PSMB9 antibody
- Known as:
- PSMB9 (anti-)
- Catalog number:
- orb125048
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- PSMB9 antibody
Related genes to: PSMB9 antibody
- 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: PSMB9 antibody
Related articles to: PSMB9 antibody
- SOCS2 is known to regulate myoblast differentiation and skeletal muscle development via the GH-IGF1 axis, while its role in Hu sheep myoblast differentiation and its potential alternative signaling pathways remain largely unexplored. Proteomic profiling of SOCS2-knockout C2C12 monoclonal cell lines identified significant enrichment of differentially expressed proteins in the proteasome pathway, with PSMB9 serving as one of the most prominent candidates, though the underlying mechanism remained unclear. In this present study, the regulatory relationship between SOCS2 and PSMB9 was firstly validated, and the results showed that SOCS2 positively regulated PSMB9 expression in Hu sheep myoblasts. Functional assays further confirmed SOCS2 negatively regulated Hu sheep myoblast differentiation. Mechanistically, JASPAR database predicted potential STAT3 transcription factor binding sites in the PSMB9 promoter region, and dual-luciferase reporter assays verified that STAT3 indeed repressed PSMB9 transcriptional activity. SOCS2 regulated STAT3 protein abundance and phosphorylation by interacting with JAK1. Functionally, STAT3 promoted Hu sheep myoblast differentiation, whereas PSMB9 inhibited Hu sheep myoblast differentiation. Moreover, either STAT3 knockdown or PSMB9 overexpression could rescue the enhanced differentiation phenotype induced by SOCS2 knockdown. Collectively, this study demonstrates a novel mechanism by which SOCS2 regulates Hu sheep myoblast differentiation through STAT3/PSMB9 signaling axis. - Source: PubMed
Publication date: 2026/06/24
Xie B Y TGuo D DZhang JMeng C HZhang J LQian YCao S XLi Y X - Childhood-onset systemic lupus erythematosus (cSLE) is associated with significant morbidity and mortality. While numerous variants have been associated with adult-onset SLE, limited data exist on genetic variation within cSLE. We aimed to investigate genetic factors of early-onset cSLE, defined as onset of cSLE prior to age 10. - Source: PubMed
Publication date: 2026/06/23
Nelson MeghanMurthy ShantaMaddipatla SushmaShenoy SreekalaPonder LoriChandrakasan ShanmuganathanKugathasan SubraCutler DavePrahalad Sampath - 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
Publication date: 2026/06/05
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
Publication date: 2026/05/28
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