Ask about this productRelated genes to: PPP2R1B Blocking Peptide
- Gene:
- PPP2R1B NIH gene
- Name:
- protein phosphatase 2 scaffold subunit Abeta
- Previous symbol:
- -
- Synonyms:
- PR65B, PP2A-Abeta
- Chromosome:
- 11q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-01-25
- Date modifiied:
- 2016-05-13
Related products to: PPP2R1B Blocking Peptide
Related articles to: PPP2R1B Blocking Peptide
- BackgroundPhysical exercise shows neuroprotective and anti-inflammatory effects in Alzheimer's disease (AD) models, but whether it modulates neuroinflammation through regulation of peripheral T-cell activity is still unresolved.ObjectiveThe present study aimed to explore the mechanisms by which aerobic exercise regulates peripheral T cell-mediated immune responses and their potential contribution to neuroinflammation in AD.MethodsMale wild-type mice and APP/PS1 transgenic mice were divided into four groups: wild-type sedentary mice (WT-SE) group, wild-type exercise group (WT-EX), APP/PS1 transgenic AD sedentary mice (AD-SE) group, and APP/PS1 transgenic AD exercise mice (AD-EX) group. The sedentary groups received no exercise training, while the exercise groups underwent a 3-month treadmill aerobic exercise intervention. At the end of the intervention, T lymphocytes were isolated from spleens. Label-free proteomics combined with LC-MS/MS was used to identify differentially expressed proteins (DEPs) and perform functional and pathway enrichment analyses. Differentially expressed protein-coding genes were validated at the mRNA level using RT-qPCR.ResultsA total of 3399 proteins were quantified across the four groups. Applying a threshold of |log fold change| > 0.67 and < 0.05, 913 DEPs were identified. These DEPs were significantly enriched in biological processes including immune system processes, protein-containing complexes, and structural molecule activity, as well as signaling pathways including AD, TGF-β, and apoptosis.ConclusionsOverall, HSP90AB1, HSP90AA1, BAG5, DNAJC8, CTSD, and ANXA1 may play a role in peripheral T-cell immune dysregulation in AD, with potential implications for central neuroinflammation. Furthermore, the beneficial effects of aerobic exercise on AD-related peripheral immune alterations, and its potential modulation of neuroinflammation, may be associated with expression changes in DEPs including Ppp2r1b, Pde2a, Casp8, Apaf-1, Dnajb11, and Dnajc13. - Source: PubMed
Publication date: 2026/03/30
Ye XingHu KaiLiu Renyi - The retina is highly sensitive to oxygen and blood supply, and hypoxia plays a key role in retinal diseases such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). Müller glial cells, which are essential for retinal homeostasis, respond to injury and hypoxia with reactive gliosis, characterized by the upregulation of the glial fibrillary acidic protein (GFAP) and vimentin, cellular hypertrophy, and extracellular matrix changes, which can impair retinal function and repair. The retinal pigment epithelium (RPE) supports photoreceptors, forms part of the blood-retinal barrier, and protects against oxidative stress; its dysfunction contributes to retinal degenerative diseases such as AMD, retinitis pigmentosa (RP), and Stargardt disease (SD). Extracellular vesicles (EVs) play a crucial role in intercellular communication, protein homeostasis, and immune modulation, and have emerged as promising diagnostic and therapeutic tools. Understanding the role of extracellular vesicles' (EVs') signaling machinery of glial cells and the retinal pigment epithelium (RPE) is critical for developing effective treatments for retinal degeneration. In this study, we investigated the bidirectional EV-mediated crosstalk between RPE and Müller cells under hypoxic conditions and its impact on cellular metabolism and retinal cell integrity. Our findings demonstrate that RPE-derived extracellular vesicles (RPE EVs) induce time-dependent metabolic reprogramming in Müller cells. Short-term exposure (24 h) promotes pathways supporting neurotransmitter cycling, calcium and mineral absorption, and glutamate metabolism, while prolonged exposure (72 h) shifts Müller cell metabolism toward enhanced mitochondrial function and ATP production. Conversely, Müller cell-derived EVs under hypoxia influenced RPE metabolic pathways, enhancing fatty acid