PSMC5 _ SUG1 Chicken antibody Ab Aff - Purified
- Known as:
- PSMC5 _ SUG1 Chicken (anti-) Antibody Aff - Purified
- Catalog number:
- GTX82443
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- ACR
- Gene target:
- PSMC5 _ SUG1 Chicken antibody Aff - Purified
Related genes to: PSMC5 _ SUG1 Chicken antibody Ab Aff - Purified
- 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: PSMC5 _ SUG1 Chicken antibody Ab Aff - Purified
Related articles to: PSMC5 _ SUG1 Chicken antibody Ab Aff - Purified
- Sepsis involves dysregulated host responses with mitochondrial dysfunction as a key mechanism, yet its immune cell landscape and clinical utility are unclear. - Source: PubMed
Publication date: 2026/09/19
Le XinFan YoufenXu SidaLi JiliangCui ShengyongJin GuoyingHuang NengYu YaohuaXu Pei - Swine Acute Diarrhea Syndrome Coronavirus (SADS-CoV) is an emerging porcine enteric coronavirus that causes severe diarrhea in piglets. Type III interferon (IFN) are crucial for intestinal antiviral defense, and the capacity of SADS-CoV to disrupt IFN-III responses is critical for its replication. This study found that SADS-CoV inhibits IFN-III production through its nonstructural protein 1 (Nsp1), which degrades interferon regulatory factor 1 (IRF1) by promoting its ubiquitination and proteasomal degradation. Mass spectrometry and co-immunoprecipitation analyses revealed that SADS-CoV Nsp1 interacts with proteasomal subunits. Further research indicates that PSMB4, PSMB5, and PSMC5 are key proteasomal subunits involved in SADS-CoV Nsp1-induced IRF1 degradation. Similarly, Porcine Epidemic Diarrhea Virus (PEDV) and Transmissible Gastroenteritis Virus (TGEV) Nsp1 exhibit similar functions, highlighting the conserved role of coronavirus Nsp1 in immune evasion. Collectively, our findings uncover a new mechanism where SADS-CoV Nsp1 exploits the proteasome to degrade IRF1, countering IFN-III responses. - Source: PubMed
Publication date: 2026/09/06
Xiang YingjieZhu QinyuanCheng YueZhao XingShi KaichuangFeng ShupingHuang YuChen ZhenhaiLin ChanghuaMou Chunxiao - Parkinson's disease (PD) and related Parkinsonian conditions involve progressive disruption of mitochondrial homeostasis, redox balance, synaptic function, and proteostasis. Available therapies remain predominantly symptomatic, motivating the search for multitarget compounds acting across stress-sensitive pathways. BjPro-7a (pEDGPIPP), a proline-rich oligopeptide from Bothrops jararaca venom, exerts cytoprotective effects under oxidative stress, but its activity in an in vivo Parkinsonian-like model is unknown. Here we investigated whether BjPro-7a attenuates the behavioral and proteomic disturbances induced by 1-methyl-4-phenylpyridinium (MPP) in zebrafish larvae. Larvae were exposed to 500 µM MPP and post-treated with 10 µM BjPro-7a, followed by assessment of basal locomotion, light/dark-evoked behavior, and label-free proteomic profiling. BjPro-7a markedly reversed the MPP-induced hypolocomotor phenotype by increasing the total distance traveled, improving bout-related parameters, reducing inter-episode intervals, and restoring visually evoked responsiveness. Proteomic analysis revealed broad rescue-associated remodeling, more pronounced among proteins suppressed by MPP than among those elevated by intoxication. Functional enrichment and protein-protein interaction analyses indicated coordinated modulation of vesicle trafficking and synaptic organization, mitochondrial and bioenergetic function, redox homeostasis, and protein quality control. Representative rescue-associated proteins included VAMP2 and SNAP25A (synaptic), SDHA and UQCRFS1 (mitochondrial), G6PD and PRDX3 (redox), and PSMC5 and STIP1 (proteostasis). Together, these findings show that BjPro-7a attenuates MPP-induced dysfunction and promotes systems-level proteomic remodeling consistent with rescue in zebrafish larvae. These data support BjPro-7a as a promising candidate for future therapeutic studies in Parkinsonian-like neurotoxicity. - Source: PubMed
Publication date: 2026/07/13
Maleski Adolfo Luis Almeidada Cunha E Silva Felipe AssumpçãoPereira Bruno FioreliniAlberto-Silva Carlos - 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