Ask about this productRelated genes to: ARID5A antibody
- Gene:
- ARID5A NIH gene
- Name:
- AT-rich interaction domain 5A
- Previous symbol:
- -
- Synonyms:
- MRF-1, RP11-363D14
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-28
- Date modifiied:
- 2016-10-05
Related products to: ARID5A antibody
Related articles to: ARID5A antibody
- Adenine-thymine (AT)-rich interactive domain-containing protein 5a (Arid5a) is an RNA-binding protein (RBP) that post-transcriptionally stabilizes mRNAs encoding proinflammatory mediators, including Interleukin-6 (IL-6), thereby amplifying inflammation. However, structural basis and regulatory mechanisms of Arid5a function remain poorly defined. In this study, we identified and characterized a conserved allosteric site within the ARID domain that regulates Arid5a-mediated mRNA stabilization. Using integrative in silico modeling and in vitro assays, 2 picolinamide-based inhibitors, NFP1 and NFP2, were designed to specifically engage the allosteric site constituent residues. Mutational and functional analyses revealed Tyr88 and Val91 as key regulatory elements within the allosteric site, essential for transmitting conformational regulation upon ligand engagement. Pharmacological inhibition of the allosteric site disrupted Arid5a interaction with target RNA stem-loop structure, reduced stability of Il6 mRNA, and attenuated inflammatory responses in Lipopolysaccharide (LPS)-stimulated macrophages. Furthermore, Arid5a inhibitors reduced the stability of other target mRNAs, including Signal transducer and activator of transcription 3 (Stat3) and OX40, in polarized T helper 17 (Th17) cells. In a murine model of LPS-induced septic shock, treatment with NFP1 or NFP2 significantly improved survival, reduced clinical severity, and mitigated tissue damage in vital organs. These findings identify a new mechanism regulating Arid5a activity and present Arid5a allosteric inhibition as a promising therapeutic strategy for managing systemic inflammation including sepsis. - Source: PubMed
Hanieh HamzaMetwally HozaifaKishimoto Tadamitsu - Head and neck squamous cell carcinoma (HNSCC) is characterized by a highly immunosuppressive tumor microenvironment (TME), with tumor-associated macrophages (TAMs) playing a central role in resistance to therapy. The immune checkpoint molecule CD47, known for its "don't eat me" signal, and EphA3, a receptor tyrosine kinase, are both upregulated in radiation-resistant HNSCC. However, their cooperative role in regulating TAMs and therapeutic resistance remains poorly understood. - Source: PubMed
Publication date: 2026/05/15
Kim Song HeeKim Ji WonKim Min SeokCha Hee JeongKim Seong WhoHan Myung Woul - Chronic kidney disease (CKD) is a major global health burden with substantial morbidity and mortality. Proteinuria is strongly associated with adverse renal outcomes, and podocyte pyroptosis is increasingly recognized as a key driver of glomerular filtration barrier disruption. - Source: PubMed
Publication date: 2026/05/01
Zhao MingmingDuan HangyuZhang JianingShi YueHe LinghuiXu JianlongYin YundongZhang Yu - The microtubule-stabilizing drug paclitaxel remains the standard of care for various solid malignancies but frequently leads to chemotherapy-induced peripheral neuropathy (CIPN). CIPN is a leading cause for premature treatment termination and a significantly reduced quality of life in long-term cancer survivors. The molecular mechanisms of neuro-axonal degeneration, neuroinflammation, and pain in patients treated with paclitaxel remain incompletely understood, and there are currently no predictive biomarkers or preventive treatments. We used human iPSC-derived sensory neurons exposed to paclitaxel to comprehensively model the pathophysiology of CIPN. Neurotoxicity was assessed over time using viability assays and sequential RNA sequencing, as well as deep proteome and lipidomic analyses. We observed a time and dose-dependent decline of cell viability at clinically relevant paclitaxel doses. Sequential RNA sequencing defined JUN as an early immediate gene, followed by the overexpression of genes of the neuronal stress response (e.g., ARID5A, WEE1, DUSP16, GADD45A), neuronal injury and apoptotic pathways (e.g., ATF3, HRK, BBC3 [PUMA], BCL2L11 [BIM], CASP3), neuroinflammation and nociception (CALCB, MMP10, IL31RA, CYSLTR2, C3AR1, TNFRSF12A) and neuronal transduction (e.g., CAMK2A, STOML3, PIRT), while key enzymes of lipid biosynthesis were markedly downregulated (e.g., LSS, HMGCS1, HMGCR, DHCR24). Deep proteome analyses following 48 h of exposure to 100 nM paclitaxel revealed a strong correlation of differentially expressed RNA with proteins, and a marked degradation of essential axonal transport proteins such as kinesins, stathmins, and scaffold proteins. Consistent with the downregulation of rate-limiting enzymes of lipid biosynthesis, lipidome analysis confirmed deregulation of neuronal lipid homeostasis. In summary, paclitaxel induces transcriptomic and proteomic signatures of the neuronal stress response, neuroinflammation, nociception, and disturbed metabolism. These may explain, in part, the clinical phenotype of sensory loss, hypersensitivity, and neuropathic pain frequently observed in patients suffering from CIPN, but constitute pharmacologically addressable targets. - Source: PubMed
Publication date: 2026/02/10
Schinke ChristianMaierhof Smilla KHew LoisFernandez Vallone ValeriaFrahm SilkeTelugu Narasimha SwamyDiecke SebastianIvanov AndranikKovács RichardBeule DieterKirchner MarieluiseMertins PhilippBrüning UlrikeKirwan Jennifer AStachelscheid HaraldEndres MatthiasHuehnchen PetraBoehmerle Wolfgang - Cartilage development and homeostasis require precise regulation by transcriptional and epigenetic networks. PRDM16 is a transcription factor containing zinc finger domains that enable protein-DNA and protein-protein interactions, as well as domains with the capacity for histone methyltransferase activity. However, the detailed molecular mechanisms by which PRDM16 regulates chondrogenesis and chondrocyte identities remain largely unknown. Using our osteochondral lineage-specific, conditional knockout mouse model ( , Prdm16 cKO), we found that loss of Prdm16 in osteochondral lineage cells delays, but does not fully inhibit, endochondral ossification and bone formation in the knee joint. Furthermore, Prdm16 cKO male mice exhibit comparable OA severity between injured and non-injured joints, suggesting that PRDM16 may exert a chondroprotective function. In our hiPSC-derived chondrocyte model, we observed significantly reduced pellet size and DNA content in cells with modulated PRDM16 expression compared to Control, implying a link between PRDM16 and chondrocyte viability. Integrated analysis of single cell RNA-sequencing and CUT&RUN-sequencing revealed that PRDM16 regulates chondrocyte cell fate decisions by altering chromatin accessibility and DNA binding at promoter/enhancer regions of genes essential for chondrogenesis and chondrocyte hypertrophy. Indeed, PRDM16 governs the expression of key chondrogenic regulators including , , , , and hypertrophic driver . Overall, our results provide evidence that PRDM16 serves as an essential genetic and epigenetic regulator of chondrogenesis and chondrocyte phenotype specification in the knee joint through DNA binding and by modulating H3K4me3 histone mark deposition. - Source: PubMed
Publication date: 2026/01/31
Fadial EloiseHansen VictoriaKulzhanova GulzadaTashbib Eliya TazreenaChinta DeekshaKlee AlexisShammas HelenPradhan GourangoWu Chia-Lung