TIS11B / ZFP36L1 pSer92 antibody Ab
- Known as:
- TIS11B / ZFP36L1 pSer92 (anti-) Antibody
- Catalog number:
- 1488089
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- TIS11B / ZFP36L1 pSer92 antibody
Related genes to: TIS11B / ZFP36L1 pSer92 antibody Ab
- Gene:
- ZFP36L1 NIH gene
- Name:
- ZFP36 ring finger protein like 1
- Previous symbol:
- BRF1
- Synonyms:
- RNF162B, Berg36, ERF1, TIS11B, cMG1
- Chromosome:
- 14q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-09
- Date modifiied:
- 2016-06-30
Related products to: TIS11B / ZFP36L1 pSer92 antibody Ab
Related articles to: TIS11B / ZFP36L1 pSer92 antibody Ab
- 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 - Sepsis-induced acute respiratory distress syndrome (ARDS) is a fatal inflammatory lung injury. The integrated stress response (ISR) may play stage-dependent roles in lung injury, but its clinical relevance in sepsis-induced ARDS remains unclear. We aimed to identify ISR-related biomarkers and explore their potential mechanisms. - Source: PubMed
Gao YeWang NiXiao Zhaoyang - Cellular senescence plays a critical role in physiological and pathological processes. This study aims to elucidate the contribution of cellular senescence-related genes to disease etiology. We investigated a cohort study of 439,501 individuals, which included 22 cancers and 9 non-cancer diseases. We found that HLA-E and HLA-G-associated senescence in epithelial and immune cells were specific oncogenic factors for prostate and lung cancers. MAP2K4 was implicated as a risk factor for breast cancer, while ZFP36L1 and STAT3 were associated with a reduced risk of inflammatory bowel disease (IBD). Notably, ETS2-mediated inhibition of the senescence-associated secretory phenotype (SASP) was associated with decreased disease risk. Furthermore, single-cell level analysis confirmed that the dynamics of these marked gene expressions in immune cells was related to reduced disease risk, while upregulation in epithelial cells correlated with increased disease risk. In parallel, co-localization analyses corroborated these associations, explaining potential regulatory mechanisms underlying disease risk variants. These findings enhance our understanding of how cellular senescence works on disease susceptibility and provide potential targets for therapeutic interventions and precision medicine approaches. - Source: PubMed
Publication date: 2026/08/30
Liu BinWu WeidongLiu ChangFeng PengyaLiu SimengGong ShanshanLi YingyingLi YaMi JunZheng PengyuanWen HongtaoXue XiaMi Yang - The innate immune system provides the first line of defense against invading pathogens and relies on tightly regulated mechanisms to initiate and resolve inflammatory responses. In addition to transcriptional control, post-transcriptional regulation of messenger RNA (mRNA) plays a critical role in determining the magnitude and duration of immune responses. Among those key regulators, the ZFP36 family of CCCH-type zinc-finger RNA-binding proteins, including ZFP36, ZFP36L1, and ZFP36L2, plays a central role in controlling the stability and translation of inflammatory, immune-related, and viral RNAs. This review focuses on the ZFP36 family of RNA-binding proteins and highlights their emerging roles in inflammation, immune cell development and differentiation, and antiviral immunity, with a particular focus on ZFP36L1 and ZFP36L2. Recent evidence has identified ZFP36L1 as a broad-spectrum antiviral factor that restricts multiple RNA viruses through distinct molecular mechanisms. A detailed understanding of the molecular mechanisms underlying ZFP36L1- and ZFP36L2-mediated antiviral activity and immune regulation will facilitate rational development of host-directed antiviral therapeutics and their strategic integration with vaccination strategies to limit viral replication, shedding, and transmission, thereby improving the control of emerging and re-emerging viral diseases. - Source: PubMed
Publication date: 2026/07/27
Bhowmik MalabikaMomin ToobaThakur NeeluSingh NeerajRajput Mrigendra - T follicular helper (Tfh) cells are critical for germinal centers (GC), the specialized microenvironment where long-lived humoral immunity is generated in response to vaccination or infection. Within the GC, B cells engage with Tfh cells and elicit their help in the form of cytokines and cell-surface co-stimulator molecules. Tfh helper activity must be rapidly available in response to B cell engagement, yet the mechanisms controlling this helper activity remain poorly characterized. Post-transcriptional regulation of mRNA decay and translation offers one way to rapidly and temporally tune Tfh cell activity. ZFP36L1, a member of the ZFP family of RNA-binding proteins, is a candidate modulator of Tfh cell helper activity, as it controls cytokine production and responses in other T cell lineages, modulating their differentiation and function. We sought to determine if ZFP36L1 is also important for Tfh cell biology. In this study, we show expression of ZFP36L1 by Tfh cells. We selectively delete ZFP36L1 from Tfh cells and analyze the effect this has on the GCs. Surprisingly, we find that the GC response and affinity maturation are resilient to deletion of ZFP36L1 from Tfh cells. - Source: PubMed
Carslaw Helena AWoolliscroft SamWatson Emily MBell Sarah ELinterman Michelle ATurner MartinWebb Louise M C