Ask about this productRelated genes to: PSMA3 antibody
- Gene:
- PSMA3 NIH gene
- Name:
- proteasome subunit alpha 3
- Previous symbol:
- -
- Synonyms:
- HC8
- Chromosome:
- 14q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-03
- Date modifiied:
- 2016-10-05
Related products to: PSMA3 antibody
Related articles to: PSMA3 antibody
- Parkinson's disease (PD) is characterized by progressive dopaminergic neuronal loss driven by mitochondrial dysfunction, oxidative stress, and proteostasis collapse, for which current therapies remain symptomatic. This study investigated the neuroprotective effects of Eucalyptus citriodora essential oil (ECEO) on 6-hydroxydopamine (6-OHDA)-induced toxicity in N2a neuroblastoma cells. GC-MS analysis showed that ECEO was dominated by oxygenated monoterpenes, mainly citronellal (60.7%), isopulegol (16%), and citronellol (5.7%). In silico analysis of these constituents showed favorable ADMET profiles, predicted blood-brain barrier permeability, and non-overlapping multitarget engagement across enzymes, GPCRs and nuclear receptors. At the cellular level, ECEO pretreatment significantly restored cell viability (86.7% of control), reduced LDH release, attenuated ROS and NO, and limited mitochondrial depolarization. Quantitative 2D-gel/MALDI-TOF/TOF proteomics identified 94 differentially abundant proteins, of which 20 showed validated PD-related associations (KEGG, Gene4PD, and DisGeNET databases). ECEO pretreatment modulated 12 of these proteins across mechanistically coherent pathways: (i) reversal of 6-OHDA-induced reprogramming of energy metabolism, by normalizing the glycolytic enzymes PKM and PGK1 and restoring the TCA enzyme SUCLG2; (ii) reinforcement of proteostasis through PSMB4 and PSMA3 induction, VCP upregulation and attenuation of ER stress marker HSPA5/BiP; (iii) preservation of mitochondrial and cytoskeletal integrity through PHB1 induction and bilateral TUBB5 restoration. Overall, our results suggest that ECEO exerts significant neuroprotective effects in a cellular PD model by coordinately modulating energy metabolism, proteostasis, antioxidant defense, and structural integrity. Given its predominance in oxygenated monoterpenes the neuroprotective activity of ECEO may result from the combined contribution of the major constituents supporting further investigation in age-related neurodegeneration. - Source: PubMed
Publication date: 2026/08/17
Abidi AmelShaba EnxhiVantaggiato LorenzaKouki OumaymaMasmoudi-Kouki OlfaBini LucaUlivieri CristinaLandi ClaudiaGhrairi Taoufik - Ubiquitin-independent degradation (UID) by the 20S proteasome represents a key pathway for mainly regulating intrinsically disordered proteins (IDPs), yet the degron motifs that govern this process remain poorly defined. In this chapter, we describe experimental strategies to identify UID degrons that mediate degradation by the catalytic 20S proteasome particle. Combining high-throughput 20S substrate assays in vitro with analyses of PSMA3 C-terminal binding proteins, we identified numerous IDPs, including p21, as potential substrates. Using bimolecular fluorescence complementation (BiFC) and split-luciferase reporter assays, we mapped the degron within p21. Systematic mutagenesis and peptide- and fragment-based assays delineated the minimal degron sequence, while CRISPR-Cas9-mediated editing of the endogenous protein confirmed its physiological role in proteasomal turnover. This integrated workflow-spanning degron mapping to functional validation-provides a generalizable framework for uncovering ubiquitin-independent degrons. - Source: PubMed
Shaul Yosef - Heart failure with preserved ejection fraction (HFpEF) is an increasingly common form of heart failure (HF) that is best understood as a systemic, multiorgan syndrome rather than a disease of left-ventricular filling alone. This review has three specific aims: first, to synthesize genetic and molecular pathways that are most relevant to non-ischemic HFpEF; second, to distinguish HFpEF-enriched mechanisms from evidence extrapolated from ischemic cardiomyopathy or HFrEF; and third, to consider translational implications for populations with high consanguinity, including the Kingdom of Saudi Arabia. The available evidence indicates that chronic inflammatory signaling involving CCL2, CCL5, TLR3, PTGS2/COX-2, IL-6/JAK/STAT3, NF-kB, and NLRP3 acts upstream of endothelial