LMP7
- Known as:
- LMP7
- Catalog number:
- Y214149
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- LMP7
Related genes to: LMP7
- Gene:
- PSMB8 NIH gene
- Name:
- proteasome subunit beta 8
- Previous symbol:
- LMP7
- Synonyms:
- RING10, D6S216E, PSMB5i, beta5i
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-25
- Date modifiied:
- 2019-04-23
Related products to: LMP7
Related articles to: LMP7
- The human placenta plays a critical role as an immune and mechanical barrier. Notwithstanding, viral pathogens can still cross this barrier. Previously, differential gene expression has been described for protein-coding genes in human-induced-pluripotent-stem-cell-derived (hiPSC-derived) trophoblasts (TBs) from dizygotic twins discordant for congenital Zika syndrome (CZS), in which only one of the twin subjects presented the microcephaly phenotype. However, the involvement of long non-coding RNAs (lncRNAs) in TB development and in the TB response to ZIKV infection remained unexplored. To address this gap, we constructed a trophoblast-specific, lncRNA-enriched transcriptome resource and used it to define co-expression networks linking lncRNAs to trophoblast differentiation and to the antiviral response to ZIKV infection. Here, public RNA-Seq data from hiPSCs and hiPSC-derived TBs from dizygotic twins discordant for CZS were re-mapped to the human reference genome (GRCh38) using an ad hoc compiled hiPSC-TB-specific transcriptome enriched for lncRNAs, followed by differential expression analysis, co-expression network analysis and gene ontology (GO) enrichment. Expression validation by RT-qPCR of a set of novel and known lncRNAs associated with trophoblast differentiation and ZIKV infection was obtained. When comparing hiPSCs and TBs, 218 known and 26 novel lncRNAs were differentially expressed (DE) (FDR < 0.001). Correlated modules were enriched with GO terms related to "epithelial cell differentiation" and "tissue morphogenesis". Upon comparing TBs derived from the dizygotic twins, before and after ZIKV infection, 96 known and 6 novel lncRNAs were DE (FDR < 0.05). Correlated modules were enriched with interferon-related GO terms, including "regulation of defense response to virus" and "response to interferon". ZIKV-infected TBs from microcephaly-affected twins showed a 2.5-fold lower number of DE protein-coding genes and a 2-fold lower number of DE lncRNAs, compared with ZIKV-infected TBs from non-affected twins. These results indicate lncRNAs associated with TB development and response to ZIKV infection, highlighting candidates to be prioritized in future functional studies, such as , , , and imprinted and lncRNAs. - Source: PubMed
Publication date: 2026/08/15
Souza-Lopes ThallesFischer-Carvalho AgathaFreire Caio FPoli Pedro JFerreira Raiane OAmarante Maria F CZatz MayanaTahira Ana CAmaral Murilo SVerjovski-Almeida Sergio - Proteasome β (PSMB) subunits are essential components of the proteasome complex and play important roles in antigen processing and immune regulation. In this study, we identified 14 Psmb genes in grass carp (Ctenopharyngodon idella), including seven constitutive Psmbs (Psmb1-7), three immunoproteasome genes (Psmb8-10), two thymoproteasome-related paralogs (Psmb11a and Psmb11b), and two telelost-specific members (Psmb12 and Psmb13). Comparative genomic analyses showed that grass carp Psmb genes are highly conserved in genomic organization, gene synteny, and predicted β-subunit-like protein structures, supporting the evolutionary conservation of the proteasome β-subunit family in fish. Phylogenetic and syntenic analyses further revealed lineage-specific expansion of immunoproteasome-related Psmb genes in teleost fish, with Psmb12 and Psmb13 likely derived from duplications of Psmb9 and Psmb10, respectively. Tissue expression analysis suggested functional divergence among duplicated Psmb members, as constitutive Psmbs were relatively enriched in the brain, whereas immunoproteasome-related and teleost-specific Psmbs were highly expressed in immune- and mucosa-associated tissues. Moreover, GCRV-I infection rapidly induced Psmb8-10 and Psmb11b expression in CIK cells. IFN-γ induced a broader set of Psmb genes than IFNa, whereas IL-10 selectively suppressed several Psmbs. Together, these findings highlight the evolutionary conservation, expansion, and immune-related diversification of the Psmb family in teleost fish. - Source: PubMed
