Mouse G-CSF ELISA kit (4X96T)
- Known as:
- Mouse G-CSF Enzyme-linked immunosorbent assay test reagent (4X96T)
- Catalog number:
- LF-EK50636
- Product Quantity:
- 4
- Category:
- Elisa Kits
- Supplier:
- Abfron
- Gene target:
- Mouse G-CSF ELISA kit (4X96T)
Related genes to: Mouse G-CSF ELISA kit (4X96T)
- 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: Mouse G-CSF ELISA kit (4X96T)
Related articles to: Mouse G-CSF ELISA kit (4X96T)
- Peri-implantitis (PI) is a multifactorial chronic inflammatory disease characterized by persistent mucosal inflammation and progressive marginal bone loss, yet the tissue architecture and cellular programs that sustain chronic inflammation remain incompletely defined. Here, we integrate single-cell and spatial transcriptomic analyses with targeted validation to map the PI microenvironment and its regulatory circuits. PI lesions exhibit marked immune enrichment, including expansion of CXCR4⁺ aged neutrophils with enhanced survival signaling consistent with apoptosis delay. Spatial and communication analyses reveal a PI-specific stromal-myeloid organization in which fibroblast-rich regions are closely associated with myeloid hotspots and display heightened CXCL- and CSF-related signaling. Within the fibroblast compartment, inflammatory myofibroblasts emerge as a prominent predicted source within a CXCL/CSF-enriched secretory program, with CXCL6 and CSF3 highlighted as candidate mediators of neutrophil recruitment and survival. Functionally, blockade of the CXCR2 axis reduces neutrophil infiltration and mitigates peri-implant bone resorption. Upstream regulatory analyses nominate STAT4 as a candidate upstream regulator of the inflammatory stromal program; pharmacologic perturbation with lisofylline reduces CXCL6/CSF3 expression, weakens neutrophil chemotaxis, partially restores apoptosis sensitivity, and alleviates inflammation and bone loss in vivo. Together, these findings support a stromal-neutrophil circuit that sustains chronic inflammation in PI and highlight stromal inflammatory programs and neutrophil recruitment/survival pathways as potential therapeutic entry points. - Source: PubMed
Publication date: 2026/07/01
Lin WeiminAltayar Bassam AJiang ShuangHe KunZhao YiWu QinghengLin YumengXing MalcolmYuan Quan - Severe congenital neutropenia (SCN) is a genetically heterogeneous condition. Reaching a molecular diagnosis is important for management, prognostication, and risk assessment. We present the first confirmatory report of a previously proposed SCN due to a homozygous pathogenic loss-of-function variant in CSF3. Our report supports this new gene-disease relationship in humans. - Source: PubMed
Publication date: 2026/06/25
Almannai MohammedAlhanshani Ahmed ABakur KhadijahAlkuraya Fowzan S - Syphilis serofast, characterized by persistent seropositivity despite adequate treatment and symptom resolution, poses significant clinical challenges. This study investigated the immunological basis of serofast status, focusing on CD3 T-cell populations and cytokine profiles. - Source: PubMed
Publication date: 2026/06/20
Qiang DiPeng MinZhang WangyuTan Mengjun - The development of vaccines against Mycoplasma ovipneumoniae (MO) and the screening of novel therapeutic agents are hindered by the lack of a stable animal model for evaluation. Hu sheep, as a predominant breed in intensive farming systems, are highly susceptible to MO infection. Therefore, we established a MO infection model in Hu sheep to investigate the reasons for their susceptibility to MO. We collected tissue samples from the lung junction at the interface between diseased and healthy areas for pathological examination and transcriptomic analysis. Differentially expressed genes were screened and subjected to functional enrichment analysis, enabling an in-depth discussion of the mechanisms by which MO damages the lungs of Hu sheep. The study found that following infection with MO, Hu sheep exhibit a gradual rise in body temperature during the initial phase of infection. After several days of persistent fever, the temperature gradually returns to normal, while body weight shows a downward trend. Twenty-one days after infection with MO, hepatization of lung tissue was observed in the right apical lobe of the lung in Hu sheep. Histopathological sections from the lesion-control interface revealed thickened alveolar septa with extensive infiltration of red blood cells and inflammatory cells. Transcriptome sequencing identified 899 differentially expressed genes (|log2(Fold Change)| ≥ 1, padj≤ 0.05), comprising 535 upregulated genes and 364 downregulated genes. GO enrichment analysis indicates that the core functions of differentially expressed genes are concentrated in two biological processes: immune system processes and immune responses. KEGG enrichment analysis revealed that differentially expressed genes were significantly enriched across 28 distinct signaling pathways, identifying multiple key metabolic pathways associated with MO infection. These primarily encompassed the IL-17 signaling pathway, Toll-like receptor signaling pathway, NF-κB signaling pathway, TNF-α signaling pathway, and natural killer cell-mediated cytotoxicity pathways. We have additionally identified multiple genes associated with MO infection, including CCL19, CCL20, TNFSF11, CXCL8, CXCL11, CCR10, CSF3, IL2RA, CXCL1, CD40, BBOX1, and BPIFB1. These discoveries lay the groundwork for establishing MO infection models and investigating the mechanisms underlying sheep susceptibility. - Source: PubMed
Publication date: 2026/06/16
Zhao GuangxinCheng GuojieLiu WenjunGuo KepengSun YanmingZhang Yanbing - Neutrophil extracellular traps (NETs) are increasingly recognized as key regulators of tumor progression, yet the molecular circuitry that governs their induction in cancer remains elusive. Here, we identify the RNA-binding protein RBFOX2 as a tumor suppressor that curtails glioma growth by coordinately restraining tumor cell proliferation and NETosis. RBFOX2 expression is markedly reduced in glioma and positively correlates with patient survival. Mechanistically, RBFOX2 binds to 5-hydroxymethylcytidine (5hmC)-modified sites within PDGFB mRNA and promotes its decay, thereby dampening AKT-SP1 signaling and repressing CSF3 transcription. This repression limits neutrophil-mediated NET formation in the tumor microenvironment, as confirmed in PAD4 mice and upon CSF3 neutralization. Collectively, our study uncovers a 5hmC-dependent post-transcriptional mechanism linking RBFOX2 to NETosis control and glioma suppression, revealing RBFOX2 as a potential biomarker and therapeutic lever and establishing a broader paradigm in which RNA-binding proteins couple post-transcriptional RNA modification and immune regulation in tumor evolution. - Source: PubMed
Publication date: 2026/06/11
Chen XiDai WeiweiWang HanlinFang JianingYin BowenLiu ChangweiChen YulingWu RuixinCai YihengBian ShashaHai RihanLi JinZhu YiqianShu Minfeng