Mouse Khdrbs1 Antibody (C-term) Blocking Peptide
- Known as:
- Mouse Khdrbs1 Antibody (C-terminus) Blocking Peptide
- Catalog number:
- BP19343b
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- Mouse Khdrbs1 Antibody (C-term) Blocking Peptide
Related genes to: Mouse Khdrbs1 Antibody (C-term) Blocking Peptide
- Gene:
- KHDRBS1 NIH gene
- Name:
- KH RNA binding domain containing, signal transduction associated 1
- Previous symbol:
- -
- Synonyms:
- Sam68, p62, FLJ34027
- Chromosome:
- 1p35.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-28
- Date modifiied:
- 2016-10-05
Related products to: Mouse Khdrbs1 Antibody (C-term) Blocking Peptide
Related articles to: Mouse Khdrbs1 Antibody (C-term) Blocking Peptide
- Atherosclerosis (AS) is driven by intertwined inflammatory responses and vascular wall remodeling, yet the core regulatory networks and actionable targets underlying plaque formation remain incompletely defined. Bulk transcriptomic data from GSE43292, comprising paired advanced carotid plaques and distant early-stage lesion tissues from 32 patients, were analyzed to identify differentially expressed genes (DEGs), followed by WGCNA and intersection with GeneCards-derived AS-related genes. Candidate genes were mapped to a STRING PPI network, and hub genes were prioritized using four Cytoscape algorithms (MCC, EPC, Stress, Degree). Functional annotation (GO/KEGG), immune infiltration, and single-gene GSEA were performed. A 10 × scRNA-seq dataset (GSE159677) was used for cell-type annotation, compositional comparison, cell-cell communication, and hub-gene localization. Drug prediction was conducted, followed by molecular docking of candidate compounds with hub proteins. Finally, an oxLDL-induced in vitro model was used for validation by CCK-8, ROS staining, Western blotting, and qRT-PCR. Seven hub genes (SMAD4, CASP8, PARP1, CRKL, CDK6, VDAC1, KHDRBS1) were identified. Enrichment analyses linked these hubs to cell death/stress regulation, immune-related programs, and vascular remodeling. Immune infiltration suggested marked immune reconfiguration in plaques. Single-gene GSEA highlighted coordinated remodeling of vascular smooth muscle contraction, gap junction signaling, and lipid/NAD-associated metabolism. scRNA-seq analysis indicated joint contributions from myeloid and vascular structural cells, with hub genes showing cell-type-biased enrichment. Quercetin emerged as a candidate compound; docking supported favorable multi-target binding (strongest for PARP1 and CDK6). Experimentally, oxLDL upregulated hub-gene mRNA/protein levels, while quercetin significantly attenuated these increases. We define an AS-associated hub-gene network with single-cell context and provide convergent computational and experimental evidence that quercetin exerts endothelial-protective effects consistent with multi-target modulation of the hub-gene network, supporting its therapeutic potential in AS. - Source: PubMed
Publication date: 2026/07/07
Huang DajunLiu YingWang YilanHu JinmingTang HanzhangYin YongjunKong Lingqiu - Tissue-derived small extracellular vesicles (sEVs) are vital mediators of intercellular communication; however, the molecular landscape of their long RNA cargo, including full-length mRNAs and long noncoding RNAs, and the mechanisms controlling specific RNA sorting into sEVs are still poorly understood. Here, we successfully isolated sEVs from five anatomical regions of healthy porcine lung and performed polyadenylated transcriptome profiling using short- and long-read sequencing. - Source: PubMed
Publication date: 2026/07/02
Liu JinxiuYu NaixiangWei JiachengZhang Zhou - RNA-binding proteins (RBPs) of the STAR family play key roles in mammalian development, yet their contributions to lineage specification remain incompletely understood. Here, using CRISPR-Cas9 knockout models combined with multi-omics approaches, we investigate the functions of two STAR proteins, SAM68 and QKI, in mouse embryonic stem cells (mESCs). Both RBPs support mESC proliferation, self-renewal, and efficient differentiation into cardiomyocytes. Although SAM68 and QKI belong to the same protein family, they control largely distinct regulatory programs during differentiation. We uncover an unexpected role for SAM68 in cardiomyocyte specification through multiple post-transcriptional