Ask about this productRelated genes to: PSMD3 Blocking Peptide
- Gene:
- PSMD3 NIH gene
- Name:
- proteasome 26S subunit, non-ATPase 3
- Previous symbol:
- TSTA2
- Synonyms:
- S3, P58, Rpn3
- Chromosome:
- 17q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-28
- Date modifiied:
- 2016-10-05
Related products to: PSMD3 Blocking Peptide
Related articles to: PSMD3 Blocking Peptide
- Methylchloroisothiazolinone (CMIT) and polyhexamethylene guanidine (PHMG) are antimicrobial biocides associated with pulmonary toxicity, although their comparative cellular stress mechanisms remain unclear. Here, we investigated how CMIT and PHMG differentially alter the proteome of human alveolar epithelial A549 cells under subcytotoxic conditions. Cells were exposed to CMIT or PHMG, and global proteomic profiling was performed using label-free liquid chromatography-tandem mass spectrometry. Differentially expressed proteins (DEPs) were identified at a 1% false discovery rate with an absolute log2 fold change ≥1. Functional analyses were conducted using Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Ingenuity Pathway Analysis, and selected proteins were validated by western blotting. Comparative toxicoproteomics revealed distinct stress-response signatures induced by the two biocides. CMIT preferentially altered proteins associated with proteostasis, oxidative stress, and protein quality control, whereas PHMG was characterized by coordinated depletion of ribosome-associated and translation-related proteins. A total of 73 and 155 DEPs were identified in CMIT- and PHMG-treated cells, respectively, with 22 proteins shared between treatments. Western blotting confirmed PSMD3, TUBB2A, and GLRX1 as CMIT-responsive proteins and THRAP3, DHX15, and RPL4 as PHMG-responsive markers. These findings provide comparative mechanistic insight into how CMIT and PHMG induce distinct epithelial stress responses and identify candidate protein markers that may support future in vitro assessment of biocide-induced pulmonary toxicity. - Source: PubMed
Publication date: 2026/09/06
Jeong Ye-EunJeon Min JeongYoun Hyung-SunHan JiyouLee Mi-Young - The genetic architecture of idiopathic inflammatory myopathies (IIMs) remains incompletely defined. When increasing sample size is not feasible, cross-trait analysis of genetically correlated diseases offers an effective strategy for discovering risk loci. Using summary statistics of IIM and B cell lymphoma subtypes, we applied conditional false discovery rate (condFDR) and multi-trait analysis of genome-wide association studies (GWASs) (MTAG) to detect genetic associations with IIM risk. Single-nucleotide polymorphisms (SNPs) outside the human leukocyte antigen (HLA) region meeting significance thresholds (condFDR < 0.01 or p <5 × 10 for MTAG) were clumped and subjected to both functional annotation in FUMA and Gene Ontology (GO) biological process enrichment analysis using clusterProfiler. We identified six previously unreported loci, including three associated with dermatomyositis (chr12:58674304T>C, chr13:110799415C>T, and chr17:38103285G>A (hg19)) and three associated with polymyositis (PM) (chr4:971496T>C, chr6:396321C>T, and chr6:32650631C>A). All non-HLA loci act as expression quantitative trait loci (eQTL) or localize within enhancer regions. Notably, these include cis-eQTLs for known IIM risk-associated genes (GSDMB, DGKQ, SLC26A1, and IDUA) as well as genes implicated in synaptic vesicle cycle (SVC) pathways, immune regulation (IKZF3, ORMDL3, IRF4, DUSP22, and SPON2), protein homeostasis (ATP23 and PSMD3), lipid metabolism (PGAP3, ORMDL3, STARD3, and DGKQ), and myopathy (COL4A1). GO analysis revealed significance for SVC pathways in PM (FDR < 0.05). These findings advance our understanding of IIM pathogenesis from a genetic perspective and highlight candidate regulatory variants for further mechanistic investigation. - Source: PubMed
Publication date: 2026/07/24
