Ask about this productRelated genes to: KHDRBS3 antibody
- Gene:
- KHDRBS3 NIH gene
- Name:
- KH RNA binding domain containing, signal transduction associated 3
- Previous symbol:
- -
- Synonyms:
- T-STAR, Etle, etoile, SALP, SLM2, SLM-2
- Chromosome:
- 8q24.23
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-28
- Date modifiied:
- 2016-05-23
Related products to: KHDRBS3 antibody
Related articles to: KHDRBS3 antibody
- The aim of this study was to better understand the genomic architecture behind performance-related traits in sport horses. In this study, we conducted a haplotype-based genome-wide association study (GWAS) for 36 conformation and free jumping phenotypes recorded during routinely conducted young horse evaluation tests involving 380 Swedish Warmblood (SWB) horses. The horses were evaluated by expert judges using both traditional and linear evaluation systems. All samples were genotyped using the 670K Affymetrix® Axiom® Equine Genotyping Array, haplotypes were first phased, and haplotype blocks were calculated for a total of 78,000 haplotypes. To assess the association between the haplotypes and studied traits, a single trait linear mixed model was used, correcting for sex and the date-location in which the evaluation took place. In the analysis, a total of 11 haplotype blocks were found to be significantly associated with a total of six traits: height at withers, the conformation traits hooves and correctness in movement, and the free jumping traits technique: haunches, carefulness, and distance estimation. In the proximity of those haplotypes (windows size ± 500 kb), 33 protein-coding genes, 31 IncRNAs, and one miRNA were found. Within those regions, key candidate genes were located such as LCORL and KHDRBS3, associated with body size and growth, as well as COL12A1, MYO6, and FILIP1, involved in musculoskeletal development and muscle elasticity and strength. The haplotype-based GWAS approach proved to be a useful method since it helped in the detection of aggregated genetic effects. Future studies with larger sample sizes and using novel tools for objective phenotyping will be essential to further investigate the genetic mechanisms behind sports performance. - Source: PubMed
Publication date: 2026/04/10
Ablondi MichelaEriksson SusanneGelinder Viklund ÅsaMikko Sofia - Oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV) employs a biphasic life cycle consisting of latency and lytic replication to achieve lifelong infection. Despite its essential role in KSHV persistence and tumorigenicity, much remains unknown about how KSHV lytic reactivation is regulated. Leveraging high-throughput transcriptomics, we identify microRNA-31-5p (miRNA-31-5p) as a key regulator of KSHV lytic reactivation, capable of modulating expression of KSHV lytic genes and progression through the lytic cascade. Mechanistically, miR-31-5p controls the KSHV lytic switch by regulating expression of the RNA-binding protein KHDRBS3. miR-31-5p-mediated KHDRBS3 repression results in decreased nascent transcription of crucial viral lytic genes including the main KSHV transcription factor RTA. We characterize KHDRBS3 as a major host factor that is critical for KSHV lytic replication and uncover its key role in KSHV lytic gene transcription. Our results highlight a pivotal role for the miR-31-5p/KHDRBS3 axis in modulating KSHV reactivation and provide insights into gene-expression regulation of lytic KSHV. - Source: PubMed
Publication date: 2026/04/01
Lee Soo MiAvalos Christopher LMiliotis ChristosDoh Hanna MChan EricaKaye Kenneth MSlack Frank J - Recurrent implantation failure (RIF) remains a major challenge in assisted reproductive technology, and the molecular mechanisms underlying endometrial receptivity are incompletely understood. This study aimed to comprehensively characterize transcriptomic alterations, including alternative splicing events (ASEs), differential gene expression (DEGs), and immune cell dynamics across different phases of endometrial receptivity in women with RIF. Endometrial biopsies were collected from 90 healthy fertile controls and 73 RIF patients during pre-receptive, receptive, and post-receptive