Human Polyclonal PSMB9 Ab
- Known as:
- Human Polyclonal PSMB9 Antibody
- Catalog number:
- a1771
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal PSMB9
Ask about this productRelated genes to: Human Polyclonal PSMB9 Ab
- Gene:
- PSMB9 NIH gene
- Name:
- proteasome subunit beta 9
- Previous symbol:
- LMP2
- Synonyms:
- RING12, beta1i, PSMB6i
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-18
- Date modifiied:
- 2016-10-05
Related products to: Human Polyclonal PSMB9 Ab
Related articles to: Human Polyclonal PSMB9 Ab
- Rheumatoid arthritis (RA) is a systemic immune-related disease characterized by chronic synovial inflammation and progressive joint destruction. However, the molecular mechanisms and diagnostic biomarkers underlying RA remain unclear. In this study, we aimed to identify potential biomarkers for clinical diagnosis of RA and to investigate their association with immune infiltration. By integrating differentially expressed genes analysis (DEGs) and weighted gene co-expression network analysis (WGCNA), we identified PSMB9 as a hub gene associated with RA. Gene set enrichment analysis (GSEA) and immune infiltration analysis revealed a strong association between RA and macrophage infiltration. Single-cell RNA sequencing datasets also suggest that PSMB9 is not only highly expressed in macrophage but is also present in synovial cells. We employed cellular thermal shift assay (CETSA) combined with Western blot to validate the interaction between sinomenine (SIN) and the target protein. CETSA results demonstrated that, compared with the control group, SIN increased the thermal stability of PSMB9, suggesting direct binding between the two. Western blot experiments further confirmed that PSMB9 protein expression was significantly downregulated following SIN treatment. PSMB9 may serve as potential diagnostic biomarker and therapeutic targets for RA. Moreover, our data suggest SIN may exert anti-inflammatory effects through regulation of PSMB9. This study also provides an additional insight into the underlying mechanisms involved in the progression of RA and discover a new molecular target for SIN. - Source: PubMed
Publication date: 2026/05/29
Zhang CuiLio ChonkitLi NanaYu YangLuo Jinfang - Epigenetic modifications may illuminate mechanisms by which HIV and antiretroviral therapy (ART) exposure during critical developmental periods affect biological pathways and chronic comorbidity risk. We examined genome-wide DNA methylation (DNAm) in youth with perinatally-acquired HIV (YPHIV) compared to perinatally HIV-exposed uninfected youth (YPHEU) at two timepoints. In YPHIV, we assessed associations of HIV RNA viral load, CD4 count, and inflammation with DNAm alterations. - Source: PubMed
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Shiau StephanieBrummel Sean SHu JunjieDouglas JasmineZumpano FrancescaCorley MichaelJao JenniferPurswani MurliPatel KunjalMarsit Carmen J - Patients with lung cancer brain metastases can benefit from immune checkpoint inhibitors (ICI). However, intracranial responses are often limited and not always concordant with activity seen in extracranial disease. Defects in IFNγ signaling and HLA class-I antigen presentation machinery (APM) on malignant cells can drive immune evasion and ICI resistance, and have traditionally been viewed as interdependent. The possible role of these alterations in non-small cell lung cancer (NSCLC) brain progression remains poorly understood. - Source: PubMed
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Vilariño Noeliade Rodas Miguel LópezVillalba-Esparza MariaRajendran Barani KumarHuang BoyuHijazo-Pechero SaraCostantini AdrienRanjan KishuRamos-Paradas JavierLu Benjamin YNadal ErnestGoldberg Sarah BNguyen Don XSchalper Kurt A - Complex human diseases exhibit substantial clinical heterogeneity driven by poorly understood molecular mechanisms, while many also lack sufficient molecular and omics data for mechanistic investigation, hindering therapeutic development. We introduce PiMInfer, a phenotype-to-mechanism framework that leveraged largely available real-world clinical data-based deep phenotypic characterizations with a biomedical knowledge graph approach to resolve disease clinical heterogeneity into phenotype-informed molecular modules, thereby accelerating therapeutic target discovery. We applied PiMInfer to investigate Hidradenitis Suppurativa (HS), an autoimmune skin disease with poorly understood pathogenesis and limited treatment options. PiMInfer identified a coherent, phenotype-informed HS gene module (PiHSM) and functional endotypes, which were validated using multimodal evidence. In silico drug repurposing using PiHSM prioritized Carfilzomib, targeting the immunoproteasome subunit PSMB9, essential for MHC Class I antigen presentation. Preclinical testing using human patient lesional skin explants confirmed its anti-inflammatory activity and demonstrated a significant downregulation of IFN-γ, IL-17, and mTOR signaling pathways within HS lesional microenvironment through single-cell RNA sequencing. PiHSM-based network predictions further suggest a potential enhanced efficacy of combining Carfilzomib with approved HS agents. Collectively, PiMInfer provides a scalable framework that bridges real-world phenome-wide comorbid associations to mechanism-anchored therapeutic discovery, enabling a paradigm shift in precision medicine approaches for complex diseases with limited molecular characterization and in need of better therapeutic strategies. - Source: PubMed
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