PSMB7 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- PSMB7 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00005695-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- PSMB7 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: PSMB7 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- PSMB7 NIH gene
- Name:
- proteasome subunit beta 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 9q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-22
- Date modifiied:
- 2016-10-05
Related products to: PSMB7 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: PSMB7 293T Cell Transient Overexpression Lysate(Denatured)
- Sweet syndrome (SS) is an autoinflammatory neutrophilic dermatosis characterized by abrupt-onset inflammatory skin lesions and systemic symptoms, yet its molecular pathogenesis remains incompletely defined. To delineate disease-specific inflammatory programmes, we performed NanoString-based transcriptomic analysis of SS skin lesions and compared them with healthy control skin and pyoderma gangrenosum, a related neutrophilic dermatosis. SS exhibited a distinct inflammatory transcriptional signature marked by robust upregulation of type I and II interferon-stimulated genes, including CXCL9, CXCL10, GBP1, GBP5, IFIT2 and IRF7, distinguishing SS from both control groups. Cell type deconvolution analysis revealed enrichment of dendritic cells, consistent with a prominent type I interferon-driven immune response. In parallel, SS lesions demonstrated altered immunoproteasome gene expression, with upregulation of immunoproteasome subunits PSMB8, PSMB9 and PSMB10 and downregulation of the constitutive subunit PSMB7 suggesting functional remodelling of proteasomal activity. Together, these findings support a model in which dendritic cell-driven interferon signalling promotes immunoproteasome remodelling and sustains neutrophilic inflammation in Sweet. This study identifies a prominent interferon signalling as a defining molecular feature of SS and highlights potential therapeutic opportunities within the interferon-JAK/STAT and proteasome pathways. - Source: PubMed
Calabrese LauraMoltrasio ChiaraRomagnuolo MaurizioStadler Pia-CharlotteFiocco ZenoNeulinger-Muñoz MatthiasAoki RuiD'Onghia MartinaRubegni PietroKerl KatrinSatoh Takashi KMarzano Angelo VFrench Lars E - Psoriasis is a chronic inflammatory skin disease. Narrow-band ultraviolet B (NB-UVB) phototherapy is an effective, cost-efficient, and safe treatment for plaque psoriasis; however, predictors of treatment response remain limited. - Source: PubMed
Publication date: 2026/05/25
Yu YingyuanLi BingjieWang YuQu ZhengkaiWang XinJiang YuxiongZhong XiaoyuanChen YoudongHuang DaweiBi XinlingLu JiajingDing YangfengGong YuGu JunZhang XilinShi Yuling - Dysregulated immunometabolism is central to the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD). Although polyamines contribute to cellular stress responses and immune-cell function, their cell-type-specific transcriptional associations within the hepatic immune microenvironment remain incompletely understood. - Source: PubMed
Publication date: 2026/04/29
Zou PengSun LinLin Zhibin - Lung adenocarcinoma (LUAD) leads to death primarily due to its high metastatic potential. Risk assessment methodologies currently predicated on histopathological and imaging features possess a limited capacity to predict metastatic potential. Therefore, integrating single-cell transcriptomics and CT radiomics to identify key molecular drivers of metastasis and establishing a noninvasive imaging prediction model for LUAD is important. - Source: PubMed
Publication date: 2026/03/16
Wu ShengqianHu TaoCao ZhikaiLin ChengbinHuang ShuoLi YingxiZhu KeyunTian YaoHe Jinxian - This study investigated mitochondrial permeability transition-driven necrosis-related genes (MPTDNRGs) and its association with lung adenocarcinoma (LUAD). We systematically investigated their genetic variation, expression patterns, and prognostic value. A risk prediction model for MPTDNRGs was contrasted using Cox regression and least absolute shrinkage and selection operator regression analyses. MPTDNRG scores were used to quantify LUAD subtypes. We evaluated their value in the tumor microenvironment (TME), tumor mutational burden (TMB), prognostic prediction, and drug sensitivity in LUAD. The expression level, copy number variation, methylation, and microRNA (miRNA) status of PSMB7 were analyzed. We also analyzed the expression and knockdown efficiency of PSMB7 in LUAD by immunohistochemical staining, real-time fluorescence quantitative polymerase chain reaction, and western blotting. PSMB7 function in LUAD cells and in vivo was assayed using Cell Counting Kit 8, colony formation, wound healing, Transwell assays, flow cytometry, and mouse models. Seven MPTDNRG features were successfully constructed to predict LUAD prognosis and validated in an external cohort. Patients were categorized into high- and low-risk groups based on risk scores. The high-risk group exhibited shorter survival times, lower TME scores, weaker TME cell infiltration, and higher TMB scores than the low-risk group. Cancer stem cell index, mutation frequency, and drug sensitivity significantly differed between the two groups. MPTDNRG score could independently predict LUAD. PSMB7 was highly expressed in various tumors, and copy number variation, methylation, and miRNA expression significantly differed among different cancers. PSMB7 was highly expressed in LUAD tissues and cell lines. PSMB7 knockdown inhibited cancer cell proliferation, migration, invasion, and epithelial - mesenchymal transition, and promoted apoptosis. PSMB7 exerted tumorigenic effects in mice. In conclusion, we comprehensively demonstrated the characterization of MPTDNRGs in LUAD and constructed a new risk prediction model. Meanwhile, PSMB7 was shown to be a possible new target for LUAD treatment. - Source: PubMed
Publication date: 2025/12/28
Liu LinGao MingjunHe WenboWang MengmengZhou SidingWang XiaolinShu Yusheng