CSTF2 Mouse Monoclonal Antibody
- Known as:
- CSTF2 Mouse Monoclonal Antibody
- Catalog number:
- BIN-001478-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CSTF2 Mouse Monoclonal Antibody
Related genes to: CSTF2 Mouse Monoclonal Antibody
- Gene:
- CSTF2 NIH gene
- Name:
- cleavage stimulation factor subunit 2
- Previous symbol:
- -
- Synonyms:
- CstF-64
- Chromosome:
- Xq22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-12
- Date modifiied:
- 2016-04-05
Related products to: CSTF2 Mouse Monoclonal Antibody
Related articles to: CSTF2 Mouse Monoclonal Antibody
- Viral infection can reprogram host gene expression by selectively remodeling the cellular epitranscriptome. N -methyladenosine (m A) is a reversible RNA modification that is dynamically altered during infection by viruses, including Zika virus (ZIKV), yet the mechanisms underlying transcript-specific m A changes remain poorly understood. Here, we integrated glyoxal and nitrite-mediated deamination of unmethylated adenosine sequencing (GLORI-seq) and METTL3 RNA immunoprecipitation and sequencing to generate a comprehensive map of m A dynamics during ZIKV infection. We identified over 2,000 dynamically regulated m A sites, with m A-increased genes enriched for JAK/STAT and TGF-β signaling pathways, both central to immune regulation. Many m A changes arose from ZIKV-induced noncanonical polyadenylation, which generated new RNA isoforms that are preferentially targeted by METTL3. Consistently, depletion of the cleavage stimulation factors CSTF2 and CSTF2T impaired alternative isoform expression and subsequent ZIKV-induced m A methylation. Overall, this work reveals that ZIKV reshapes the host epitranscriptome through coordinated changes in RNA processing and redirected METTL3 targeting, establishing mechanistic frameworks for infection-induced m A remodeling. - Source: PubMed
Publication date: 2026/03/28
Aufgebauer Caroline JNelson Theodore MHouerbi NadiaVeenbaas Seth DTegowski MatthewLuo EstherSivasudhan EnakshiGoneos MichaelCollier PaulProszynski JacquelineRyon KristaViolette Evan MTouré Savanna AMeyer Kate DMason Christopher EHorner Stacy M - Gastric cancer is a fatal malignancy that is frequently diagnosed at an advanced stage worldwide, and current treatments are limited. The RNA-binding protein CSTF2 is associated with the prognosis of many cancers, but the role it plays in gastric cancer remains unknown. - Source: PubMed
Publication date: 2025/11/27
Feng LiangCao ZhiguoShi XiaoqiLiu WenhaoXu WeiweiYu ChangjunNing JieChen Changyu - Epitranscriptomic changes in the transcripts of cancer related genes could modulate protein levels. RNA editing, particularly A-to-I(G) editing catalyzed by ADAR1, has been implicated in cancer progression. RNA editing events in the 3' untranslated region (3'UTR) can regulate mRNA stability, localization, and translation, underscoring the importance of exploring their impact in cancer. Here, we performed an in silico analysis to detect breast cancer enriched RNA editing sites using the TCGA breast cancer RNA-seq dataset. Notably, the majority of differential editing events mapped to 3' untranslated regions (3'UTRs). We confirmed A-to-I(G) editing in the 3'UTRs of MDM2 (Mouse Double Minute 2 homolog), GINS1 (GINS Complex Subunit 1), and F11R (Junctional Adhesion Molecule A) in breast cancer cells. RNA immunoprecipitation with ADAR1 antibody confirmed the interaction between ADAR1 and MDM2, GINS1, and F11R 3'UTRs. ADAR1 knockdown revealed decreased editing levels, establishing ADAR1 as the editing enzyme. A reporter assay for MDM2, an oncogene overexpressed mostly in luminal breast cancers, demonstrated that RNA editing enhances protein expression, in agreement with reduced MDM2 protein levels in ADAR1 knockdown cells. Further exploration into the mechanisms of 3'UTR editing events revealed an interaction between ADAR1 and CSTF2, a core component of the polyadenylation machinery, as identified through biotin-based proximity labeling mass spectroscopy, and co-immunoprecipitation experiments. Furthermore, CSTF2 knockdown reduced both ADAR1 and MDM2 protein levels. Our findings highlight implications for MDM2 regulation by ADAR1-dependent 3'UTR RNA editing and present an interplay between RNA editing on 3'UTRs and the mRNA polyadenylation machinery. These results improve our understanding of ADAR1's role in cancer-associated 3' UTR RNA editing and its potential as a therapeutic target. - Source: PubMed
Publication date: 2025/05/17
Almeric ElanurKaragozoglu DenizCicek MustafaDioken Didem NazTac Huseyin AvniCicek EsraKirim Busra AytulGurcuoglu IrmakSezerman Osman UgurOzlu NurhanErson-Bensan Ayse Elif - Oral squamous cell carcinoma (OSCC) is a prevalent and devastating malignancy of the oral cavity that profoundly affects patient survival and quality of life (QOL). Cleavage Stimulation Factor Subunit 2 (CSTF2) is known to influence tumor development across multiple cancer types. However, its specific association with patient prognosis and immune cell infiltration in OSCC remains insufficiently understood. - Source: PubMed
Publication date: 2025/02/07
Aierken ZumulaitiMuhetaer MuertizaLei ZhangAbudourousuli Ainiwaerjiang - Alternative cleavage and polyadenylation (APA) have gained increasing attention in cancer biology, yet its role in modulating anti-tumor immune response remains largely unexplored. Here, we identify the cleavage stimulation factor 2 (CSTF2), an APA-related gene, as a pivotal suppressor of anti-tumor immunity in pancreatic ductal adenocarcinoma (PDAC). CSTF2 promotes tumor development by inhibiting the infiltration and cytotoxic immune cell recruitment function of TCRαβCD4CD8NK1.1 innate αβ T (iαβT) cells. Mechanistically, CSTF2 diminishes CXCL10 expression by promoting PolyA polymerase alpha (PAPα) binding to the 3' untranslated regions of CXCL10 RNA, resulting in shortened PolyA tails and compromised RNA stability. Furthermore, we identify Forsythoside B, a selective inhibitor targeting the RNA recognition motif of CSTF2, can effectively activate anti-tumor immunity and overcome resistance to immune checkpoint blockade (ICB) therapy. Collectively, our findings unveil CSTF2 as a promising therapeutic target for sensitizing PDAC to ICB therapy. - Source: PubMed
Publication date: 2025/02/19
He XiaoweiLiu JiZhou YifanZhao SihanChen ZimingXu ZilanXue ChunlingZeng LingxingLiu ShuangLiu ShaoqiuBai RuihongWu ShaojiaZhuang LishaLi MeiZhao HongzheZhou QuanboLin DongxinZheng JianHuang XudongZhang Jialiang