Ask about this productRelated genes to: RAD23A Blocking Peptide
- Gene:
- RAD23A NIH gene
- Name:
- RAD23 homolog A, nucleotide excision repair protein
- Previous symbol:
- -
- Synonyms:
- HHR23A, MGC111083
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-20
- Date modifiied:
- 2016-10-05
Related products to: RAD23A Blocking Peptide
Related articles to: RAD23A Blocking Peptide
- Multiple myeloma (MM) is a plasma cell malignancy characterized by genomic instability and a high dependency on proteasome activity. Accordingly, DNA-damaging agents and proteasome inhibitors (PIs) are frontline therapies; however, therapeutic resistance inevitably develops. RAD23A, a dual-function protein involved in nucleotide excision repair and proteasome-mediated protein degradation, is highly expressed in MM and is associated with poor patient survival. Here, we demonstrate that depletion of RAD23A exerts potent anti-MM activity both in vitro and in vivo. Inducible CRISPR/Cas9 knockout (iKO) or shRNA-mediated knockdown of RAD23A in MM cell lines, including PI-resistant models, markedly suppressed cell proliferation. RAD23A loss impaired DNA repair capacity, triggered activation of the stress-associated eIF2α-ATF4 axis and promoted caspase-dependent apoptosis. Quantitative proteomic profiling of RAD23A-iKO cells confirmed upregulation of apoptotic and stress-response pathways, accompanied by downregulation of DNA repair and deubiquitination pathways. In an MM xenograft model, RAD23A depletion significantly reduced tumor growth and prolonged survival. Collectively, these findings identify RAD23A as a critical survival factor in MM and highlight its potential as a novel therapeutic target. - Source: PubMed
Publication date: 2026/07/15
Wan XuepingDu TingFang TengWang MinxingRay ArghyaWen KennethMusa Md AbuGarbicz FilipCarrasco Ruben DSamur Anil AFulciniti MariateresaTalluri SrikanthSong YanMunshi Nikhil CAnderson Kenneth C - Type 2 diabetes mellitus (T2DM) and sarcopenia demonstrate a significant comorbidity, particularly in the elderly, yet the molecular mechanisms linking them, especially through oxidative stress, remain incompletely understood. This study aimed to identify oxidative stress-related hub genes involved in T2DM-associated sarcopenia (T2DS) by integrating single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data with machine learning. We analyzed scRNA-seq datasets (GSE244515, GSE268953) to characterize cellular heterogeneity and bulk RNA-seq datasets (GSE202295, GSE226151) for differential expression. Cell type annotation revealed key involvement of neuromuscular junctions and myofibers. Functional enrichment analyses highlighted pathways like the proteasome, TNF signaling, and ubiquitin-mediated proteolysis. From an initial set of oxidative stress-related genes, a comprehensive machine learning framework comprising 127 algorithm combinations was employed. The Lasso+Stepglm[both] model identified 12 candidate genes. Subsequent Protein-Protein Interaction (PPI) network analysis refined this to seven core hub genes: TNFRSF1B, PSMA2, UBE2D1, UBE2N, HSP90AA1, RAD23A, and DNAJB1. These genes are functionally interconnected, primarily implicating TNFRSF1B-mediated inflammatory signaling that activates the ubiquitin-proteasome system, leading to enhanced protein degradation-a key pathway in muscle atrophy. ROC curve analysis confirmed the strong diagnostic value of these hub genes across training, test, and external validation sets. Our findings systematically reveal novel oxidative stress-related hub genes and mechanisms in T2DS, providing potential biomarkers and therapeutic targets for this debilitating condition. - Source: PubMed
Publication date: 2026/07/07
Zhu GuangwenZou KaiLiang YiXie LitingChen Qiu - The scalable production of recombinant adeno-associated viruses (rAAVs) remains a critical challenge in gene therapy manufacturing. While HEK293 and insect cell systems dominate current production platforms, each presents significant limitations in cost, scalability, and product quality. Chinese hamster ovary (CHO) cells represent an attractive alternative given their established use in biopharmaceutical manufacturing, yet their inability to efficiently support rAAV assembly has hindered development of CHO-based rAAV bioprocesses. Here, we investigate the molecular basis of this limitation by expressing individual AAV and adenoviral helper proteins in CHO cells and characterizing their effects using integrated transcriptomic and proteomic analyses. Functional enrichment analyses revealed that mitochondrial biogenesis was broadly