BRUNOL6 Blocking Peptide
- Known as:
- BRUNOL6 Blocking Peptide
- Catalog number:
- 33r-7452
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- BRUNOL6 Blocking Peptide
Related genes to: BRUNOL6 Blocking Peptide
- Gene:
- CELF6 NIH gene
- Name:
- CUGBP Elav-like family member 6
- Previous symbol:
- BRUNOL6
- Synonyms:
- -
- Chromosome:
- 15q23
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-28
- Date modifiied:
- 2017-01-20
Related products to: BRUNOL6 Blocking Peptide
Related articles to: BRUNOL6 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 - The ubiquitin-proteasome system plays a crucial role in neuroblastoma progression, yet the regulation of key degradation targets remains incompletely understood. By integrating transcriptomic and proteomic data, we identified nine candidate proteins, including CELF6, whose degradation is potentially mediated by ubiquitination. Survival analyses revealed that high CELF6 expression correlated with a favorable prognosis. Functional assays demonstrated that CELF6 suppresses neuroblastoma cell proliferation without affecting apoptosis. Mechanistically, the E3 ubiquitin ligase MDM2 directly interacts with CELF6, promoting its degradation via K48-linked ubiquitination. MDM2 overexpression accelerates CELF6 degradation, while its inhibition stabilizes CELF6 protein levels, an effect reversed by proteasome inhibitors. Furthermore, MDM2-driven neuroblastoma cell proliferation is dependent on CELF6 depletion. These findings establish MDM2 as a key regulator of CELF6 stability and highlight the MDM2-CELF6 axis as a potential therapeutic target in neuroblastoma. - Source: PubMed
Publication date: 2025/10/21
Zhao ZhenzhenZhang BaoZhang XuLi Changchun - Excitotoxicity and altered RNA regulation by RNA-binding proteins (RBPs) are two prevalent hallmarks in multiple neurodegenerative disorders. However, global effects of excitotoxicity on RNA secondary structure and RNA-protein interactions are largely unknown. To address this, we have performed protein interaction profile sequencing (PIP-seq) in NMDA-treated primary neurons. Our results show that NMDA treatment alters RNA structure, which correlates, in opposite directions depending on the intragenic region, with changes in mRNA abundance. Moreover, NMDA treatment increases and alters RNA-protein binding sites defining subsets of transcripts functionally associated with synaptic functions and neurodegenerative disorders. Finally, we identify two RNA motifs enriched in protein binding after NMDA treatment, and several RBPs binding to them , including CELF6 and YBX3, which show NMDA-dependent changes in their protein levels. Overall, we provide extensive datasets that can be leveraged to bridge the mechanistic gap between two hallmarks of neurodegeneration: excitotoxicity and RNA regulation by RBPs. - Source: PubMed
Publication date: 2025/05/06
Alvarez-Periel ElenaKramer Marianne CAkay-Espinoza CaglaJackson Daniel PTasca Julia AGarcia Benjamin AGregory Brian DJordan-Sciutto Kelly L - Emerging evidence indicates the essential role of cancer stem cells (CSCs) in the development and progression of various cancers, including colorectal cancer (CRC). CELF6, a member of the cytosine-uridine-guanine-binding protein (CUG-BP), Elav-like family (CELF), has been reported to be downregulated in CRC tissues. This study aims to elucidate the role and underlying mechanisms of CELF6 in CRC progression. - Source: PubMed
Fu ZhimingWang XiangChen ZhijuWang BaochunHuang WeiweiLiu Xin - Rheumatoid arthritis (RA) is one of the most common forms of arthritis. Extracorporeal shockwave therapy (ESWT) has been identified as a viable alternative therapeutic approach in light of the present protracted clinical course of pharmacological treatment, and changes in levels of marker proteins in the blood samples of RA patients can be utilized to assess treatment outcomes. - Source: PubMed
Publication date: 2024/08/21
Zhang MeiMa ZhongyuanSuguro RinkikoZhu MenglinChen Esther XinyiDong XinChen MeixiuCheng LinlingSu BolunZhu Yizhun