CD2BP2 (N Terminus)
- Known as:
- CD2BP2 (N Terminus)
- Catalog number:
- Y213374
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CD2BP2 ( Terminus)
Related genes to: CD2BP2 (N Terminus)
- Gene:
- CD2BP2 NIH gene
- Name:
- CD2 cytoplasmic tail binding protein 2
- Previous symbol:
- -
- Synonyms:
- LIN1, Snu40, PPP1R59, U5-52K
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-18
- Date modifiied:
- 2017-06-12
Related products to: CD2BP2 (N Terminus)
Related articles to: CD2BP2 (N Terminus)
- Pancreatic ductal adenocarcinoma (PDA) is an aggressive malignancy that lacks reliable biomarkers to guide treatment decisions. Effective prognostic tools are needed to improve its clinical management. We conducted a comprehensive proteomic analysis on 115 PDA patient samples with matched adjacent normal tissue. A 20-protein diagnostic panel was identified (LGALS1, ANXA2, LGALS3BP, CTSD, S100P, COL12A1, SFN, THBS2, CTHRC1, THBS1, SERPINB5, LAMC2, POSTN, CEACAM6, CTSE, PLEC, PKM, S100A11, TAGLN2, ALDOA). Consensus clustering analysis identified four prognostic proteomic subtypes. Subtypes with poorer prognoses exhibited upregulation of neutrophil degranulation, extracellular matrix remodeling, focal adhesion, Mesenchymal Epithelial Transition, collagen formation, and PI3K-Akt-mTOR-related pathways, indicating a predominance of basal-like and activated stromal features. In tumors with homologous recombination deficiency or Catalogue of Somatic Mutations in Cancer Signature-3, several immune-related proteins were enriched. An 18-protein (PURB, SDCBP2, CD2BP2, GALM, SERPINA3, OAS3, FAN1, ZPR1, KRT2, NUDT2, SMNDC1, SERPINA4, CUTA, WDR36, POSTN, CLEC11A, PEX14, and PI4KA) risk score was developed and validated using multicox regression analyses with LASSO regularization. The risk score demonstrated independent prognostic significance for overall survival and recurrence, and was validated in an independent proteomic dataset generated using a different proteomic technology. This study thus introduces four novel prognostic PDA subtypes, and an 18-protein risk score validated in an independent dataset, which shows promise for improving survival prediction and could serve as a valuable tool for personalized treatment guidance. - Source: PubMed
Aref Adel TGrealey JasonPathan MohashinNoor ZainabAnees AsimAzad A K MSmith Daniela LeeHumphries Erin MBucio-Noble DanielKoh Jennifer M SSykes Erin KWilliams Steven GLyons Ruth JLucas NatashaXavier DylanSahni SumitMittal AnubhavSamra Jaswinder SPearson John VWaddell NicolaKondrashova OlgaChou AngelaSioson LorettaSheen Amy Hains Peter GRobinson Phillip JZhong QingReddel Roger RGill Anthony J - Long noncoding RNAs (lncRNAs) play critical roles in the initiation and progression of breast cancer. However, the specific mechanisms and biological functions of lncRNAs in breast cancer remain incompletely understood. Bioinformatics analysis identifies a novel lncRNA, CD2BP2-DT, that is overexpressed in breast cancer and correlates with adverse clinicopathological features and poor overall survival. Both in vivo and in vitro experiments demonstrate that CD2BP2-DT promotes proliferation of breast cancer cells. Mechanistically, NAT10 mediates the N4-acetylcytidine (ac4C) modification of CD2BP2-DT, enhancing its RNA stability and expression. More importantly, CD2BP2-DT enhances the stability of CDK1 mRNA by mediating YBX1 phase separation, thereby promoting the proliferation of breast cancer cells. In conclusion, the lncRNA CD2BP2-DT is identified as a crucial driver of breast cancer cell proliferation through the YBX1/CDK1 axis, highlighting its potential as a promising biomarker and therapeutic target for breast cancer. - Source: PubMed
Publication date: 2025/02/20
Wang HongyuZhao BozhiZhang JiayuHu QunyuZhou LinlinZhang YinghuiCai YixinQu YuansongJiang TaoZhang Dongwei - DNA replication is a crucial biological process that ensures the accurate transmission of genetic information, underpinning the growth, development, and reproduction of organisms. Abnormalities in DNA replication are a primary source of genomic instability and tumorigenesis. During DNA replication, the assembly of the pre-RC at the G1-G1/S transition is a crucial licensing step that ensures the successful initiation of replication. Although many pre-replication complex (pre-RC) proteins have been identified, technical limitations hinder the detection of transiently interacting proteins. The APEX system employs