Ask about this productRelated genes to: PSMD2 antibody
- Gene:
- PSMD2 NIH gene
- Name:
- proteasome 26S subunit, non-ATPase 2
- Previous symbol:
- -
- Synonyms:
- S2, P97, TRAP2, MGC14274, Rpn1
- Chromosome:
- 3q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-28
- Date modifiied:
- 2016-10-05
Related products to: PSMD2 antibody
Related articles to: PSMD2 antibody
- Fetal brain development is crucial for lifelong neurological health, yet the impact of environmental heavy metal pollutants such as cadmium (Cd) remains incompletely understood. As a typical environmental heavy metal pollutant, Cd is widely encountered by various populations, including pregnant women, and disrupts zinc and copper ion homeostasis-processes essential for fetal brain development. However, cell-type-specific vulnerabilities underlying Cd-induced developmental neurotoxicity have been underexplored in human models. In this study, we employed cortical organoids with single-cell RNA sequencing (scRNA-seq) to evaluate the Cd-induced cell-type-specific developmental neurotoxicity and elucidate molecular mechanisms. scRNA-seq revealed that Cd exposure induced cell cycle arrest concurrent with zinc and copper ion dyshomeostasis in proliferating neural populations, inducing the loss of inhibitory neurons. Mechanistically, Cd activated ribosome biogenesis and mitochondrial energy metabolism across all cell types, while enhancing Cd detoxification in astrocytes and inducing astrocyte dysfunction. Furthermore, Cd disrupted axon guidance as evidenced by decreased axonal growth length and enhanced aberrant intercellular communication via robust binding Glu and Asp of PSMD2, TUBA1B and CFL1. Finally, MEA assays revealed that Cd exposure impaired neural network activity in cortical organoids. Our study reveals previously unrecognized mechanisms by which environmentally relevant cadmium disrupts human corticogenesis at the single-cell level, providing compelling evidence for the developmental neurotoxicity of this ubiquitous pollutant and supporting efforts to reduce prenatal Cd exposure for lifelong neurological health. - Source: PubMed
Publication date: 2026/05/22
Huang YanWang ZhiqiuLi HaoWang ZhongLuo GuimingZhao LujunZeng PingliZhu XizhiXue AiqinBian GuohuiSong DailiHe MaoyangHuang YinaGao HongZhang XinCen XiaoboBu Qian - Tumor-infiltrating CD8 cells recognize neoantigens created by tumor-specific mutations. Nonetheless, even after checkpoint inhibitor therapy, most patients progress. A deeper understanding of anti-tumor responses could facilitate development of better therapies. To enable such studies, we applied TCXpress, a high throughput platform that clones fully expressible TCRs from single cells into retro- or lenti- viral vectors without sequencing or gene synthesis, to study TCRs from CD8 cells infiltrating mouse MC38 tumors. We expressed cloned TCRs in reporter cells and interrogated TCR specificity by coculturing them with B6WT3 cells transduced with tandem minigenes encoding predicted neoantigens. We isolated TCRs reactive against epitopes from mutant Rpl18, Adpgk, Psmd2, and Zc3h7b along with self-reactive TCRs that recognized normal B6 and MC38 cells. Importantly, we successfully treated MC38-bearing mice with T cells transduced with anti-Rpl18 TCRs. These results establish a system that could be used to study many types of T cell responses and validates a therapeutic approach that could be tested in the clinic. - Source: PubMed
Publication date: 2026/04/28
Rowe Alexander MChaurasia SmritiWei WenzhongGarcía-Diéguez LauraQuerry KatherineSchiebel Johnathon GSmolak ChristyMuralles Alexander GWikenheiser DanielQuann KevinPirner CollinCodispot KentinShlomchik Mark JShlomchik Warren D - 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 - Feline nasal lymphoma (FNL) is the most common nasal tumor in cats. Although some negative prognostic factors for FNL have been previously reported, further studies on its molecular pathophysiology are needed. In the present study, we conducted comprehensive investigations of gene expression profiles (GEPs) in FNL. GEPs were compared between 17 FNL tissues and peripheral blood mononuclear cell (PBMC) samples of 3 healthy cats by RNA-sequencing. Then, we extracted differentially expressed genes (DEGs), and the differences in their mRNA expression levels were validated by RT-qPCR using 31 FNL, 3 lymph node (LN), and 3 PBMC samples. Finally, immunohistochemistry was performed to validate the expression of the focused protein in 11 FNL tissues and LN of 3 healthy cats. The comparisons of GEPs between FNL and PBMC samples identified 7208 DEGs. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that 76 pathways including those related to tumor biology were significantly enriched with DEGs. Part of the extracted pathways commonly included DEGs related to proteasome. RT-qPCR analysis showed a trend toward increased expression of PSMD2 and PSMB5 genes in the FNL samples. In addition, immunohistochemistry also showed that PSMD2 protein expression was comparable and higher when compared with those of germinal centers and other areas of normal lymph nodes, respectively. Our results showed dysregulation of various pathways related to tumor biology and suggested upregulation of genes and proteins related to the proteasome in FNL. Future studies are needed to clarify their associations with the pathogenesis of FNL. - Source: PubMed
Publication date: 2026/04/07
Tsuruta TakumiTomiyasu HirotakaSakuma HirokiShimano ShotaroNagao ItsumaToyoda HirotoFukuoka RayOhmi AkiFujita NaokiMomoi YasuyukiOhshima TakafumiFujiwara-Igarashi AkiTakahashi NaohiroChambers James KUchida KazuyukiGoto-Koshino YukoOkuda Masaru - Helicobacter pylori (H. pylori) has been identified as a pathogenic factor in gastric cancer (GC). Building on our previous findings that VacA upregulates TRAF1, which in turn transcriptionally activates OASL, we explored the role of this TRAF1-OASL-PANoptosis axis in GC using clinical samples, cell lines, and mouse models. Functional assays (CCK-8, colony formation, migration, invasion, TUNEL) demonstrated that TRAF1 promotes GC cell proliferation, migration, and invasion via OASL, while suppressing apoptosis. RNA-seq revealed that upregulation of TRAF1 and OASL, combined with H. pylori infection in gastric epithelial cells, enriched pathways associated with PANoptosis. Rescue experiments showed that TRAF1 knockdown increased PANoptosis, and this increase was attenuated by the pan-caspase inhibitor Z-VAD-FMK, whereas subsequent OASL overexpression reversed the suppression of PANoptosis caused by TRAF1 knockdown, whereas LPS further induced PANoptosis. Both in vitro and in vivo models confirmed that H. pylori infection triggers PANoptosis. Co-Immunoprecipitation assays uncovered a protein interaction between OASL and the ZBP1-PANoptosome. Critically, under H. pylori infection conditions, OASL overexpression rescued the PANoptosis suppressed by TRAF1 knockdown in gastric epithelial cells. This study demonstrates that H. pylori infection induces PANoptosis, and defines a pathway wherein TRAF1 promotes PANoptosis by regulating OASL-mediated activation of the ZBP1-PANoptosome. Our findings reveal a novel, context-dependent duality of the TRAF1/OASL axis: it promotes PANoptosis, contributing to mucosal damage during the precancerous inflammatory stage, yet in established GC, this axis appears to suppress PANoptosis, facilitating tumor progression. These insights provide a theoretical foundation for targeting this pathway in treating H. pylori-associated gastritis-cancer progression. - Source: PubMed
Publication date: 2026/04/06
Zhang MinglinYang XueerXie JieCai TingZhao XuelinLiu XiaomingWang Fen