metabolism, intracellular vesicular trafficking, and the biosynthesis of mitochondrial co-factors such as ubiquinone. Proteomic analysis revealed significant modulation of key regulatory proteins. In Müller cells, hypoxic RPE-EV exposure led to reduced expression of Dyskerin Pseudouridine Synthase 1 (DKc1), Eukaryotic Translation Termination Factor 1 (ETF1), and Protein Ser/Thr phosphatases (PPP2R1B), suggesting alterations in RNA processing, translational fidelity, and signaling. RPE cells exposed to hypoxic Müller cell EVs exhibited elevated Ribosome-binding protein 1 (RRBP1), RAC1/2, and Guanine Nucleotide-Binding Protein G(i) Subunit Alpha-1 (GNAI1), supporting enhanced endoplasmic reticulum (ER) function and cytoskeletal remodeling. Functional assays also revealed the compromised barrier integrity of the outer blood-retinal barrier (oBRB) under hypoxic co-culture conditions. These results underscore the adaptive but time-sensitive nature of retinal cell communication via EVs in response to hypoxia. Targeting this crosstalk may offer novel therapeutic strategies to preserve retinal structure and function in ischemic retinopathies. - Source: PubMed
Publication date: 2025/08/07
Mansour Alaa MGad Mohamed SHabib SamarElmasry Khaled - Protein phosphatase 2A (PP2A) is crucial for regulating cellular pathways, with its holoenzyme assembly affecting enzyme function and substrate selection. The PP2A holoenzyme comprises scaffold A-, regulatory B-, and catalytic C-subunits, each with various isoforms. Here, we examine structural and biochemical characteristics of the A-subunit isoforms (Aα and Aβ) and identify different biophysical properties that may promote distinct PP2A functions. Our molecular dynamics simulations and cryo-EM analyses define structural differences in the isoforms that reside primarily at the N-terminus of the A-subunit where it interfaces with regulatory B-subunits. Kinetic analyses show Aβ has a lower binding affinity in complexes with B56 subunits and exhibits unique aggregative properties as a monomeric protein. These findings suggest that the different physicochemical properties between A-subunit isoforms are key to PP2A holoenzyme assembly and function. We predict that the Aβ serves as a reservoir, ensuring that serine-threonine phosphatase activity is maintained during high regulatory demand. - Source: PubMed
Publication date: 2025/07/24
Day AlexanderHuang WeiLeonard DanielO'Connor Caitlin MNarla GouthamTaylor Derek J - Transcriptomic profiling has shown that exposure to PM, a common air pollutant, can modulate gene expression, which has been linked to negative health effects and diseases. However, there are few population-based cohort studies on the association between PM exposure and specific gene set expression. In this study, we used an unbiased transcriptomic profiling approach to examine gene expression in a mouse model exposed to PM and to identify PM-responsive genes. The gene expressions were further validated in both the human cell lines and a population-based cohort study. Two cohorts of healthy older adults (aged ≥ 65 years) were recruited from regions characterized by differing levels of PM. Logistic regression and decision tree algorithms were then utilized to construct predictive models for PM exposure based on these gene expression profiles. Our results indicated that the expression of five genes (, , , , and increased with PM exposure in both cell-based assay and population-based cohort studies. Furthermore, the predictive models demonstrated high accuracy in classifying high-and-low PM exposure, potentially supporting the integration of gene biomarkers into public health practices. - Source: PubMed
Publication date: 2025/06/30
Wei Yu-ChungCheng Wen-ChiLin PinpinZhang Zhi-YaoChen Chi-HsienWu Chih-DaGuo Yue LeonWang Hung-Jung - Hepatoblastoma is the most prevalent liver cancer affecting children, and its intricate causes are closely linked to genetic variations. This study interrogated the influence of the miR-34b/c rs4938723 T > C polymorphism in hepatoblastoma predisposition in a Han Chinese children study population, comprising 193 cases and 773 controls from East China. - Source: PubMed
Publication date: 2025/07/01
Zhang WenliZhu JinhongBian JunZhou ChunleiZhang ShouhuaHe ShaohuaLu HongtingWang YizhenHe Jing