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
Ask about this productRelated 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
- 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 - Acrossocheilus fasciatus is an emerging economically important fish species in China, and Streptococcus agalactiae infection may pose a potential threat to its aquaculture. However, the epigenetic regulatory mechanisms underlying the response of A. fasciatus to S. agalactiae infection remain unclear. In this study, histological observation, RNA-seq, and ATAC-seq were integrated to systematically investigate tissue damage, transcriptomic changes, and chromatin accessibility dynamics in the brain of A. fasciatus after S. agalactiae infection. Histopathological analysis showed obvious lesions in the brain, intestine, and spleen of infected fish. ATAC-seq analysis revealed marked changes in chromatin accessibility in the brain, with 128,083, 163,535, and 142,031 accessible chromatin peaks identified at 0 h, 48 h, and 72 h, respectively. RNA-seq analysis identified 5406 and 7840 differentially expressed genes at 48 h and 72 h, respectively. These genes were mainly associated with biological processes such as immune response, response to stimulus, and signal transduction and were enriched in immune-related pathways, including cytokine-cytokine receptor interaction and TNF signaling pathway. Integrated ATAC-seq and RNA-seq analysis at 48 h identified 2193 overlapping genes showing both differential chromatin accessibility and differential expression. Among them, 513 genes exhibited increased chromatin accessibility accompanied by transcriptional upregulation and were mainly enriched in the NF-κB signaling pathway, T cell receptor signaling pathway, and TNF signaling pathway. Further analysis identified several candidate immune-related genes, including BCL6, CXCL12, SOCS3, CSF3, IL7R, and RHOH. Motif enrichment analysis suggested that transcription factors such as PHA-4, COUP-TFII, EAR2, Nkx6.1, and Isl1 may be involved in infection-associated transcriptional regulation. This study provides the first epigenetic insight into the brain response of A. fasciatus to S. agalactiae infection and offers a new framework for understanding host immune regulation in this species. - Source: PubMed
Publication date: 2026/06/02
Fang WenbinHuang RenxuanWu ZihangTong WanqingHu MinghaoLi YanhongZheng Shanjian