phases. High-throughput RNA sequencing was performed, and bioinformatic analyses were conducted to identify ASEs, DEGs, immune cell composition, and RNA-binding protein (RBP) networks. Skipped exons and mutually exclusive exons were the predominant splicing events observed. Both ASEs and DEGs were significantly enriched in pathways regulating cell adhesion, cytoskeletal organization, and immune modulation. KHDRBS3 emerged as a potential key RBP involved in splicing regulation during the window of implantation. Immune profiling revealed dynamic alterations in CD8 + T cells, NK cells, and monocytes between non-receptive and receptive phases, suggesting immune dysregulation associated with implantation failure. Drug repurposing analysis identified several small molecules targeting ASE-related genes, offering promising therapeutic options for RIF. These findings highlight the coordinated changes in alternative splicing, gene expression, and immune cell composition that characterize endometrial receptivity and provide insights that may guide the development of novel diagnostic biomarkers and targeted interventions to improve reproductive outcomes. - Source: PubMed
Publication date: 2026/02/18
Wang Mao-LiLu Bing-JieLu XiangLi LuSun Xiao-XiChen Jiu-ChengLiu HuChen ChenWu HanLi Da-JinZhang Wen-Bi - 25-Hydroxyvitamin D (25(OH)D), a metabolite of vitamin D, has demonstrated anticancer properties; however, the role of alternative splicing in mediating these effects remains poorly understood. In this study, we reveal for the first time that 25(OH)D exerts antitumor effects by promoting exon 13 skipping of KDM6A (KDM6A Δexon13), which suppresses the proliferation and stemness of breast cancer cells and lacks H3K27 demethylase activity. Mechanistically, CUT&Tag and RNA-seq analyses demonstrated that KDM6A Δexon13 induces the accumulation of H3K27me3 at the promoter region of TRAP1, thereby inhibiting its transcription. Consequently, the downregulation of TRAP1 reduces Smad2/3 phosphorylation. Furthermore, KHDRBS3 was identified as the splicing factor of KDM6A Δexon13 and was regulated by 25(OH)D. Notably, 25(OH)D exhibited a synergistic effect with GSK-J4, a specific inhibitor of KDM6A, in suppressing breast cancer cell growth. Collectively, our findings uncover a novel anticancer mechanism of 25(OH)D, highlight the critical role of KDM6A Δexon13 in breast cancer progression, and provide further evidence supporting the correction of 25(OH)D deficiency in breast cancer patients. - Source: PubMed
Publication date: 2026/02/17
Ma LingjunSheng XingyeWang LexinWan XinyuChen RuiLi XuanZheng RanXu LuZha XiaomingWang Jue - Osteoarthritis (OA) is a common chronic degenerative joint disease. Chondrocytes undergo dynamic changes during the pathogenesis of OA, and the destruction of the extracellular matrix (ECM) and its homeostatic disruption are hallmarks of OA. This study explores the roles of transcriptional and alternative splicing (AS) mechanisms in regulating extracellular matrix (ECM) homeostasis in osteoarthritis (OA), using bulk and single-cell RNA-sequencing data. By analyzing two OA transcriptome datasets, we identified differentially expressed genes (DEGs) that are enriched in ECM-related pathways and constructed a regulatory network between differentially expressed transcription factors (DE TFs) and ECM-related DEGs. This revealed the potential roles of transcription factors ELF3 and DDIT3 in regulating the expression of , , and . Single-cell RNA-sequencing data further validated the expression patterns of and in distinct chondrocyte subtypes. Additionally, by analyzing AS events, we identified the RNA-binding protein (RBP) KHDRBS3 as a regulator of AS for the ECM-related gene . Aberrant changes in these events may impact the ECM environment of chondrocytes and contribute to the pathogenesis of OA. This study, for the first time, dissects the regulatory models in OA cartilage at both transcriptional and post-transcriptional levels. These findings provide novel potential targets for early diagnosis and intervention strategies in OA. - Source: PubMed
Publication date: 2025/12/16
Ye XiguangZheng ChunyanLi Hao