Publication date: 2026/08/22
Xu JingGao WaJia ZhaoFeng JianhuaLei WenjingZhu LiwenYan HuiZhuo PeilinWang JunyaZou Jun - Type I interferonopathies are a heterogeneous group of monogenic autoinflammatory disorders characterized by dysregulated type I interferon (IFN-I) signaling due to pathogenic variants that affect nucleic acid sensing, processing, or downstream signaling pathways. Mutations in genes including TREX1, RNASEH2A/B/C, SAMHD1, ADAR1, STING1 (TMEM173), PSMB8, COPA, and DNASE1L3 lead to persistent activation of innate immune pathways, particularly the cGAS-STING, MDA5, and Toll-like receptor pathways, with subsequent JAK-STAT signaling and sustained overexpression of interferon-stimulated genes. Chronic IFN-I activation promotes endothelial dysfunction, vascular inflammation, and tissue injury, providing a mechanistic link between interferonopathies and vasculitic disorders. Clinically, these conditions present with diverse manifestations, including chilblains, livedo reticularis, necrotizing cutaneous vasculopathy, panniculitis, interstitial lung disease, cerebral vasculopathy, and glomerulonephritis, often resembling autoimmune diseases such as primary central nervous system vasculitis, systemic lupus erythematosus (SLE), poliarteritis nodosa (PAN), immune complex vasculitis, and ANCA-associated vasculitis (AAV). A persistently elevated interferon gene signature represents a valuable diagnostic biomarker that distinguishes these disorders from most classical autoimmune vasculitides and facilitates early recognition. Timely genetic testing is essential to establish an accurate diagnosis, guide patient management, and avoid treatment delays. The present review summarizes the molecular mechanisms linking IFN-I dysregulation to endothelial injury and vasculitis, discusses the clinical spectrum and diagnostic challenges of monogenic interferonopathies, and highlights emerging targeted therapies, particularly Janus kinase inhibitors, that support precision medicine approaches for interferon-driven inflammatory diseases. - Source: PubMed
Publication date: 2026/08/07
Gürbüz NidaIsmayilova ShamsAhmadova GulnarÇiftçi RenaAksu GüzideBerdeli Afig - To explore the molecular mechanisms and key pharmacodynamic basis of for alleviating cancer-related fatigue (CRF) during chemotherapy for breast cancer. - Source: PubMed
Li ZhuangShi HuanChen JietingLiang YuqiWu YingchaoZuo QianChen Qianjun - Loss-of-function mutations in PSMB8/beta5i and other components of the 20S proteasome result in multi-organ diseases, such as Chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature (CANDLE) syndrome. Neurocognitive dysfunction associated with CANDLE suggests that proteasomal mutations may impact neuronal function and development early in life. We generated cerebral organoids (COs) from induced pluripotent stem cells (iPSCs) made from CANDLE patients. The COs from CANDLE iPSCs exhibited impaired neuronal development when compared to COs from healthy control iPSCs. Impaired neuronal maturation in CANDLE COs was correlated with increased polyamines, which were also elevated in CANDLE patient CSF. The proteasome-regulated Ornithine decarboxylase (ODC), the rate limiting enzyme in polyamine biosynthesis, was elevated in CANDLE neurons. Inhibition of ODC reversed polyamine overproduction and repaired neuronal maturation in CANDLE COs, suggesting a potential therapeutic avenue for intervention. These findings demonstrate that dysfunction of the proteasome affects neuronal development through overproduction of polyamines via dysregulation of ODC and offer insight into potential therapeutic strategies for CNS-related proteasomal dysfunction. - Source: PubMed
Publication date: 2026/08/04
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