mechanisms. SAM68 modulates alternative splicing and promotes the biogenesis of a subset of cardiac-enriched circular RNAs, through binding to intronic regions flanking back-splice junctions and potentially through association with NF90/110. In addition, SAM68 binds untranslated regions of key differentiation-related transcripts, including Gata4 mRNA, and functions in ribonucleoprotein complexes to regulate their translation. Together, these findings identify SAM68 as a multifunctional regulator coordinating multiple layers of RNA metabolism-including splicing, circRNA biogenesis, and translation-during cardiomyocyte differentiation and provide insight into how STAR proteins shape post-transcriptional gene regulatory networks during early development. - Source: PubMed
Broglia LauraDasti AlessandroAntonelli Maria CarlaAoun GuyD'Agostino SabrinaVandelli AndreaArmaos AlexandrosDelli Ponti RiccardoWolf SarahKlostermann MelinaArnal Segura MagdalenaTian Tian VMariani DavideColantoni AlessioParonetto Maria PaolaGustincich StefanoZarnack KathiBechara EliasTartaglia Gian Gaetano - We employed an integrated bioinformatics screening approach along with Mendelian randomization (MR) analysis to explore potential genetic targets for varicose veins of lower extremities (VVs) and identify potential treatment options for VVs. Differential expression analysis was conducted using R software to identify differentially expressed genes (DEGs) of VVs from the Gene Expression Omnibus database. Weighted gene co-expression network analysis (WGCNA) was performed to identify co-expression networks. Functional enrichment analyses were conducted for the identified genes. A protein-protein interaction network was constructed to analyze the interactions among the identified genes. Additionally, genome-wide association studies data for VVs were downloaded for MR analysis. Various methods, including inverse-variance weighted, were employed to assess potential causal associations with VVs risk, followed by sensitivity analysis. The DEGs identified from the VVs Gene Expression Omnibus dataset included 180 upregulated genes and 335 downregulated genes. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analysis revealed that the downregulated DEGs were significantly associated with nuclear protein-containing complexes and nucleic acid binding (P < .05). WGCNA highlighted a highly significant "turquoise" module comprising 78 downregulated genes (P = 2e - 04). The protein-protein interaction network analysis of the significant DEGs and the WGCNA "turquoise" module identified 224 nodes and 491 edges, uncovering several hub genes such as BRCA1, NCBP2, GTPBP4, HDAC2, KHDRBS1, and HNRNPR. Detailed functional enrichment analysis indicated involvement in tumor-like cellular proliferation and differentiation processes, including protein acetylation, RNA splicing, and metabolic processes. MR analysis revealed a causal association between the tumor-related gene Ecto-NOX disulfide-thiol exchanger 2 (ENOX2) and the risk of VVs, with a statistical significance (odds ratio: 1.0016; 95% confidence interval: 1.0003-1.0029; P = .015) according to inverse-variance weighted analysis. Sensitivity analysis confirmed the absence of heterogeneity and horizontal pleiotropy in the observed associations (P > .05). "Leave-one-out" validation analysis did not indicate any changes. Our study unveils the involvement of ENOX2 and the related mechanisms in the pathogenesis of VVs, suggesting their potential as genetic targets for treatment. - Source: PubMed
He QiuruiZhang XiaohongTao ChenChen ChenmingYan Weiming - Metabolic remodeling, marked by maladaptive shifts in substrate use and energy production, is a hallmark of pathologic cardiac hypertrophy. Yet the mechanisms linking stress signaling to impaired myocardial glucose oxidation remain incompletely defined. Sam68 (Src-associated in mitosis, 68 kDa; also known as [KH domain-containing, RNA-binding, signal transduction-associated protein 1]), a STAR (signal transduction and activation of RNA) family RNA-binding protein, has not previously been implicated in cardiac metabolic control. - Source: PubMed
Publication date: 2026/05/22
An JunqingHan ChaoshanJiang YingShi JiaweiLi HuadongWang ChenqiHuang JianrongXu ShiyueNi JieCao YangpoFeng YuliangLyu QingDong NianguoQin Gangjian