Ask about this productRelated genes to: ELAVL2 Blocking Peptide
- Gene:
- ELAVL2 NIH gene
- Name:
- ELAV like RNA binding protein 2
- Previous symbol:
- -
- Synonyms:
- HuB, HEL-N1
- Chromosome:
- 9p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2016-10-05
Related products to: ELAVL2 Blocking Peptide
Related articles to: ELAVL2 Blocking Peptide
- - Source: PubMed
Publication date: 2026/04/20
Feng WeiZhu Yu-FengLi Kai-YuanXu Xiao-ShuangZhang Bo-YuZhou Jian - Sheep are an economically important livestock species, and reproductive performance is a key trait affecting productivity. The Dorper × Hu hybrid sheep (DHS), widely bred in China, provides a valuable model for studying the genetic basis of prolificacy. This study aimed to investigate the genomic architecture and identify candidate genes associated with high litter size in DHS using whole-genome selective sweep analysis and genome-wide association study (GWAS). A total of 31 DHS individuals with complete reproductive records were sequenced and compared with publicly available genomic data from 20 Hu sheep (HUS) and 10 Dorper sheep (DPS). Population genetic structure and diversity were assessed using phylogenetic trees, principal component analysis (PCA), and ADMIXTURE analysis. To identify key genomic regions associated with litter size, we performed selective sweep analysis between the polytocous and monotocous subpopulations of DHS using multiple methods within a 50 kb sliding window framework, including FST, θπ ratio, XP-CLR, and XP-EHH; we also conducted GWAS. DHS exhibited a distinct genetic structure with admixed ancestry and elevated genetic diversity. Genetic diversity analysis showed that DHS retained moderate levels of heterozygosity and polymorphism, comparable to or exceeding those of its parental breeds. Comparative analysis between polytocous and monotocous DHS identified reproduction-associated genes, including , , , and , enriched in pathways such as ovarian steroidogenesis, insulin secretion, and circadian entrainment. Furthermore, genome-wide association study (GWAS) identified 140 significant loci ( < 10) associated with reproductive traits. From these, 10 candidate SNPs were selected for validation through single-marker association analysis in 200 DHS individuals, among which two loci-g.88680390 C>A (/) and g.18197516 T>C ()-showed significant correlations with litter size. These findings enhance our understanding of the genetic basis of prolificacy in DHS and provide valuable molecular markers for genomic selection in sheep-breeding programs. - Source: PubMed
Publication date: 2025/12/04
Qiao LiyingMa KeYao QuanhongZhang SiyingPang ZhixuWang WannianCai KeLiu Wenzhong - Gliomas are complex and among the most lethal central nervous system (CNS) disorders. While they are notoriously heterogeneous, evidences suggest critical involvement of intricate interactions between RNA-binding proteins (RBPs) and their diverse partners, in the pathogeneses of gliomas. In this study, we used RNA sequencing data from the Cancer Genome Atlas (TCGA) to identify differentially expressed genes (DEGs). After selection of differentially expressed RBPs from these DEGs, systematic investigation of their transcriptomic changes during glioma progression was undertaken. Extensive in silico assessments allowed the creation of their interactome and pathway, identifying potential biological effects of these differentially expressed RBPs. Construction of regulatory networks of these differentially expressed RBPs and their topological analysis discovered key RBPs such as PABPC1, EIF4A2, RPS3, EEF1A1, RPS6, ELAVL2, CPEB1, and CELF5, which are largely involved in alternative splicing and ribosomal biogenesis. Moreover, we also identified differentially expressed RBPs such as YBX1, ELAVL2, and IGF2BP1, which may be involved in the formation of stress granules in gliomas. We also identified highly mutated RBPs, such as RPSA, RPL5, CPEB4, and SMAD7, in gliomas. Further, RBPs like RPS8, RPL5, RPS3A, EEF1A1, and EIF4E1B were found to be strongly correlated with patients' overall survival. Taken together, our analyses identified several candidate RBPs which might serve as potential targets for oncological measures against gliomas. - Source: PubMed
Publication date: 2025/12/08
Haque ShafiulMathkor Darin MansorBabegi Ashjan SaeedAhmad FarazArumugam Mohanapriya - This research aims to investigate the remote regulatory role of plasma exosomal miR-375-3p in diabetic periodontitis and to design a local drug-loading material to retard periodontal tissue destruction. - Source: PubMed
Publication date: 2025/11/26
Xue HanxiaoZhang HongmingYuan YunJin XiayueHuang Hui - Neurodegeneration is increasingly recognized not as a linear trajectory of protein accumulation, but as a multidimensional collapse of biological organization-spanning intracellular signaling, transcriptional identity, proteostatic integrity, organelle communication, and network-level computation. This review intends to synthesize emerging frameworks that reposition neurodegenerative diseases (ND) as progressive breakdowns of interpretive cellular logic, rather than mere terminal consequences of protein aggregation or synaptic attrition. The discussion aims to provide a detailed mapping of how critical signaling pathways-including PI3K-AKT-mTOR, MAPK, Wnt/β-catenin, and integrated stress response cascades-undergo spatial and temporal disintegration. Special attention is directed toward the roles of RNA-binding proteins (e.g., TDP-43, FUS, ELAVL2), m6A epitranscriptomic modifiers (METTL3, YTHDF1, IGF2BP1), and non-canonical post-translational modifications (SUMOylation, crotonylation) in disrupting translation fidelity, proteostasis, and subcellular targeting. At the organelle level, the review seeks to highlight how the failure of ribosome-associated quality control (RQC), autophagosome-lysosome fusion machinery (STX17, SNAP29), and mitochondrial import/export systems (TIM/TOM complexes) generates cumulative stress and impairs neuronal triage. These dysfunctions are compounded by mitochondrial protease overload (LONP1, CLPP), UPR maladaptation, and phase-transitioned stress granules that sequester nucleocytoplasmic transport proteins and ribosomal subunits, especially in ALS and FTD contexts. Synaptic disassembly is treated not only as a downstream event, but as an early tipping point, driven by impaired PSD scaffolding, aberrant endosomal recycling (Rab5, Rab11), complement-mediated pruning (C1q/C3-CR3 axis), and excitatory-inhibitory imbalance linked to parvalbumin interneuron decay. Using insights from single-cell and spatial transcriptomics, the review illustrates how regional vulnerability to proteostatic and metabolic stress converges with signaling noise to produce entropic attractor collapse within core networks such as the DMN, SN, and FPCN. By framing neurodegeneration as an active loss of cellular and network "meaning-making"-a collapse of coordinated signal interpretation, triage prioritization, and adaptive response-the review aims to support a more integrative conceptual model. In this context, therapeutic direction may shift from damage containment toward restoring high-dimensional neuronal agency, via strategies that include the following elements: reprogrammable proteome-targeting agents (e.g., PROTACs), engineered autophagy adaptors, CRISPR-based BDNF enhancers, mitochondrial gatekeeping stabilizers, and glial-exosome neuroengineering. This synthesis intends to offer a translational scaffold for viewing neurodegeneration as not only a disorder of accumulation but as a systems-level failure of cellular reasoning-a perspective that may inform future efforts in resilience-based intervention and precision neurorestoration. - Source: PubMed
Publication date: 2025/08/20
Voicu VictorToader CorneliuȘerban MateiCovache-Busuioc Răzvan-AdrianCiurea Alexandru Vlad