G-CSF, Mouse Protein
- Known as:
- G-CSF, Mouse Protein
- Catalog number:
- z03163-50
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- G-CSF Mouse Protein
Related genes to: G-CSF, Mouse Protein
- 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: G-CSF, Mouse Protein
Related articles to: G-CSF, Mouse Protein
- 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 - Mycoplasma pneumoniae pneumonia (MPP) can cause serious extrapulmonary complications, including life-threatening thrombosis. This study aimed to elucidate the roles of neutrophils and neutrophil extracellular traps (NETs) in vascular endothelial cell (EC) activation in pediatric MPP-associated thrombosis. We analyzed the relationship between neutrophils and thrombosis in children with MPP and used mouse models of neutrophilia (Csf3 plasmid injection), neutropenia (Csf3 deficient, Csf3-/-), and defective NETs formation (Pad4 deficient, Pad4-/-). The effects of neutrophils and NETs on EC activation were further examined in vivo, in vitro, and in human samples. Elevated neutrophil count was observed in patients with thrombosis and functioned as a potential diagnostic marker as well as a risk factor for MPP-associated thrombosis. EC activation was enhanced in MPP mice with neutrophilia but attenuated in neutropenic or Pad4-/- mice. NETs activated ECs through TLR2 and JAK/STAT3 signaling, and inhibition of NETs formation (Cl-amidine), TLR2 (C29), and JAK (upadacitinib) each attenuated this response. Strong correlations among neutrophils, NETs, EC activation, and thrombosis were observed in pediatric patients. These findings suggest that neutrophils promoted thrombosis in MPP via NETs-mediated EC activation involving TLR2 and JAK/STAT3 signaling. This study provides mechanistic insights into the inflammatory-thrombotic processes in MPP-associated thrombosis and offers a rationale for further investigation of neutrophils, NETs, TLR2, and JAK/STAT3 signaling in this context. - Source: PubMed
Publication date: 2026/09/22
Huang XiaZhu YifanGuo YunLv TianGu HaiyanLuo YingyingLi DanSun HangZhao DeyuLiu Feng - Excessive conjunctival fibroblast proliferation is a major factor in postoperative scarring following ophthalmic surgery. While Rebamipide is clinically used for dry eye and has anti-inflammatory effects, its direct impact on the transcriptomic profiles and inflammatory signaling of conjunctival fibroblasts remains unclear. We aimed to elucidate the gene expression pathways by which Rebamipide modulates the inflammatory and fibrotic responses of Primary Human Conjunctival Fibroblasts (HCFCs). - Source: PubMed
Publication date: 2026/09/09
Kinari GenTagami MizukiKira YukimiHaruna YusukeMisawa NorihikoMizukami YoichiHonda Shigeru