ELAVL1 Mouse Monoclonal Antibody
- Known as:
- ELAVL1 Mouse Monoclonal Antibody
- Catalog number:
- BIN-001994-M02
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- ELAVL1 Mouse Monoclonal Antibody
Related genes to: ELAVL1 Mouse Monoclonal Antibody
- Gene:
- ELAVL1 NIH gene
- Name:
- ELAV like RNA binding protein 1
- Previous symbol:
- HUR
- Synonyms:
- HuR, Hua, MelG
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-12
- Date modifiied:
- 2015-07-22
Related products to: ELAVL1 Mouse Monoclonal Antibody
Related articles to: ELAVL1 Mouse Monoclonal Antibody
- Aging involves morphological and functional changes across different organs, but how these changes are linked among the different organs remains to be elucidated. Here, we uncover a central role of platelets in systemic aging. In aged mice, the levels of platelet-secreted pro-inflammatory factors (PSPF) increased greatly in the serum and platelets, leading to a diffuse increase of platelet infiltration in the brain, liver, lung, kidney, and aortic root. The RNA-binding protein HuR/ELAVL1, a major regulator of RNA metabolism, promoted the production of PSPF in platelets. Platelet-specific deletion of HuR reduced the expression of PSPF in platelets, alleviated platelet infiltration in the brain, liver, lung, kidney, and aortic root, and delayed systemic aging. By using single-nucleus sequencing, platelet-specific HuR ablation was found to alleviate p53 and pro-inflammatory signaling pathways in liver, lung, and brain tissues in aged mice. Our findings highlight a role of platelets in coordinating aging traits across organs. - Source: PubMed
Publication date: 2026/05/07
Liu CihangWang YingXia TianjiaoLin JingLiao QianzanLi YanyanZhang YiqiangMiao CongxiuYi XiaSun LuyangMa ZhengliangCheng XiaoleiJiang BinTian FengJu ZhenyuLiu BaohuaKong WeiFu YiYang ZhongzhouLiu JunlingTang HaoGu XiaopingWang Wengong - Cellular senescence arises through replicative exhaustion or acute stress, yet whether these distinct triggers share a reproducible transcriptional organization has remained unresolved. Seven public human fibroblast RNA-seq datasets were integrated across both trigger types, moving from differential expression through Gene Ontology and Reactome enrichment to protein-protein interaction network embedding within a single harmonized framework. Both triggers converged on concordant repression of replication and chromatin programs alongside induction of inflammatory and extracellular matrix outputs. Cross-trigger combination identified 263 commonly repressed and 112 commonly induced GO terms, with consistently higher enrichment scores in the repressed set, and 145 versus 13 shared Reactome pathways. Conserved induction of calcium ion homeostasis and membrane potential regulation, and conserved repression of RHO GTPase-Formin signaling, extended the shared program beyond canonical SASP biology into dimensions not previously described in human fibroblasts. Interactome embedding, applied here for the first time in a cross-trigger senescence framework, identified ten genes occupying both induced and repressed neighborhoods simultaneously, a structural layer invisible to enrichment analysis alone. ELAVL1 coordinates SASP output and growth arrest post-transcriptionally, while suppressed PARP1 alongside active ATM defines a self-reinforcing damage configuration. These results provide a quantitative cross-study reference and a structured basis for senotherapeutic candidate prioritization. - Source: PubMed
Publication date: 2026/05/07
Shahzaib MohdAprile DomenicoSquillaro TizianaAlessio NicolaPeluso GianfrancoDi Bernardo GiovanniGalderisi Umberto - Type 2 high asthma is driven by coordinated GATA3 dependent programs in CD4 T cells and group 2 innate lymphoid cells (ILC2). Although biologics targeting IL4, IL5, or IL13 benefit subsets of patients, many remain symptomatic, suggesting that upstream regulatory mechanisms may sustain type 2 inflammation. We investigated whether HuR (ELAVL1), an RNA-binding protein that stabilizes GATA3 and Th2 cytokines mRNA, regulates type 2 inflammatory programs in allergic asthma. Using a house dust mite (HDM) model in vivo, HuR inhibition with the small molecule KH3 reduced lung inflammation, suppressed Th2 cytokine expression, accelerated Gata3 mRNA decay in lung CD4 T cells, and attenuated airway hyperresponsiveness toward control levels. In ex vivo activated human lung CD4 T cells, KH3 accelerated GATA3 mRNA decay with minimal effects on RORC or TBX21 and selectively reduced Th2 cytokine secretion, while IL10 and IL2 were unchanged. Similarly, ILC2s isolated from peripheral blood mononuclear cells (PBMCs) of type 2 high asthmatic donors showed reduced GATA3 mRNA stability and diminished Th2 cytokine production following KH3 treatment. Single-cell transcriptomic analysis of bronchoalveolar lavage fluid after allergen challenge demonstrated co-enrichment of ELAVL1 and GATA3 within Th2 clusters in human airways. Together, these findings identify HuR as a post-transcriptional regulator of GATA3 driven type 2 inflammation in allergic asthma. - Source: PubMed
Publication date: 2026/04/27
Atasoy UlusFattahi FatemehYaekle LauraHolden JuliaTepper BrandonHussein KareemMeier JoshuaXu LiangNerella SrilaxmiLei JingBentley KelleyHershenson MarcHuang Steven K - This study aims to investigate the impact and molecular mechanism of ELAVL1 in promoting macrophage M1 polarization in Crohn's disease (CD) by upregulating S100A8 expression. - Source: PubMed
Publication date: 2026/05/03
Jia LinChen YingtaiLu Ying - Nuclear export of viral RNAs is essential for the replication of hepatitis B virus (HBV). Our previous study demonstrated that ELAVL1 (embryonic lethal, abnormal vision, Drosophila-like 1) mediates the nuclear export of HBV RNAs via the chromosome region maintenance 1 (CRM1) pathway by recognizing and binding to the AUUUA motifs within these transcripts. Here, we identify Ras-related nuclear protein (RAN) and RAN-binding protein 3 (RANBP3) as critical downstream regulators of this CRM1-mediated RNA export pathway. We show that RANBP3 recruits RAN-GTP to assemble an export-competent quaternary complex (CRM1-HBV RNAs-RANBP3-RAN-GTP). The functional significance of this complex is underscored by the findings that its disruption, through knockdown of RANBP3/RAN, or by introducing CRM1 mutations that prevent cofactor binding, severely impairs HBV RNA export and viral replication. Together, our study thus elucidates a precise regulatory mechanism governing HBV RNA trafficking and highlights RANBP3 and RAN as potential antiviral targets.IMPORTANCEEfficient nuclear export of hepatitis B virus (HBV) RNAs is essential for viral replication, yet the regulatory mechanisms controlling this process remain poorly defined. This study identifies Ras-related nuclear protein (RAN) and RAN-binding protein 3 (RANBP3) as key host cofactors that drive chromosome region maintenance 1 (CRM1)-mediated export of HBV transcripts by assembling an export-competent complex with viral RNAs. Disrupting this pathway profoundly impairs RNA export and downstream steps of the viral life cycle. By defining how HBV harnesses the RANBP3-RAN-CRM1 axis for RNA trafficking, our work reveals a previously unrecognized layer of host dependency and highlights RANBP3 and RAN as promising targets for antiviral intervention. - Source: PubMed
Publication date: 2026/04/30
Wang MengfeiChen QuanZheng YingchengYin JiatongZhu GuoguoZhao KaitaoXu ZaichaoHua RongZhou MengZhang LuZhao GaihongYang ShipengAmat ZulihumaXia YuchenCheng Xiaoming