Ask about this productRelated genes to: Psmc1 Blocking Peptide
- Gene:
- PSMC1 NIH gene
- Name:
- proteasome 26S subunit, ATPase 1
- Previous symbol:
- -
- Synonyms:
- S4, p56
- Chromosome:
- 14q32.11
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-27
- Date modifiied:
- 2015-08-12
Related products to: Psmc1 Blocking Peptide
Related articles to: Psmc1 Blocking Peptide
- While both high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) are known to benefit physical health, their comparative effects on cognitive function in Alzheimer's disease (AD) remain unclear. Here, using equal number 3.5 months old male (28 ± 2 g) and female (24.0 ± 1.1 g) 5 × FAD transgenic mice, we demonstrate that HIIT and MICT improve AD pathology and cognitive performance, as evidenced by reduced amyloid-β deposition and enhanced hippocampal synaptic plasticity. Both exercise modalities significantly elevated lactate levels in the blood and hippocampus of AD mice. The functional consequences of this increase, however, were not linear. We found that while low lactate (2 mM) universally enhanced excitatory postsynaptic potentials in the hippocampus, high lactate (7 mM) was inhibitory, with no significant effects observed at intermediate concentrations (4 and 6 mM), an effect independent of genotype. To mechanistically link lactate dynamics to functional benefits, we performed lactylation-based proteomics. This revealed that HIIT and MICT differentially modulated protein lactylation-both reduced lactylation of glutamatergic synaptic proteins, but HIIT specifically upregulated lactylation of necroptosis-related proteins (CypA/Cyp40), while MICT downregulated proteasome-related proteins (Psmc1/Psmα7). Our findings suggest that exercise-induced lactate dynamically regulates brain function via protein lactylation, offering a novel therapeutic avenue for AD. - Source: PubMed
Publication date: 2026/04/16
Chen LimingYe YuweiGuo XiaoqinLi RuiXia SijiaChen FengWang SinuoCao YajunHu ZhongyiQiu YuxiWang LiumuChi DongruiYang MinguangTao JingLiu Weilin - Serrated adenocarcinoma (SAC) represents a molecularly heterogeneous subtype of colorectal carcinoma (CRC) linked to the serrated pathway. It is aimed to clarify the molecular mechanisms underlying SAC development. Digital slides from The Cancer Genome Atlas (TCGA) colorectal adenocarcinoma Firehose Legacy dataset (632 cases) were reviewed, and cases were classified as SAC, partial-SAC, or classical CRC. Genomic alterations, mRNA expression, and DNA hypermethylation were compared using cBioPortal. Enrichment analyses were performed via WebGestalt, and protein-protein interaction (PPI) networks with hub genes were identified using STRING and Cytoscape. Statistical significance was defined as < 0.05 and < 0.05. The results revealed that the groups showed significant differences in the expression of 327 genomic alterations, 20 mRNAs, and 21 methylated genes ( < 0.0001, < 0.0001). Hub genes were , , , , , , , , , and . The pathways associated with differently expressed genes were the following: cell structure and morphology (phagocytic vesicle, microvillus, endocytosis, and immobile cilium), protein kinase activity (particularly MAPK), and immunological mechanisms. The hub genes act as molecular bridges connecting the observed genomic and epigenetic variations, particularly driving chromatin-related regulation and MAPK signaling pathways. In particular, , , , , and genes offer promising molecular targets for future therapeutic approaches in SACs. - Source: PubMed
Publication date: 2026/02/04
Sagnak Yilmaz ZeynepDemir Kececi SibelSagol OzgulSarioglu Sulen - The mechanisms underlying carfilzomib (CFZ)-induced cardiotoxicity remain incompletely elucidated. In this study, we used human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) to characterize the transcriptional impact of CFZ and to evaluate whether atorvastatin could prevent these deleterious transcriptional changes. hiPSC-CMs were treated with 1 µM CFZ, CFZ + atorvastatin, atorvastatin, or vehicle control, followed by RNA sequencing, differential expression analyses, and pathway analyses. Transcriptomic profiling revealed a marked upregulation of genes in multiple proteasome subunits, including ATPase components (, , , ) and non-ATPase regulatory subunits (, , ), suggesting a strong compensatory activation of proteostasis and protein quality-control pathways in response to CFZ exposure. In addition, several of the most significantly altered genes were those implicated in cardiomyopathy and heart failure, such as and , and many heat-shock proteins, indicating the activation of cardiac stress-response pathways relevant to CFZ-associated cardiotoxicity. Atorvastatin co-treatment partially reversed a subset of CFZ-induced transcriptional changes, particularly within cholesterol biosynthesis and lipid-regulatory pathways (e.g., and ) but did not restore the CFZ-mediated downregulation of sarcomeric genes. Together, these findings define a multifactorial signature of deleterious CFZ-induced transcriptional changes and suggest that atorvastatin may provide partial metabolic, but not structural, cardio protection. - Source: PubMed
Publication date: 2026/01/29
Tantawy MarwaWang DanxinGbadamosi MohammedYu FahongZhang YanpingAlomar Mohammed EShain Kenneth HBaz Rachid CBruno Katelyn AGong Yan - In the context of increasing consumer demand for high-quality meat, this study aimed to evaluate the effects of 4% fermented goji berry residue supplementation on meat quality and flavor characteristics in finishing Tan sheep. - Source: PubMed
Publication date: 2026/01/01
Zhan CongLi MengLi DanLi PanZhang QimingWu MirouZhong GuoweiXu Xiaochun - Transcriptome-wide association studies (TWASs) are powerful for identifying gene-trait associations by integrating gene expression and genome-wide association data, but findings may be impacted by the choice of gene expression reference. We performed TWAS of cardiovascular outcomes using multi-tissue and ancestry-matched gene expression references. We used data from the Chronic Renal Insufficiency Cohort Study for participants of African (AFR, n = 1,512) and European (EUR, n = 2,067) ancestry and three outcomes: all-cause stroke, coronary heart disease, and heart failure. We performed TWASs using EUR and AFR predicted gene expression reference panels and multi-tissue TWAS by integrating gene expression from 10 GTEx selected tissues. TWAS identified KDELR2 associated with heart failure in AFR participants using matched AFR reference panel (p = 4.7 × 10), although findings were near significant using the EUR mismatched reference panel (p = 5.6 × 10). PSMC1 was associated with coronary heart disease in TWAS of CRIC EUR using AFR reference panel, and this gene was not present in the EUR-trained gene expression model. Multi-tissue TWASs identified KHDRBS2 significantly associated with all-cause stroke in CRIC AFR participants (p = 4.0 × 10). Variants near KDELR2 have been associated with coronary artery disease, which is a main cause of heart failure, while KHDRBS2 has been associated with cardiovascular risk factors in genome-wide association studies. Our findings highlight differences in gene discovery for TWAS of cardiovascular disease applied to high-risk participants based on participant ancestry and gene expression reference panels, and gains to identify genes compared with traditional genome-wide association approaches. - Source: PubMed
Publication date: 2026/01/08
Lin Bridget MWen JiaHorimoto Andrea R V RZhou LingboHuang ShuaiDobre MirelaGo Alan SLi YunFranceschini Nora