UPF1 antibody - middle region (ARP36350_P050)
- Known as:
- UPF1 (anti-) - middle region (ARP36350_P050)
- Catalog number:
- arp36350_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- UPF1 antibody - middle region (ARP36350_P050)
Related genes to: UPF1 antibody - middle region (ARP36350_P050)
- Gene:
- UPF1 NIH gene
- Name:
- UPF1 RNA helicase and ATPase
- Previous symbol:
- RENT1
- Synonyms:
- HUPF1, KIAA0221, NORF1, pNORF1, smg-2
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-11
- Date modifiied:
- 2019-01-25
Related products to: UPF1 antibody - middle region (ARP36350_P050)
Related articles to: UPF1 antibody - middle region (ARP36350_P050)
- The coding sequence of an mRNA directs its own decay, yet how codons, codon context, and amino acids collectively regulate mRNA stability remains poorly understood. Here we use a massively parallel reporter assay to decode this regulatory layer in zebrafish embryos. We find that codon pairs and amino acid pairs regulate mRNA stability beyond the level of individual codons. This regulation depends on the identity and order of neighboring codons and their encoded amino acids in a translation-dependent manner. The relative contributions of codon and amino acid combinations to mRNA stability can be quantified using machine learning. We further found that endogenous mRNAs are regulated by codon pairs, thereby governing developmental gene regulation and biological function. This codon context-dependent decay requires deadenylation and decapping by Cnot7 and Dcp2, with Upf1 acting on long non-optimal ORFs. Together, our results redefine codon optimality as a context-dependent, pair-level code with implications for RNA biology and therapeutic mRNA design. - Source: PubMed
Publication date: 2026/09/17
Lee HaejeongMusaev DamirVejnar Charles EKrishna SrikarNguyen Trung DucStrayer Ethan CMessih Mario AbdelTakacs Carter MBeaudoin Jean-DenisGiraldez Antonio J - Dysregulation of target genes of nonsense-mediated decay (NMD) in the brain remains sparsely known in tauopathies. PS19 transgenic mice expressing human mutant P301S tau were evaluated for levels of lncRNA Gas5, a target of NMD. The results show Gas5 decreased in the brains of PS19 mice as they aged. We evaluated the consequences of blocking the NMD-mediated turnover of Gas5 using a small molecule administered intranasally to PS19 mice. The results show NPC86 disassociated Upf1 and Gas5, thereby hindering NMD. NPC86 treatment increased Gas5 levels in the cortex of male PS19 mice concurrent with a highly significant decrease in pTau S214 and neuroinflammatory genes while increasing insulin signaling. Consequently, digital spatial profiling identified Gas5-regulated genes and pathways. NPC86 treatment enhanced neuronal homeostasis, synaptic vesicle transport and mitochondrial function and downregulated neuroinflammatory pathways. The nodal genes in Parkinson's signaling pathway, the multiple sclerosis signaling pathway, the Gα(s) signaling pathway, the neuroinflammation signaling pathway, and the interferon gamma signaling pathway were decreased in response to NPC86. The study demonstrates the potential of selectively stabilizing NMD-target lncRNA Gas5 levels to alleviate early neurodegenerative pathology in tauopathy. - Source: PubMed
Publication date: 2026/08/27
Krause-Hauch MeredithWang BangmeiPatel Rekha SVerdina LauraHedrick AshleyBlair Laura JDharap AshutoshCai JianfengPatel Niketa A - Effective T cell responses against pathogens require a rapid yet tightly controlled remodeling of the proteome, and RNA binding proteins (RBPs) are key in this process. For instance, the RBP ZFP36L1 prevents excessive protein production and thereby limits immunopathology. ZFP36L1 is primarily known to mediate mRNA decay, but it can also regulate other processes. How its mode of action relates to its interaction partners is, however, not well-understood. Here, we mapped the ZFP36L1 interactome in primary human T cells. Using proximity labeling, we identified known and new interactors that regulate 3'UTR-mediated RNA degradation, deadenylation, stress granule/p-body formation, as well as 5'UTR-mediated translation repression and mRNA decapping. Snapshot analysis uncovered the ZFP36L1 interactome dynamics and RNA (in)dependency throughout T cell activation. Intriguingly, proximity labeling also uncovered regulators of ZFP36L1 protein expression. This included the helicase UPF1, which not only interacts with ZFP36L1 protein but that may also promote its protein expression. Altogether, this comprehensive interactome map underlines the versatility of interactions with ZFP36L1 and their possible role in cellular function. - Source: PubMed
Publication date: 2026/09/09
Jurgens Anouk PPopović Brankavan Alphen Floris PjSteinmetz MaximeWardak LeymaBradarić AntoniaEngels Sandervan der Zwaan Carmenvan den Biggelaar MaartjeHoogendijk Arie JBéthune JulienWolkers Monika C - Current targeted therapeutics for asthma focus on the T2 immune response, providing symptomatic management without addressing the issues of recurrence. Identifying key pathophysiological determinants in airway epithelium enables novel therapeutics to prevent asthma recurrence. Here we demonstrate that TDP-43, as the master regulator of RNA metabolism, is induced in airway epithelial cells by host allergen exposure and promotes asthmatic airway responses through dampening nonsense-mediated decay (NMD) by modulating UPF1 expression, resulting in accumulation of pathogenic and NMD-sensitive transcripts including CHRM1 encoding receptor that transduces the signaling of vagally-derived neurotransmitter acetylcholine. TDP-43 also facilitates airway influenza A virus replication. Intranasal application of lipid nanoparticles carrying antisense oligonucleotides targeting TDP-43 effectively reduce asthma-like pathologies in mice. Our findings indicate that targeting airway TDP-43 is therapeutically possible for asthma and influenza A virus infection-complicated asthma exacerbations. - Source: PubMed
Publication date: 2026/07/23
Yuan YanmeiTang WenzhuFeng XixiZhang ChunleiLiao YingyingTang MeiyanHe JianWan ShengpengPan GuihongLai XiaojiangXue QingWang Jun - SMG1, a phosphatidylinositol 3-kinase-related kinase (PIKK) family serine/threonine kinase, is a key regulator of nonsense-mediated mRNA decay (NMD) through phosphorylation of UPF1 and plays important roles in genome stability, p53 activation, and tumor suppression. Although 77 phosphorylation sites have been reported on SMG1, their regulatory significance has not been systematically characterized. - Source: PubMed
Publication date: 2026/08/07
Pai Apoorva K ADcunha LeonaGopalakrishnan Athira PerunellyUmmar SamseeraRajeev Athira CRaju Rajesh