KHDRBS1 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- KHDRBS1 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00010657-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- KHDRBS1 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: KHDRBS1 293T Cell Transient Overexpression Lysate(Denatured)
- 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: KHDRBS1 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: KHDRBS1 293T Cell Transient Overexpression Lysate(Denatured)
- Polymerase theta-mediated end-joining (TMEJ) is a stand-alone mutagenic DNA double-strand break (DSB) repair pathway that becomes critical when high-fidelity repair is compromised. Although the enzymatic mechanism of TMEJ has been extensively studied in recent years, its regulation remains poorly understood. Here, we identify and characterize the RNA-binding protein Sam68 (also known as Khdrbs1) as a modulator of TMEJ in mammalian cells. We demonstrate that Sam68 is required for proper expression of Polq, the gene encoding polymerase theta (Polθ), the central factor in TMEJ; loss of Sam68 results in reduced TMEJ at CRISPR-induced DSBs. Mechanistically, Sam68 promotes correct splicing of Polq messenger RNA by suppressing the inclusion of a conserved poison exon (PE) that introduces a premature termination codon in the transcript. This function depends on the RNA-binding domain of Sam68. Genetic deletion of the PE restores Polq expression and rescues TMEJ activity in Sam68-depleted cells. Together, these findings establish alternative splicing as a direct mechanism controlling TMEJ capacity and reveal a conserved regulatory mechanism that tunes mutagenic DSB repair through modulation of Polθ abundance. - Source: PubMed
van Wezel Marloes DKool Hannekevan den Heuvel Dianavan Schendel RobinBarazas MarcoLuijsterburg Martijn STijsterman MarcelSchimmel Joost - The CCL5/CCR5 axis plays a pivotal role in tumor progression and metastasis. We previously reported CCR5 promoted melanoma EMT and metastasis by upregulating TGFβ1 expression via the PI3K/AKT/GSK3β pathway. However, the full spectrum of downstream events triggered by CCR5 activation remains poorly understood. - Source: PubMed
Publication date: 2026/06/22
Xie LifenZhu TianhuiHe AnWu QinZeng JinfengHuang LiqinZhang LingLiu Jie - 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