Mouse Anti-Human PSMC5 Antibodies
- Known as:
- Mouse Antibody toHuman PSMC5 Antibodies
- Catalog number:
- JI-04-00450
- Product Quantity:
- 317 μg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human PSMC5 Antibodies
Related genes to: Mouse Anti-Human PSMC5 Antibodies
- Gene:
- PSMC5 NIH gene
- Name:
- proteasome 26S subunit, ATPase 5
- Previous symbol:
- -
- Synonyms:
- SUG1, p45/SUG, TBP10, p45, S8, TRIP1, SUG-1
- Chromosome:
- 17q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-12-08
- Date modifiied:
- 2015-08-12
Related products to: Mouse Anti-Human PSMC5 Antibodies
Related articles to: Mouse Anti-Human PSMC5 Antibodies
- Polyamine metabolism plays an essential role in glioma progression and the tumor microenvironment (TME). However, its prognostic and immunotherapeutic significance remains incompletely understood. We integrated transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) to construct a prognostic risk model via Least Absolute Shrinkage and Selection Operator (LASSO) regression. This model was externally validated using the GSE108474 and GSE43378 cohorts. Multivariable Cox regression was employed to identify key prognostic predictors, while consensus clustering was applied to stratify patients into distinct molecular subtypes. A robust 19-gene signature was established to calculate risk scores, effectively categorizing patients into high- and low-risk groups with significantly divergent survival outcomes. From this signature, five genes were identified as independent prognostic factors via multivariable Cox analysis. Ultimately, three prioritized core candidate biomarkers (AGMAT, PSMC5, and SMS) were extracted, among which SMS exhibited exceptionally high individual diagnostic efficacy. Furthermore, consensus clustering delineated two distinct subgroups (C1 and C2). The C1 subtype exhibited a less immune-infiltrated phenotype but higher PD-L1 expression and elevated TIDE scores, indicating stronger immune evasion and poorer survival. In contrast, the C2 subtype was characterized by robust immune cell infiltration, a more favorable prognosis, and a superior computationally predicted response to immunotherapy. In conclusion, our polyamine metabolism-related gene signature may serve as a promising candidate biomarker for evaluating clinical outcomes and computationally estimated immunotherapy efficacy in glioma. While this risk model and molecular subtyping framework offer novel insights for therapeutic stratification, prospective clinical validation is required. - Source: PubMed
Publication date: 2026/06/29
Hu MengchaoXu LiangHua XiangtingZhang ChaoyongLi Huaixu - Colorectal cancer (CRC) metastasis requires coordination between tumor-intrinsic programs and the surrounding microenvironment, yet how proteasomal regulation intersects with the epitranscriptome in this process remains unclear. Here, analyses of TCGA, GEO, and an institutional cohort of 146 CRC patients identified PSMC5 upregulation as associated with metastatic progression and poor prognosis. Mechanistically, PSMC5 promoted SMURF1-dependent K11-linked ubiquitination of METTL14 at K263, leading to METTL14 destabilization, global m⁶A remodeling, and activation of EMT-associated malignant phenotypes. Rescue experiments further supported METTL14 as a functional downstream effector of PSMC5. Integrative single-cell, spatial transcriptomic, and multiplex immunofluorescence analyses showed that PSMC5-high epithelial states were associated with spatially organized "regulatory islands," defined here as PSMC5-high epithelial nests with peripheral Treg and M2 enrichment together with relative CD8⁺ T-cell exclusion. , SMURF1 silencing restored METTL14 expression and attenuated PSMC5-driven tumor growth and lung metastasis. Collectively, these findings define a PSMC5/SMURF1/METTL14 axis that links proteasomal regulation to epitranscriptomic remodeling and metastatic progression in CRC, and identify this pathway as a candidate therapeutically actionable axis. - Source: PubMed
Publication date: 2026/05/11
Zhang YiYang XiaoZhong HuaDing ChengshengXu XimoShao YanfeiSun BinZhang WendongMa JunjunFeng BoZheng MinhuaHe Zirui - Investigate how Ca /calmodulin dependent protein kinase kinase 2 (CaMKK2) orchestrates a catabolic shift in chondrocytes during early osteoarthritis (OA). - Source: PubMed
Publication date: 2026/05/12
Ding XinchunLi YongHansen KasiMosley Amber LYeh Elizabeth SDoud Emma HSankar Uma - The global impact of pulmonary tuberculosis (PTB) is compounded by a limited understanding of modifiable risk factors. While caffeine is the most consumed psychoactive substance, its causal relationship with PTB and the underlying immunological mechanisms remain unknown. - Source: PubMed
Publication date: 2026/04/20
Zhu LiangyuZheng ZidaHuang XunLu HaoranChen ZhiqiangWu HanxinPeng LiTao LvyanBai YueYang RuiBao RuianLuo SuyiMa WeijiangSong JieqinTang JiaomeiLi BingxueBao FukaiLiu Aihua - 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
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