi-RuiLei Yang-YangZhu Hai-YanGuan Wei