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)
- 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 - C/EBPβ regulates oncogene-induced senescence (OIS) and the senescence-associated secretory phenotype (SASP) through activation by ERK1/2 and CK2. In tumor cells, C/EBPβ activity is suppressed by its 3'UTR via a mechanism termed 3'UTR regulation of protein activity (UPA), which spatially segregates transcripts from kinase-rich perinuclear endosomes. Here, we identify kinase-proximal mRNA decay as the underlying mechanism. The mRNA decay factors UPF1 and STAU1/2 localize to perinuclear endosomes and promote degradation of transcripts, thereby preventing C/EBPβ phosphorylation and activation. Disruption of this pathway restores C/EBPβ activity and induces senescence. , deletion of a G/U-rich regulatory element (GRE) in the 3'UTR impairs the progression of Kras-driven lung tumors and biases cells toward an AT2-like differentiation state with reduced EMT-associated transcriptional reprogramming. RAS-expressing fibroblasts show enhanced OIS that requires upregulation of the pro-senescent cytokine S100a9. These findings identify perinuclear mRNA decay as a mechanism suppressing C/EBPβ activity and senescence in cancer. - Source: PubMed
Publication date: 2026/08/04
Salotti JacquelineAsif NidaBasu SrikantaDas AniruddhaHu LinshanYang MeiKarim BaktiarSaylor KarenMartin NancyScheiblin David AMisra SwetaLuke Brian TAndresson ThorkellYi MingGalloux MélissaLockett StephenTessarollo LinoJohnson Peter F - The RNA lariat debranching enzyme DBR1 is essential for intron turnover and RNA metabolism, yet its broader impact on transcriptome regulation remains incompletely defined. To elucidate the consequences of DBR1 depletion, we performed transcriptome-wide RNA sequencing of DBR1-knockdown and wild-type HEK293 cells. Differential expression analysis revealed widespread perturbations in pathways linked to RNA splicing, mRNA surveillance, translational control, and stress-granule biology. Many of the most significantly altered transcripts encode splicing factors and RNA quality-control components, underscoring DBR1's influence on post-transcriptional regulation. Alternative splicing analysis showed changes across multiple event types, with exon skipping accounting for >50% of events, followed by mutually exclusive exons, alternative 5' and 3' splice sites, and retained introns, indicating that DBR1 depletion induces pervasive splicing defects. Direct spliceosome inhibition using isoginkgetin (blocks tri-snRNP recruitment) and pladienolide B (targets SF3B1) reproduced the DBR1-KD mis-splicing patterns of cell signaling genes and factors involved in RNA metabolism, supporting a functional link between DBR1 activity and alternative splicing. Notably, DBR1 knockdown revealed a subset of transcripts that are both NMD-sensitive and enriched within stress granules. Consistent with this observation, G3BP1 immunopurification and confocal microscopy further support a role for DBR1 and UPF1 in stress-granule dynamics, suggesting that these factors may participate at distinct stages to influence mRNA fate under stress conditions. Together, these findings indicate that DBR1 functions beyond lariat RNA turnover as a common regulator of RNA processing, transcriptome stability, and stress granule homeostasis, revealing intricate crosstalk between RNA splicing and RNA quality control pathways in human cells. - Source: PubMed
Publication date: 2026/08/04
Barwell TiffanyEmbree Caleb MReid RobertDreau DidierSingh GuramritChakrabarti Kausik