ZFP36L2 antibody - center region (OAAB13102)
- Known as:
- ZFP36L2 (anti-) - central region (OAAB13102)
- Catalog number:
- oaab13102
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZFP36L2 antibody - center region (OAAB13102)
Related genes to: ZFP36L2 antibody - center region (OAAB13102)
- Gene:
- ZFP36L2 NIH gene
- Name:
- ZFP36 ring finger protein like 2
- Previous symbol:
- BRF2
- Synonyms:
- ERF2, RNF162C, TIS11D
- Chromosome:
- 2p21
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-09
- Date modifiied:
- 2016-10-05
Related products to: ZFP36L2 antibody - center region (OAAB13102)
Related articles to: ZFP36L2 antibody - center region (OAAB13102)
- To systematically identify RING finger protein (RNF) biomarkers with diagnostic value in sepsis and to explore their potential as therapeutic targets. - Source: PubMed
Publication date: 2026/08/29
He XiaoleiLiu JunWu HaoLiu Qingquan - - Source: PubMed
- 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 - Phenotypic plasticity is a hallmark of cancer; however the molecular switches required for cell-fate reprogramming are poorly understood. During intestinal wound-healing and colorectal cancer (CRC) metastasis, differentiated cells can dynamically dedifferentiate into an intestinal stem cell (ISC) state to drive epithelial regeneration and metastatic outgrowth. Here we show that the RNA-binding protein ZFP36L2, which is mutated in 5-10% of CRC, is a pivotal stress-responsive orchestrator of dynamic dedifferentiation. In mouse colon regeneration models, ZFP36L2 ablation inhibits dedifferentiation, ISC gene expression and function and impairs intestinal regeneration. In human CRC, loss of ZFP36L2 function abrogates metastatic seeding and the outgrowth of LGR5 canonical metastases while promoting lineage plasticity and non-canonical differentiation into heterogeneous cell states. Mechanistically, ZFP36L2 binds to stress-associated mRNAs that contain AU-rich 3' untranslated regions, which induces the formation of dynamic biomolecular condensates associated with mRNA degradation and termination of the stress response. Together, these data show that ZFP36L2 acts as an important molecular switch that couples stress sensing with phenotypic plasticity. This in turn drives cellular dedifferentiation essential for re-establishing the ISC state during wound healing and metastasis. In ZFP36L2-deficient CRC, the inability to re-enter the LGR5 state during metastatic outgrowth promotes non-canonical lineage plasticity, which is associated with poor clinical outcomes. - Source: PubMed
Publication date: 2026/08/05
Jiang QingwenRaghavan Manisha SRodriguez Aileen MLallo MorganTam Cyrus LHartner SaskiaForsyth BritneyMahmoud AhmedZincke FabianZhao HuiyongMoorman AndrewBalkaran SashaLuckett KathleenPintar JuraRomin YevgeniyChan EricSantella AnthonyMödl BernadetteShah FarheenBaali IlyesKharas Michael Gde Stanchina ElisaUrganci NilShia JinruPe'er DanaSanchez-Vega FranciscoKoche RichardMorris QuaidChan Joseph MGanesh Karuna - The ZFP36 family proteins (TTP, ZFP36L1, and ZFP36L2) are RNA-binding proteins that function as key post-transcriptional regulators of gene expression. They bind AU-rich elements (AREs) in target mRNA 3'UTRs, recruit the CCR4-NOT deadenylation complex to trigger mRNA decay, and maintain homeostasis in immunity, barrier function, and stem cell fate. Rather than acting on single targets, all family members share a conserved mRNA destabilization mechanism, with outcomes determined by member-specific expression, kinase-mediated regulation, and cell-type-dependent target availability. Dysregulation of this network stabilizes mRNAs encoding pro-inflammatory cytokines, immune checkpoints, and oncogenes, driving pathogenesis of inflammation, autoimmunity, cancer, cardiovascular and neurodegenerative diseases. Individual family members exert context-dependent and sometimes opposing effects, so their net function depends on the specific cellular and disease context. Therapeutic strategies targeting ZFP36 activity, including phosphatase agonism and epigenetic modulation, have shown promising preclinical results, but clinical translation remains early. This review summarizes the molecular regulatory networks of the ZFP36 family and their physiological and pathological roles, emphasizing the mechanistic principles that unify family-member function and the contextual factors that diversify it, to provide a foundation for future therapeutic development. - Source: PubMed
Publication date: 2026/07/17
Wen YuxuanPeng LichaoWang Jing