GMCSF protein (Mouse)
- Known as:
- GMCSF protein (Mouse)
- Catalog number:
- 30r-2189
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- GMCSF protein (Mouse)
Related genes to: GMCSF protein (Mouse)
- 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
Related products to: GMCSF protein (Mouse)
Related articles to: GMCSF protein (Mouse)
- Colorectal cancer (CRC) remains the most prevalent malignancy of the digestive system globally and ranks second in cancer-related deaths worldwide. Metabolic reprogramming is one of the hallmarks of cancer. Aspartate is a proteinogenic non-essential amino acid with several essential functions in cancer cells. SLC1A3 is the main aspartate transporter, but its role in CRC needs to be elucidated. We found that SLC1A3 is significantly overexpressed in CRC tissues compared to adjacent normal tissues, and elevated SLC1A3 expression is associated with poor prognosis. Further, SLC1A3 could enhance the proliferation, invasion, migration of CRC cells and organoids by activating the DAG/PKC/MDM2 signaling axis. In addition, we revealed that SLC1A3 in CRC cells could induce the immunosuppressive M2 phenotype of macrophages via upregulating IL17c and CSF2. In sum, these findings suggest that SLC1A3 plays a dual role in CRC progression and may represent a promising target for therapeutic intervention. - Source: PubMed
Publication date: 2026/04/26
Deng ChaoZhou YouSong SijieLiu HongtaoLiao SiqiZhou LiChen SiyuanZhou ZhihangHe SongLiu Bingrong - Cryptococcus gattii is an emerging fungal pathogen that is acquired through the respiratory tract and causes invasive infections in both immunocompromised and otherwise healthy people. Many of these apparently immunocompetent patients are subsequently found to have autoantibodies against the pleiotropic cytokine GM-CSF. In this study, we investigated the potential role of GM-CSF (or CSF2) in the host response to C. gattii using a murine model of infection. Interestingly, infected Csf2-/- mice were found to have significantly improved survival and decreased lung fungal burden compared to wild type (WT) mice. We determined that during C. gattii infection, GM-CSF promotes the differentiation of monocytes into alveolar and interstitial macrophages. When these macrophages are ablated in CCR2-DTR+ mice, there is a corresponding improvement in survival with decreased lung fungal burden, thus phenocopying Csf2-/- mice. WT bone-marrow derived macrophages challenged with C. gattii and interstitial and alveolar macrophages from infected WT mice are unable to undergo M1 polarization, suggesting that monocyte-derived macrophages (moMacs) are rendered permissive for fungal proliferation. Therefore, GM-CSF and moMacs mediate immune responses that are harmful to the host. We further found that GM-CSF and moMacs preferentially promote the influx of eosinophils over neutrophils into the infected lung which is associated with substantial inflammatory lung pathology. Ablation of neutrophils using Mrp8cretg iDTR+ mice significantly increased C. gattii burden in the lungs, indicating that GM-CSF and moMacs block the entry of these beneficial, fungal-clearing granulocytes during infection. Altogether, our results show that GM-CSF plays a key role in impeding host anti-fungal responses to C. gattii by coordinating monocyte-derived macrophages and granulocyte activity and crosstalk. - Source: PubMed
Publication date: 2026/04/07
Ricafrente AlisonAcharya SreemoyeeChen ShuyiAbass AdizaArshakyan AelitaOlson Tyler JTrivedi ApurwaHeung Lena J - Cow's milk allergy (CMA) is one of the most common food allergies in childhood frequently associated with body growth impairment and micronutrient deficiencies. Immunonutrition approach with selected bioactive compounds may have beneficial effects on nutritional status and immune tolerance mechanisms. We evaluated the effects of an immunonutrition approach, based on the use of a novel multicomponent food supplement containing prebiotics, postbiotics, vitamin D3, docosahexaenoic acid (DHA), extracts, and Quercetin in children with CMA. - Source: PubMed
Publication date: 2026/03/16
Carucci LauraCaldaria ErikaOglio FrancaIorio Raffaele FedericoMauriello VittoriaMasino AntonioCoppola Serena - Myofibroblastic cancer-associated fibroblasts (myoCAFs) represent a crucial stromal cell subpopulation associated with tumor growth, relapse, and metastasis. In this study, we identify a noncanonical mechanism through which head and neck cancer cells regulate myoCAF activation. Co-culture with tumor organoids promoted the expression of cytokine interaction-related genes and myoCAF phenotypic markers in paracancerous fibroblasts (PFs). Cytokine and tissue array analyses revealed that upregulation of colony-stimulating factor-2 (CSF2) in tumor cells correlated with overexpression of nicotinamide N-methyltransferase (NNMT) in CAFs. Notably, CSF2 treatment enhanced myoCAF properties in a NNMT-dependent manner, while NNMT overexpression remained largely unaffected by transforming growth factor-β (TGF-β). In both assembled organoid and xenograft models, tumor growth was reduced when either CSF2 in cancer cells or CSF2 receptor subunit CSF2RA in CAFs was knocked down. Mechanistically, CSF2 induced FOS phosphorylation at Ser32, promoting nuclear translocation of phosphorylated FOS (p-FOS) to regulate NNMT transcription. In drug screening assays, CSF2 blockade partially overcame resistance to TGF-β inhibition. These findings establish the CSF2/FOS/NNMT axis as a TGF-β-independent pathway driving myoCAF activation. - Source: PubMed
Publication date: 2026/03/28
Li RuiYang XiaoLi YitongDuan YilingWu YufeiZhao HuiShang Zhengjun - Allergic diseases, encompassing allergic asthma, atopic dermatitis, food allergies, have emerged as substantial global public health challenges, with IgE-stimulated mast cell and basophil playing pivotal roles in disease pathogenesis. Our prior research has indicated the potential therapeutic effects of Ginkgo biloba leaf (GBL) extracts in IgE-mediated mast cell degranulation. The present study aimed to identify key genes and pathways associated with IgE-mediated mast cell and basophil responses and explore the mechanisms of GBL components. Initially, DEGs and WGCNA analysis were employed to preliminarily identify candidate genes associated with IgE stimulation in GSE96696 dataset. Subsequently, transcriptomic analysis was conducted on an anti-DNP IgE-induced RBL-2H3 degranulation model to validate the key genes, including Egr1, Tnfaip3, Nfkbid, Il13, Nfkbia, Il3, Il4, Ccl7, Cdkn1a, Csf2, Rel, alongside crucial signaling pathways such as NF-κB, and PI3K-AKT pathways. Machine learning algorithms were then applied to confirm the predictive capacity of key genes. Building upon these findings, molecular biology experiments, molecular docking, and molecular dynamics simulations demonstrated that GBL flavonoids, including quercetin, amentoflavone, ginkgetin, and bilobetin, significantly inhibited the release of cytokines, blocked calcium ion influx, and suppressed degranulation potentially by targeting RELA and AKT1. Collectively, our findings not only identify key genes for IgE-mediated response but also provide preliminary mechanistic insights into GBL. - Source: PubMed
Publication date: 2026/03/19
Ren YueWu MinxuanLiu KaiyangZhang LingheZhang YanlingQin Wen