Human G-CSF Protein Vector: E.Coli
- Known as:
- Human G-CSF Protein Vector: E.Coli
- Catalog number:
- 10240-H00E
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human G-CSF Protein Vector: .Coli
Related genes to: Human G-CSF Protein Vector: E.Coli
- Gene:
- CSF3 NIH gene
- Name:
- colony stimulating factor 3
- Previous symbol:
- GCSF, G-CSF, C17orf33
- Synonyms:
- MGC45931
- Chromosome:
- 17q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
- Gene:
- CSF3R NIH gene
- Name:
- colony stimulating factor 3 receptor
- Previous symbol:
- CD114
- Synonyms:
- GCSFR
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-12-10
- Date modifiied:
- 2019-04-23
Related products to: Human G-CSF Protein Vector: E.Coli
Related articles to: Human G-CSF Protein Vector: E.Coli
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Publication date: 2026/10/02
Zhou XiaoweiLuo FanyanHu QinghuaYu MeihongLi Kaixuan - Macrophages are major contributors to inflammatory responses in acute kidney injury (AKI) and rapidly alter their gene expression through epigenetic regulation. This study focused on ASXL1, a chromatin modifier regulating histone marks consisting of H3K27me3 (repressive) and H3K4me3 (activating) in M1 macrophages. We found that ASXL1-positive M1 macrophages were significantly increased in the unilateral ischemia-reperfusion injury kidneys of male mice in the acute phase. In cultured M1 macrophages, RNA sequencing revealed that Asxl1 knockdown upregulated inflammatory response genes such as Il6 and Il1b. Conversely, the expression of anti-apoptotic genes Csf3 and Lcn2 was suppressed, and pathways related to interleukin-17 signaling and Fcγ receptor-dependent phagocytosis were downregulated. In co-culture experiments, Asxl1 silencing in M1 macrophages induced more severe apoptosis and reduced proliferation of mouse renal cortical tubular cells. Mechanistically, chromatin immunoprecipitation analysis demonstrated that Asxl1 knockdown significantly decreased H3K27me3 levels at the Il6 and Il1b promoter regions and H3K4me3 levels at the Csf3 and Lcn2 promoter regions in M1 macrophages. These findings indicate that ASXL1 suppresses excessive inflammatory cytokine expression and preserves anti-apoptotic activity through histone modifications, while maintaining phagocytic capacity in M1 macrophages. ASXL1 in M1 macrophages thus attenuates inflammatory activation and macrophage-mediated renal tubular cell damage in AKI. - Source: PubMed
Ogura YoshiyasuSugasawa TakehitoNangaku MasaomiMimura Imari - MUC13 is a membrane-bound mucin involved in epithelial protection and barrier maintenance, but its role in nasal epithelial inflammation remains unclear. This study aimed to investigate whether MUC13 regulates inflammatory signaling in primary nasal epithelial cells (NECs). - Source: PubMed
Publication date: 2026/09/24
Zhou JiewenZhang XinyuLi MinZou YuGong YuwenZhao MengqiLi JianWen WeipingZheng Nianzhen - BackgroundNeuroinflammation, particularly involving reactive astrocytes, plays a pivotal role in Alzheimer's disease (AD) progression.ObjectiveHowever, the causal genes and regulatory pathways linking astrocyte reactivity to AD risk remain unclear.MethodsWe performed a multi-omics summary-data-based Mendelian randomization (SMR) analysis, integrating large-scale AD GWAS data with methylation (mQTLs), expression (eQTLs), and protein (pQTLs) data for 514 reactive astrocyte-related genes. Causal inference was strengthened using colocalization and tissue-specific validation, and pathway enrichment.ResultsOur multi-omics SMR analysis identified a core set of high-confidence genes related to reactive astrocytes with putatively causal roles in AD. Based on mQTL-eQTL analysis, (cg08331313), (12 CpG sites), and (4 CpG sites) demonstrated significant regulatory cascades, where methylation changes modulated gene expression and subsequently influenced AD risk. The eQTL-pQTL analysis revealed GCDH as genes with strong expression-protein correlations. Cross-tissue validation between blood and brain pinpointed a robust set of seven genes, including , , and , that consistently associate with AD risk, highlighting systemic effects. Functional and network analyses of these causal candidates revealed that they converge upon the signaling pathway as a central mechanistic hub in both peripheral blood and brain tissue. Furthermore, network analysis identified seven hub genes, including , , and , as critical regulators within this astrocyte-centered AD network.ConclusionsOur study systematically identifies genetically predicted reactive astrocyte-related genes in AD pathogenesis through multi-omics Mendelian randomization, highlighting MAPK signaling as a putatively causal mechanistic hub. - Source: PubMed
Publication date: 2026/09/23
Zhu QiChen WenjieHan Xu - This study investigates the therapeutic potential of the synthetic cannabinoid WIN55,212-2 (WIN55) in temporomandibular joint osteoarthritis (TMJOA), focusing on its capacity to attenuate cartilage degradation and modulate inflammatory pathways, thereby providing preclinical evidence to support future clinical translation. - Source: PubMed
Publication date: 2026/09/18
Guo YimanZhang XinchengZhao ShenBian CeZhu MengyaoSu ChengjunZhang YuqingLiu MiaoKurahara Lin-HaiZhang Ning