dysfunction, nitric-oxide/cGMP/PKG impairment, mitochondrial reactive oxygen species generation, and fibroblast activation. Extracellular-matrix regulators including ASPN, COL1A1, and MMP2 then amplify collagen deposition and myocardial stiffness, whereas mitochondrial genes and proteins such as ATP5C1 contribute to impaired oxidative phosphorylation, reduced ATP reserve, defective fatty-acid oxidation, and blunted mitophagy. Protein-quality-control pathways involving HSP90AA1, CCT2/CCT5, PSMA3, and stress-responsive STAT3 further link metabolic stress to proteotoxic injury. Epigenetic mechanisms, including DNA methylation and microRNAs such as miR-155, miR-1297, and miR-4649-3p, add a regulatory layer that may improve risk stratification but remains insufficiently validated for routine clinical use. In high-consanguinity settings, recessive cardiomyopathy variants can cluster in families and contribute to earlier NIHF presentations; however, population-level HFpEF-specific variant frequencies remain limited, and findings from HFrEF or dilated cardiomyopathy should be interpreted as candidate pathway evidence rather than definitive HFpEF markers. Translationally, SGLT2 inhibitors, mineralocorticoid-receptor antagonism, biomarker panels, and structured genetic evaluation provide the most clinically actionable bridge from molecular mechanisms to precision HFpEF care. - Source: PubMed
Publication date: 2026/07/11
Abou Al-Saud Sara - Recent advances in next-generation sequencing have revealed that long non-coding RNAs (lncRNAs) can encode functional micropeptides through small open reading frames (sORFs), altering the perception of the non-coding genome. In this study, we identified a 48-amino acid micropeptide named PAMP (proline-associated micropeptide), encoded by the lncRNA PSMA3-AS1, as a novel tumor suppressor in lung adenocarcinoma (LUAD). PAMP is significantly downregulated in LUAD tissues and positively correlates with favorable prognosis. Functional assays demonstrated that PAMP inhibits LUAD cell proliferation in vitro and suppresses tumor growth in vivo. Mechanistically, PAMP directly interacts with PYCR1, a key enzyme in proline biosynthesis. Structural modeling and mutagenesis revealed that the PAMP-F16 and PYCR1-N123 residues are critical for the interaction, resulting in the inhibition of PYCR1 enzymatic activity and decreased proline accumulation. Notably, synthetic PAMP administration recapitulates these anti-tumor effects, effectively reducing intracellular proline levels and impairing tumor progression in cellular and animal models. Together, our findings uncover a previously uncharacterized lncRNA-encoded micropeptide that orchestrates proline metabolic reprogramming to restrain LUAD development, offering new opportunities for metabolic intervention in precision oncology. - Source: PubMed
Publication date: 2026/06/09
Ma YunYi JianiZheng ChengcaiYang JuzeLi JiaYu MengqianQian XinyiRen JiayiWu XiaofanLu YanLiu Pengyuan - Porcine reproductive and respiratory syndrome virus (PRRSV) nonstructural protein 9 (NSP9), the viral RNA-dependent RNA polymerase (RdRp), is essential for viral replication but its comprehensive host interactome remains uncharacterized. This study employed co-immunoprecipitation coupled with liquid chromatography-tandem mass spectrometry (LC-MS/MS) to systematically identify NSP9-associated host proteins. We identified 222 high-confidence host interactors, with Gene Ontology and KEGG pathway analyses revealing significant enrichment in RNA/DNA-binding proteins, ubiquitin-proteasome pathways, metabolic regulators (amino acid/lipid biosynthesis), endoplasmic reticulum processing, and cell cycle components. Protein-protein interaction network analysis further delineated six functional modules involved in RNA processing, vesicular transport, and innate immunity. Crucially, validation studies confirmed direct binding between NSP9 and key candidates (CAPZ1, PSMA3, CDK1, USP48). Functional assessment demonstrated that CDK1 overexpression significantly inhibited PRRSV replication, implicating CDK1 as a host restriction factor. These findings collectively unveil the multifaceted role of NSP9 in subverting host machinery while identifying novel host defense mechanisms and potential targets for antiviral development against PRRSV. - Source: PubMed
Publication date: 2025/12/05
Wen WeiLiu YuhangWang WenqiangZhu ZhenbangLi Xiangdong