GM_CSF, Human, Recombinant, E.coli
- Known as:
- GM_CSF, Human, Recombinant, E.coli
- Catalog number:
- MSF0501
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- GM_CSF Human Recombinant .coli
Related genes to: GM_CSF, Human, Recombinant, E.coli
- Gene:
- CSF2 NIH gene
- Name:
- colony stimulating factor 2
- Previous symbol:
- -
- Synonyms:
- GM-CSF, GMCSF
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2018-12-12
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
Related products to: GM_CSF, Human, Recombinant, E.coli
Related articles to: GM_CSF, Human, Recombinant, E.coli
- The immunosuppressive tumor microenvironment (TME) is a cardinal driver of immune escape and resistance to immunotherapy in renal cell carcinoma (RCC). The N6-methyladenosine (mA), the most prevalent RNA modification, critically governs tumor aggressiveness and TME reprogramming. We aimed to exploit whether and how tumor-intrinsic mA modification driven by ZC3H13 (zinc finger CCCH-type containing 13) can dictate the immune landscape of RCC. - Source: PubMed
Publication date: 2026/05/20
Zheng JinxiuZhao XuetingMen QingZhou MengyiChe YuxinLiu ShengluZan LikunGuo LingzhiShao YingGao ShuhuaMa YanjieLiu XiaofengYang LijunYang Tao - Colon adenocarcinoma (COAD) remains a leading cause of cancer-related mortality worldwide, partly due to the lack of robust biomarkers for early diagnosis and accurate prognosis. Glycoproteins play critical roles in tumorigenesis and may serve as promising sources of biomarkers. This study aimed to identify glycoprotein-related candidate diagnostic and prognostic biomarkers for COAD through integrated bioinformatics approaches and experimental validation. Gene expression profiles and clinical information of COAD patients were obtained from The Cancer Genome Atlas database (TCGA). The expression data for genes associated with glycoprotein were retrieved from the UniProt database. Furthermore, we assessed the mRNA expression levels of the glycoprotein FJX1 in COAD and rectal adenocarcinoma tissues through in situ hybridization (ISH) staining using tissue microarrays. A total of 228 glycoprotein-related differentially expressed genes (DEGs) were identified, enriched in the extracellular matrix organization and signaling pathways such as PI3K-Akt and cAMP. Protein-protein interaction (PPI) network analysis revealed 10 hub genes (LIFR, CNTFR, LIF, CSF2, IL1A, CSF3, F2, FGA, FGFR2, INHBA). Survival screening and multivariate Cox regression identified FJX1 as an independent prognostic factor for overall survival after adjusting for age and stage. FJX1 mRNA was significantly overexpressed in COAD tissues compared to normal (p < 0.001), and high FJX1 expression correlated with advanced T stage, M stage, and pathological stage. ISH confirmed elevated FJX1 mRNA in tumors. Immune infiltration analysis further revealed that high FJX1 expression was associated with increased infiltration of M0 macrophages and neutrophils, and decreased resting memory CD4 T cells, suggesting a potential role in shaping the immunosuppressive tumor microenvironment. GSEA revealed significant enrichment of MAPK signaling in high-FJX1 tumors. In conclusion, this study identified 10 glycoprotein-related hub genes as candidate diagnostic biomarkers warranting further validation and established FJX1 as an independent prognostic biomarker for COAD. FJX1 overexpression is associated with tumor progression and may be linked to MAPK signaling as well as immune modulation. These findings provide a foundation for glycoprotein-based biomarker development in COAD. - Source: PubMed
Publication date: 2026/05/18
Liu HaiyunWan LinjingFang Quangang - Myocardial infarction (MI) triggers a robust inflammatory response that is essential for tissue repair but, when excessive or prolonged, drives pathological cardiac remodelling and heart failure. Colony-stimulating factor 2 (CSF2) signalling has been implicated in driving pro-inflammatory macrophage activation post-MI. Here, we investigated the role of macrophage-specific CSF2 receptor alpha (CSF2RA) signalling in post-MI remodelling using a tamoxifen-inducible genetic mouse model and permanent coronary artery ligation. Macrophage-specific Csf2ra deficiency significantly improved left ventricular systolic function post-MI without altering cardiac fibrosis burden. Functional improvement was associated with enhanced collagen scar maturation, characterised by an increased proportion of mature collagen fibres, and with accumulation of anti-inflammatory, pro-reparative macrophages within the infarct. These macrophage changes were accompanied by increased fibroblast density, consistent with altered macrophage-fibroblast crosstalk. Collectively, these findings identify macrophage-intrinsic CSF2RA signalling as a critical regulator of inflammatory resolution and scar maturation after MI and provide mechanistic support for the rationale of selective CSF2RA inhibition as a therapeutic strategy to limit adverse cardiac remodelling and improve post-infarction recovery. - Source: PubMed
