PSMC5 Pre-design Chimera RNAi
- Known as:
- PSMC5 Pre-design Chimera RNAi
- Catalog number:
- H00005705-R01
- Product Quantity:
- 20 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- PSMC5 Pre-design Chimera RNAi
Related genes to: PSMC5 Pre-design Chimera RNAi
- 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 Pre-design Chimera RNAi
Related articles to: PSMC5 Pre-design Chimera RNAi
- 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
Tantawy MarwaWang DanxinGbadamosi MohammedYu FahongZhang YanpingAlomar Mohammed EShain Kenneth HBaz Rachid CBruno Katelyn AGong Yan - Neurodevelopmental proteasomopathies are a group of disorders caused by variants in proteasome subunit genes, that disrupt protein homeostasis and brain development through poorly characterized mechanisms. Here, we report 26 distinct variants in PSMC5, encoding the AAA⁺ ATPase subunit PSMC5/RPT6, in individuals with syndromic neurodevelopmental conditions. Combining genetic, multi-omics and biochemical approaches across cellular models and Drosophila, we unveil the essential role of proteasomes in sustaining key cellular processes. Loss of PSMC5/RPT6 function impairs proteasome activity, leading to protein aggregation, disruption of mitochondrial homeostasis, and dysregulation of lipid metabolism and immune signaling. It also compromises synaptic balance, neuritogenesis, and neural progenitor cell stemness, causing deficits in higher-order functions, including learning and locomotion. Pharmacological targeting of integrated stress response kinases reveals a mechanistic link between proteotoxic stress and spontaneous type I interferon activation. These findings expand our understanding of proteasome-dependent quality control in neurodevelopment and suggest potential therapeutic strategies for neurodevelopmental proteasomopathies. - Source: PubMed
Publication date: 2025/11/26
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