peroxidase-mediated rapid labeling with high catalytic efficiency, enabling protein labeling within one minute and detection of transient protein interactions. MCM2 is a key component of the eukaryotic replication initiation complex, which is essential for DNA replication. In this study, we fused MCM2 with enhanced APEX2 to perform in situ biotinylation. By combining this approach with mass spectrometry, we identified proteins proximal to the replication initiation complex in synchronized mouse ESCs and NIH/3T3. Through a comparison of the results from both cell types, we identified some candidate proteins. Interactions between MCM2 and the candidate proteins CD2BP2, VRK1, and GTSE1 were confirmed by bimolecular fluorescence complementation. This research establishes a basis for further study of the component proteins of the conserved DNA replication initiation complex and the transient regulatory network involving its proximal proteins. - Source: PubMed
Publication date: 2025/01/25
Yao SitongYue ZhenYe ShaotangLiang XiaohuanLi YuguGan HaiyunZhou Jiaqi - Cadmium (Cd) is a widely available metal that has been found to have a role in causing nonalcoholic fatty liver disease (NAFLD). However, the detailed toxicological targets and mechanisms by which Cd causes NAFLD are unknown. Therefore, the present work aims to reveal the main targets of action, cellular processes, and molecular pathways by which cadmium causes NAFLD. As shown in the bioinformatics analysis, there were 74 main targets of action for cadmium-induced NAFLD, hemopoietic cell kinase (HCK), EPH receptor A2 (EPHA2), MYC proto-oncogene (MYC), lysyl oxidase (LOX), dipeptidyl peptidase 7 (DPP7), nuclear factor erythroid 2-related factor 2 (NFE2L2), dual specificity phosphatase 6 (DUSP6), CD2 cytoplasmic tail binding protein 2 (CD2BP2), notch receptor 3 (NOTCH3), and phospholipase A2 group IVA (PLA2G4A) were screened as core genes. Testing these core genes in other databases, three differentially expressed genes, HCK, MYC, and DUSP6 were verified and used as targets for drug prediction in DsigDB; decitabine and retinoic acid were screened as potential therapeutic drugs for NAFLD based on the p-value and the combined score. The results of molecular docking showed that the predicted drugs can bind well to the core targets. In conclusion, cadmium is associated with NAFLD; the identified cadmium-toxicity targets, HCK, MYC, and DUSP6, may serve as biomarkers for the diagnosis of NAFLD and predicted drugs, decitabine and retinoic acid may have a potential role in the treatment of NAFLD. - Source: PubMed
Publication date: 2025/01/13
Zhang LeWang RuiXue QianWang YongjieXu JiayunzhuWang ChaofanFang XinGao ShidiZhang HaiyingGuo Li - The question whether interference with the ubiquitous splicing machinery can lead to cell-type specific perturbation of cellular function is addressed here by T cell specific ablation of the general U5 snRNP assembly factor CD2BP2/U5-52K. This protein defines the family of nuclear GYF domain containing proteins that are ubiquitously expressed in eukaryotes with essential functions ascribed to early embryogenesis and organ function. Abrogating CD2BP2/U5-52K in T cells, allows us to delineate the consequences of splicing machinery interferences for T cell development and function. Increased T cell lymphopenia and T cell death are observed upon depletion of CD2BP2/U5-52K. A substantial increase in exon skipping coincides with the observed defect in the proliferation/differentiation balance in the absence of CD2BP2/U5-52K. Prominently, skipping of exon 7 in Mdm4 is observed, coinciding with upregulation of pro-apoptotic gene expression profiles upon CD2BP2/U5-52K depletion. Furthermore, we observe enhanced sensitivity of naïve T cells compared to memory T cells to changes in CD2BP2/U5-52K levels, indicating that depletion of this general splicing factor leads to modulation of T cell homeostasis. Given the recent structural characterization of the U5 snRNP and the crosslinking mass spectrometry data given here, design of inhibitors of the U5 snRNP conceivably offers new ways to manipulate T cell function in settings of disease. - Source: PubMed
Publication date: 2024/09/06
Bertazzon MiriamHurtado-Pico AlmudenaPlaza-Sirvent CarlosSchuster MarcPreußner MarcoKuropka BennoLiu FanKirsten Andor Zenon AmandusSchmitt Xiao JakobKönig BenjaminÁlvaro-Benito MiguelAbualrous Esam TAlbert Gesa IKliche StefanieHeyd FlorianSchmitz IngoFreund Christian