Publication date: 2026/04/24
Kremastiotis GeorgiosLi YongBond AndrewShanahan DaireDi Gregoli KarinaPoole Alastair WGeorge Sarah JJohnson Jason L - Breast cancer remains a significant global health challenge, necessitating the development of innovative therapeutic strategies. This study aims to integrate immunotherapy and suicide gene therapy for breast cancer treatment. The cytokines IL-2 and GM-CSF, which are crucial in orchestrating immune responses against cancer, are the focal points of investigation. This study focused on the co-expression of these cytokines alongside apoptin, a promising protein derived from chicken anemia virus, via the bidirectional survivin promoter (pAIG). The constructed vectors were transfected into MCF-7 cells, which resulted in a significant increase in gene expression. Compared with individual cytokine and apoptin vectors (pIG and pA), the pAIG vector exhibited superior efficacy, reducing cell viability and inducing apoptosis (31.7%) at 72 h post-transfection. Exploration of the interaction of apoptin revealed its association with the human PIK3R1 protein, which interacts with both cytokines, contributing to the inhibition of cell viability. Leveraging the survivin promoter for co-expression presents a promising avenue for targeted breast cancer gene therapy, potentially disrupting intricate signaling networks involved in cancer progression. This study provides valuable insights into the synergistic effects of IL-2, GM-CSF, and apoptin co-expression, offering a compelling approach to advancing breast cancer treatment. These findings contribute to the broader landscape of cancer gene therapy, emphasizing the potential of combining immunomodulatory agents and gene-directed approaches to improve therapeutic outcomes. - Source: PubMed
Barzegari OmidGhadimi FatemehShamsabadi Fatemeh TGolalipour MasoudShahbazi Majid - establishes infection in hosts by deploying effector proteins that reprogram cytokine-driven immunity. While protozoan parasite-encoded macrophage migration inhibitory factor (MIF) homologs exemplify cytokine mimicry, whether targets additional host cytokine axes remains unclear. Here, we identify a 3-ketoacyl-CoA reductase (KCR) as a noncanonical cytokine modulator that engages the granulocyte-macrophage colony-stimulating factor (CSF2) receptor alpha chain (CSF2Rα). In HEK293T cells, forward and reverse co-immunoprecipitation (Co-IP) assays demonstrated a specific interaction between KCR and murine CSF2Rα. The recombinant KCR triggered rapid activation of canonical CSF2 signaling in RAW264.7 macrophages, inducing phosphorylation of JAK2 and STAT5 to levels comparable to murine CSF2. Functionally, KCR enhanced NADPH oxidase-dependent oxidative responses, increasing intracellular reactive oxygen species (ROS) and upregulating transcripts encoding core oxidase subunits, including CYBB, CYBA, NCF1, and NCF2. KCR also promoted phagocytic capacity, elevating FITC-dextran uptake and inducing expression of complement, Fc, and scavenger receptor genes, including CR3, CD16, CD64, MSR1, and MARCO. Notably, KCR pretreatment attenuated CSF2-induced JAK2/STAT5 phosphorylation, ROS production, and phagocytosis, consistent with competitive interference with endogenous CSF2-CSF2R signaling. Together, these findings reveal KCR as a previously unrecognized factor that targets the CSF2/CSF2R axis to recalibrate macrophage effector functions, expanding the repertoire of parasite strategies for cytokine pathway modulation and highlighting CSF2-CSF2R signaling as a potential interface for mechanistic and therapeutic investigation in toxoplasmosis. - Source: PubMed
Publication date: 2026/05/09
Mei JiePu XianglinZhang MengkaiLiu YueMeng ChuangXu LixinSong XiaokaiYan RuofengLi XiangruiLu Mingmin