Che Weng IanJarvis James NSysojev Anton ÖbergZhu CatherinePatasova Karina Smedby Karin ELundberg Ingrid EWesterlind HelgaLamb Janine AHolmqvist Marie - Carbon dots offer excellent physico-chemical properties and biocompatibility for cancer theranostics systems, either as therapeutic agents themselves, or as potential drug carriers. It is, however, postulated that the drug carrier affects the mechanism of action and intracellular target molecules of a drug. Therefore, in the present study, we systematically evaluated protein alterations in HeLa cervical cancer cells after treatment with sulfur-doped carbon dots (S-CDs). Synchrotron Radiation μFTIR spectroscopy and label-free LC-MS/MS proteomics integrated with bioinformatics were used to assess molecular changes. μFTIR revealed a shift and increased intensity of α-helices, indicating structural changes in proteins as a result of the interaction between S-CDs and cells. Proteomic analysis identified 122 statistically significant ( ≤ 0.05) proteins with increased abundance and 61 with decreased abundance following S-CD exposure, many of which possess high α-helix content, consistent with μFTIR findings. Functional analyses showed that up-regulated proteins were enriched in molecular adaptor, transporter, and transcription regulator activities, particularly those involved in RNA metabolism and translation. Down-regulated proteins were dominated by protein-modifying enzymes and cytoskeletal components. Pathway enrichment analysis indicated alterations in mRNA processing, ribosomal pathways, translation factors, aminoacyl-tRNA biosynthesis, and proteasome degradation. Key hub proteins included ribosomal proteins and translation initiation factors. S-CD treatment led to opposite regulation of many proteins compared to their regulation in untreated HeLa cells including down-regulation of ribosomal proteins (RPS27L, RPS19, and RPS5), aminoacyl-tRNA biosynthesis proteins (IARS1, LARS1, and MARS1), and proteasome degradation proteins (PSMD2, PSMD3, and PSMD11), which aligns with the observed cytotoxic effect of S-CDs on cervical cancer cells. Overall, these results highlight significant proteomic and structural protein changes induced by S-CDs and support their potential for cervical cancer treatment, warranting further investigation of this nanomaterial's biological applications. - Source: PubMed
Publication date: 2026/03/26
Davalieva KatarinaRalić VanjaBozhinovski GjorgjiGemović BranislavaNešić Maja DKorićanac LelaDučić TanjaAlgarra ManuelPopović Iva AStepić MilutinPetković Marijana - Major depressive disorder (MDD) and inflammatory bowel disease (IBD) exhibit clinical associations, yet the cross-disease genetic links and shared mechanisms between them remain unclear. This study aims to explore the genetic associations between MDD and IBD and identify the shared risk loci, potential key tissues, and related genetic mechanisms. - Source: PubMed
Publication date: 2026/04/08
Ding YifanLuo QinghuaYan XiaojunDeng ChenweiShen PanXu YueqiZhang Leichang - Specific gut microbes are critically involved in the development of metabolic diseases, particularly obesity. Here, through analyses of diabetic patients and animal models, we identified Romboutsia ilealis as a novel gut bacterium that alleviates obesity and associated metabolic disorders by suppressing intestinal lipid absorption rather than altering energy expenditure. Metabolomic profiling revealed 2-oxoindole-3-acetate (OAA) as a key mediator of this effect, which was validated both in vitro and in vivo. Mechanistically, biotin-labeled OAA pull-down coupled with proteomics in the intestinal IPEC-J2 cells identified a direct interaction between OAA and the 26S proteasome subunit PSMD3, leading to destabilization of the mA-binding protein YTHDF2. Loss of YTHDF2 derepressed Rxrb mRNA, increasing CD36 and FABP2 expression and thereby promoting intestinal lipid absorption. Together, our findings uncover a previously unrecognized R. ilealis-OAA-PSMD3-YTHDF2-Rxrb signaling axis that links the gut microbiota to host metabolism, and highlight R. ilealis and OAA as potent next-generation probiotic or metabolite-based therapies for obesity. - Source: PubMed
Publication date: 2026/03/17
Zhu LuoyiHuang LiangLiu ShuqiLuo ShiqiLi YigeWang YizhenZong Xin