Polyclonal Rabbit PIK3R5 Antibody
- Known as:
- Polyclonal Rabbit PIK3R5 Antibody
- Catalog number:
- abx003425
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Polyclonal Rabbit PIK3R5 Antibody
Related genes to: Polyclonal Rabbit PIK3R5 Antibody
- Gene:
- PIK3R5 NIH gene
- Name:
- phosphoinositide-3-kinase regulatory subunit 5
- Previous symbol:
- -
- Synonyms:
- P101-PI3K, p101
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-10-13
- Date modifiied:
- 2015-11-17
Related products to: Polyclonal Rabbit PIK3R5 Antibody
Related articles to: Polyclonal Rabbit PIK3R5 Antibody
- The rumen epithelium of Tibetan sheep plays a critical role in energy metabolism and immune defense; however, its post-transcriptional regulatory mechanisms under high-altitude hypoxia stress remain unclear. In this study, we employed integrated mRNA and miRNA transcriptome sequencing to analyze the adaptive strategies of the rumen epithelium in Tibetan sheep at different altitudes. A total of 2183 differentially expressed genes (DEGs) and 135 differentially expressed miRNAs (DEmiRNAs) were identified. Functional enrichment analysis revealed that DEGs and their target genes were significantly enriched in immune-related pathways such as the NF-κB signaling pathway and cytokine-cytokine receptor interaction, as well as metabolic pathways including oxidative phosphorylation and branched-chain amino acid degradation. Integrated network analysis highlighted key regulatory pairs, including targeting and , and regulating , suggesting coordinated modulation between mitochondrial homeostasis and immune responses. Specifically, the upregulation of immune genes (, ) and heat shock proteins at TS4500m indicates enhanced mucosal immunity and stress tolerance, while altered expression of metabolic genes reflects a shift in energy substrate utilization. These findings elucidate a complex mRNA-miRNA regulatory network that enables Tibetan sheep to maintain rumen epithelial integrity and energy balance under extreme high-altitude conditions, providing novel insights into the molecular basis of hypoxia adaptation in ruminants. - Source: PubMed
Publication date: 2026/05/28
Wang LeiHuang WeiSha YuzhuHe YanyuShao PengyangChen QianlingHe YapengFan JiangfengLiu XiuDu Wenhui - Inflammatory response-related signaling pathways are associated with Atherosclerosis (AS), yet the particular inflammation-related genes underpinning this process are still not fully characterized. - Source: PubMed
Publication date: 2026/05/20
Xu XuJiang MeilingHuang ZeyunZhu Guofu - Most genetic variants in the human genome reside in non-coding regions, where they can perturb regulatory element activity to influence gene expression, thereby contributing to various phenotypes and diseases. However, identifying functionally relevant non-coding genetic variation remains challenging. Here we integrate personal genomics, allele-specific gene regulation, and deep learning predictions to map the impact of non-coding variation in its native allelic and regulatory context. Leveraging whole-chromosome haplotypes and allele-specific analyses, we establish regulatory links within individual human genomes, enabling us to evaluate functional consequences of both common and rare variants. We identify and validate hundreds of cell-type-specific transcription factor binding events disrupted by genetic variants, revealing known and novel mechanisms that underlie allele-specific chromatin accessibility and gene expression. Using this framework, we discovered a rare variant that disrupted an OCT2 binding site within a distal enhancer, thereby modulating the expression of PIK3R5 gene. Our study establishes a generalisable strategy for interpreting non-coding regulatory variation, enabling systematic dissection of variant effects across diverse biological systems and offering a framework to investigate disease mechanisms. - Source: PubMed
Publication date: 2026/04/29
Magnitov Mikhail Dvan der Weide Robin HWitvliet Aster FHernández-Quiles MiguelMartinović MorenoTeunissen HansBraccioli LucaVermeulen Michielde Wit Elzo - Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by profound molecular heterogeneity and high relapse rates, posing significant clinical challenges. Programmed cell death (PCD), encompassing diverse regulated modalities such as apoptosis, necroptosis, and ferroptosis, plays a key role in leukemogenesis and therapeutic response; however, a comprehensive prognostic framework integrating multi-modal PCD pathways in AML remains elusive. In this study, we performed a systematic transcriptomic analysis of 1624 genes associated with 13 distinct PCD forms. A novel computational pipeline combining a variational autoencoder (VAE) for dimensionality reduction and a multilayer perceptron (MLP) for classification was employed to identify robust PCD-related biomarkers, interpreted via SHapley Additive exPlanations (SHAP) analysis. This approach identified 48 candidate genes with discriminative potential between AML and normal bone marrow. Unsupervised consensus clustering based on these genes delineated two molecular subtypes exhibiting divergent clinical outcomes and immune microenvironment profiles. The subtype demonstrated an immunosuppressive phenotype, characterized by enriched regulatory T cells, M2 macrophages, and elevated expression of inhibitory immune checkpoints, correlating with inferior survival. We developed an 8-gene prognostic signature (, , , , , , and ) that effectively categorized patients into high- and low-risk groups with notable survival differences, validated across independent cohorts. A prognostic nomogram combining the risk score, age, and cytogenetic risk enhanced the prediction accuracy for overall survival. Our study presents an integrative model that connects multi-modal PCD pathways to AML prognosis, offering a new molecular subtyping system and a clinically applicable risk assessment tool for improved prognostication and personalized treatment strategies. - Source: PubMed
Publication date: 2026/03/27
Zhang ChunlongNi HaisenZhao ZiyiZhao Ning - Spinal cord injury (SCI) refers to trauma to the spinal cord resulting in functional deficits. Dysregulation of the phosphoinositide 3-kinase/serine-threonine kinase (PI3K/AKT) pathway significantly contributes to the pathogenesis of SCI. This study evaluated the role of PI3K/AKT-associated biomarkers in SCI. Transcriptomic data from SCI samples deposited in the Gene Expression Omnibus (GEO) database were analyzed. An integrative approach combining differential expression profiling, machine learning, and experimental validation was employed to identify PI3K/AKT-related biomarkers. Combinatorial strategies-including functional enrichment analysis, immune microenvironment characterization, in silico drug prediction, and ligand-receptor docking-were used to elucidate potential biomarker-driven pathological mechanisms. Quantitative reverse transcription PCR (RT-qPCR) was performed to validate biomarker expression. Four biomarkers-FGF2, IL-6, PIK3R5, and TLR2-were successfully identified. Additionally, ELOVL6, IDI1, and SQLE were co-enriched in multiple pathways, including those associated with graft-versus-host disease (GVHD) in mice. TLR2 expression exhibited the strongest positive correlation with M2 macrophages (ρ = 0.74, P < 0.001) and the strongest negative correlation with neurons (ρ = -0.73, P < 0.001). Protein-ligand interaction analysis showed the highest binding scores of TLR2 with CHEMBL1836411, resveratrol hexanoic acid, and diprovocim-1. Molecular docking further confirmed a strong binding affinity between the TLR2 receptor and these compounds. RT-qPCR demonstrated significantly elevated transcript levels of Fgf2, Il6, Pik3r5, and Tlr2 in SCI samples (P < 0.01), corroborating the bioinformatic predictions. This study identifies FGF2, IL-6, PIK3R5, and TLR2 as key biomarkers in SCI, providing potential therapeutic targets for SCI treatment. - Source: PubMed
Publication date: 2026/04/20
Chen TaibangYu LichaoCai ZhijunChen Lingqiang