suppressed across conditions, accompanied by downregulation of antiviral nuclear regulation, signaling networks, including the JAK-STATand interferon-stimulated gene pathways. Functional evaluation of host proteins identified from the omics analyses showed that overexpression of nuclear components like Mx2 and Rad23A supported rAAV production, reaching a yield of 10 vg/mL. Together, these results provide a comprehensive map of CHO cell responses to AAV and adenoviral helper elements, identify candidate host pathways influencing rAAV biogenesis, and highlight both the promise and the remaining barriers toward establishing CHO as a viable platform for large-scale rAAV manufacturing. - Source: PubMed
Publication date: 2026/06/08
Tzimou KonstantinaLópez-García GuillemSipahi Meryem IremNielsen Lars KLavado-García Jesús - The yak lung functions as a vital adaptive organ in cold, low-oxygen environments. Hypoxia can induce pathological remodeling in yak lung tissue, so we need to understand the molecular mechanisms of this remodeling. For this study, we used cross-omics comparative approaches, including transcriptomics, label-free proteomics, and untargeted metabolomics, to examine both normal and diseased yak lung tissues. From histological observations, the disease phenotype was identified as pulmonary emphysema. Our results showed a significant up-regulation of differentially expressed genes such as MTTP, CXCL8, RETN, and NNAT, while genes like SLC45A1, IL10, SDSL, and COL12A1 were clearly down-regulated. In the differential protein analysis, proteins such as RASSF4, EDC4, CTSC, and FECH were notably up-regulated, whereas CYP27A1, FKBP9, RAD23A, and PLSCR2 were significantly down-regulated. Metabolomic profiling revealed that palmitoyl-L-carnitine, decanoyl-L-carnitine, and o-acetylcarnitine were significantly higher in emphysematous lung tissue, whereas racemethionine and L-methionine S-oxide were significantly much lower. Also, when we compared of bulk RNA-seq, label-free proteomics, and untargeted metabolomics data revealed enrichment in three common pathways: the asthma pathway, the linoleic acid metabolism pathway, and the gastric acid secretion pathway. Of note, histamine levels were higher in both the asthma and gastric acid secretion pathways. While the mRNA expression level of BoLA-DQB was increased in the asthma pathway, its protein expression level was decreased. This study offers some initial cross-omics evidence about what happens. These findings give us a scientific basis for developing effective prevention and control strategies, which in turn can help the protection of yak health and the sustainable development of plateau animal husbandry. - Source: PubMed
Publication date: 2026/06/08
Chen PingZhang Jian - Lactylation is an emerging lactate-derived post-translational modification that may link tumour metabolic reprogramming, epigenetic regulation and DNA damage repair. Enhanced glycolysis and lactate accumulation are common in many tumours, and lactate has been reported to induce histone and non-histone lactylation in specific experimental contexts. Recent studies suggest that lactylation is associated with several DNA repair pathways, including base excision repair/single-strand break repair, nucleotide excision repair, homologous recombination and non-homologous end joining, and may contribute to therapy resistance in selected cancer models. Specifically, XRCC1 lactylation has been reported to promote nuclear translocation and repair activity in glioblastoma models; H4K12 lactylation has been linked to PARP inhibitor resistance through RAD23A activation in ovarian cancer models; and BLM lactylation has been associated with enhanced homologous recombination repair in bladder cancer models. Lactylation of NBS1, RAD51 and XLF has also been implicated in DNA repair regulation in specific experimental systems, although some mechanistic links are inferred from pathway activation or functional rescue experiments rather than directly demonstrated across multiple tumour types. These findings suggest that lactylation may modulate DNA repair and therapeutic response in a context-dependent manner. Targeting lactate metabolism, transport and lactylation regulators, including LDHA, MCT1/4, ACAT1, AARS1 and GCN5, or using site-specific lactylation-inhibiting peptides may improve chemotherapy and PARP inhibitor efficacy, but clinical translation remains limited by heterogeneity, metabolic plasticity, toxicity and insufficient validation. - Source: PubMed
Publication date: 2026/06/13
Wang LiningZhong SiyuZhao JiananLiu LigangLi Changyong