CUGBP2 Blocking Peptide
- Known as:
- CUGBP2 Blocking Peptide
- Catalog number:
- 33r-9274
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- CUGBP2 Blocking Peptide
Related genes to: CUGBP2 Blocking Peptide
- Gene:
- CELF2 NIH gene
- Name:
- CUGBP Elav-like family member 2
- Previous symbol:
- CUGBP2
- Synonyms:
- Etr-3, NAPOR-2, BRUNOL3
- Chromosome:
- 10p14
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-02
- Date modifiied:
- 2017-01-20
Related products to: CUGBP2 Blocking Peptide
Related articles to: CUGBP2 Blocking Peptide
- The CUG-BP and Elav-like (CELF) family of RNA-binding proteins are key regulators of post-transcriptional gene expression, coordinating alternative splicing, mRNA stability, and translation. Although individual members, particularly CELF1 and CELF2, have been extensively characterized, a systematic, paralog-resolved integration of structural determinants, regulatory mechanisms, and disease relevance across all six CELF proteins remains limited. Here, we establish an integrative framework linking conserved RNA recognition motifs and divergent linker domains to context-dependent regulatory outputs, mediated by phosphorylation, nucleocytoplasmic dynamics, and RNA network interactions. We further highlight the neuron-enriched CELF3-CELF6 subfamily, consolidating emerging evidence that extends their roles beyond neural splicing into cancer-associated regulatory programs. Notably, we delineate functional divergence within the family, with CELF1 frequently acting as an oncogenic driver in contrast to the tumor-suppressive role of CELF2, while positioning less-characterized paralogs within this regulatory spectrum. Together, this work defines a unified structure-function-disease axis for CELF proteins and provides a conceptual framework for their prognostic and therapeutic exploitation. However, current CELF-targeted strategies remain largely preclinical and face key translational challenges, including paralog selectivity, off-target effects, and delivery barriers such as limited blood-brain barrier penetration. Accordingly, the most immediate clinical utility of CELF biology is likely to lie in biomarker development and patient stratification, rather than direct therapeutic intervention. - Source: PubMed
Publication date: 2026/05/09
Ma YukangMa ChiYang AoboChen YimingGao JiajunWang QunshuWei ZhixiGao MeilingXing XianglingLiu Wancheng - Allergic Rhinitis (AR) represents a widespread chronic inflammatory condition, with especially prevalence observed in children and urban populations. - Source: PubMed
Publication date: 2026/05/01
Wang MinZhuang YueyanZhang XiaohuiLi Lijuan - Observational studies suggest that plasma proteins play a crucial role in the development and progression of obstructive sleep apnea (OSA); however, the causal relationship between plasma proteins and OSA remains controversial. This study conducted a comprehensive evaluation of the causal relationships between 4,907 plasma proteins and OSA by employing bidirectional Mendelian randomization (MR) analysis, network pharmacology strategies, and single-cell sequencing techniques. The plasma protein data used in this study were derived from Ferkingstad et al.'s research (n = 35,559), and OSA-related data were obtained from genome-wide association studies (GWAS) conducted on European populations through Finland's biobank (FinnGen). This study utilized multi-omics integration strategies, including enrichment analysis, protein-protein interaction (PPI) network construction, drug target prediction, molecular docking simulation, and single-cell transcriptome sequencing, to investigate the biological mechanisms of identified targets and evaluate their potential applications in drug development. MR analysis identified 62 plasma proteins significantly associated with OSA risk, including NTN4 (p = 0.003, OR = 1.076, CI [1.024, 1.129]) and TFF2 (p = 0.004, OR = 1.098, CI [1.029, 1.174]). Further reverse Mendelian analysis revealed causal relationships between OSA and the CELF2, NTRK3, ANTXR2, and MYOM2 genes. PPI network analysis identified 10 core genes, including IL1β, TGFβ1, EGF, SHH, and SMAD2, which participate in critical pathological processes in OSA, such as oxidative stress, inflammatory responses, and immune regulation. Through drug prediction analysis, this study identified compounds with potential therapeutic effectiveness, including 3,4-DHB, BIM IX, and 1,9-Pyrazoloanthrone, and molecular docking studies further confirmed their high binding affinity to target proteins. Single-cell sequencing revealed high expression levels of key genes in T cells and dendritic cells, thereby confirming the critical role of these cells in the pathological progression of OSA. A total of 62 candidate therapeutic targets for OSA were identified in this study, with 10 of these targets deemed important candidates for clinical trials. These findings not only enrich the understanding of the molecular pathological mechanisms underlying OSA but also offer new perspectives for developing targeted therapeutic strategies to treat the condition. By facilitating the establishment of more precise and personalized disease management approaches, these results are expected to advance the development of therapeutic drugs for OSA and substantially reduce the economic costs associated with new drug development. - Source: PubMed
Publication date: 2026/02/19
Duan LingzhiWang YanJing HaiqingWang YanqiongNing ShuyeYang ZhengfuZhang Aihua - The sensitivity of nasopharyngeal carcinoma (NPC) cells to radiation is the primary factor influencing the therapeutic effect of radiotherapy for patients with NPC. This study aimed to investigate the mechanism underlying the potential regulatory effect of long non-coding RNA (lncRNA) on the radiosensitivity of NPC cells. - Source: PubMed
Publication date: 2026/01/27
Jiang JunWang DongKang MeiQian YaqinZha TianqiShao Chang-Sheng - Alternative splicing is a fundamental mechanism underlying protein diversity. The microtubule-associated protein tau (MAPT) undergoes age-associated alternative splicing of exon 10 to generate 3R and 4R isoforms, and disruption of the 4R:3R ratio is a central feature of tauopathies. However, the molecular mechanisms regulating tau exon 10 splicing remain incompletely understood. Here, we identify the RNA-binding protein CELF2 as a key promoter of tau exon 10 inclusion. Loss of CELF2 in the mouse brain reduces exon 10 inclusion, resulting in a decreased 4R:3R ratio. We show that an intrinsically disordered region (IDR) within the CELF2 hinge domain drives protein condensation and is essential for its splicing activity. This IDR can be functionally substituted by those of FUS or TAF15. CRISPR-based imaging reveals colocalization of CELF2 condensates with tau RNA. Proteomic analyses identify NOVA2 and SFPQ as CELF2 interactors, which co-condense with CELF2 to cooperatively regulate tau exon 10 splicing. A conserved negatively charged residue (D388) within the IDR is critical for condensate formation, protein interactions, and splicing function. Finally, CELF2 condensation capacity correlates with 4R tau expression in vivo and influences locomotor and cognitive performance. These findings uncover a condensate-based mechanism for tau splicing regulation with implications for tau-related neurodegeneration. - Source: PubMed
Publication date: 2026/01/19
Chen Lizhen