KHDRBS1 MaxPab rabbit polyclonal antibody (D01)
- Known as:
- KHDRBS1 MaxPab host: rabbit pab (anti-) (D01)
- Catalog number:
- H00010657-D01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- KHDRBS1 MaxPab rabbit polyclonal antibody (D01)
Related genes to: KHDRBS1 MaxPab rabbit polyclonal antibody (D01)
- Gene:
- AAMDC NIH gene
- Name:
- adipogenesis associated Mth938 domain containing
- Previous symbol:
- C11orf67
- Synonyms:
- PTD015, FLJ21035, CK067
- Chromosome:
- 11q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-27
- Date modifiied:
- 2016-06-21
- Gene:
- C11orf54 NIH gene
- Name:
- chromosome 11 open reading frame 54
- Previous symbol:
- -
- Synonyms:
- PTD012
- Chromosome:
- 11q21
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-11
- Date modifiied:
- 2017-07-26
- Gene:
- GHITM NIH gene
- Name:
- growth hormone inducible transmembrane protein
- Previous symbol:
- -
- Synonyms:
- HSPC282, PTD010, DERP2, My021, TMBIM5
- Chromosome:
- 10q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-10
- Date modifiied:
- 2014-11-19
- 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
- Gene:
- MRPS18B NIH gene
- Name:
- mitochondrial ribosomal protein S18B
- Previous symbol:
- -
- Synonyms:
- MRPS18-2, PTD017, C6orf14, HSPC183
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-05-30
- Date modifiied:
- 2016-10-05
Related products to: KHDRBS1 MaxPab rabbit polyclonal antibody (D01)
Related articles to: KHDRBS1 MaxPab rabbit polyclonal antibody (D01)
- 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 KHDRBS1 [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 YuliangLv QingDong NianguoQin Gangjian - Retinoic acid receptor responder protein 1 is upregulated in proximal tubular epithelial cells in CKD. Soluble retinoic acid receptor responder protein 1 drives fibrosis by binding KH RNA binding domain containing, signal transduction associated 1, recruiting steroid receptor coactivator kinase, and inducing signal transducer and activator of transcription 3 phosphorylation. - Source: PubMed
Publication date: 2026/04/09
Ye LinJiang ZhuoyuanWu YongZeng YaoChen XiangjunFeng BaiyuYin LijunGao YananXu WeimingYan ShuxiangLi YuWu JinshanLi QifuChen Anqun - T cells recognize their target cells through the T cell receptor (TCR). Combining gain-of-function, single-cell and optical high-content screens, we identified RNA-based mechanisms that selectively sensitize target cells to TCR-specific T cell cytotoxicity. First, CRISPR activation screens in melanoma cells identify functionally diverse regulators of TCR-specific cytotoxicity, including SAFB, KHDRBS1, MYC, CD44, WNT3A, WNT1 and others. Expressing sensitizing hits in cancer and virally infected cells restores TCR-specific cytotoxicity. Next, we developed in situ Perturb-seq for optical pooled genetic screens with in situ detection of perturbations and spatial transcriptomic readouts. Perturb-seq and in vivo-in situ Perturb-seq show that the hits converge on shared cell-autonomous and intercellular mechanisms, map gene-environment interactions and reveal that Wnt ligands activate T cells. Introducing a scalable approach to decode gene function at the cell and tissue level, the study uncovered context-specific gene functions to restore targeted T cell-based elimination of dysfunctional cells via synthetically lethal, RNA-based interventions. - Source: PubMed
Publication date: 2026/04/07
Akana Reece VillarinYoe JeehyunLaveroni OliviaSun ChangKim Young-MinJerby Livnat