Human GM-CSF Protein Vector: HEK293
- Known as:
- Human GM-CSF Protein Vector: HEK293
- Catalog number:
- 10177-HCyH
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human GM-CSF Protein Vector: HEK293
Related genes to: Human GM-CSF Protein Vector: HEK293
- 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: Human GM-CSF Protein Vector: HEK293
Related articles to: Human GM-CSF Protein Vector: HEK293
- Chlorella vulgaris, a unicellular freshwater microalga, is widely recognised as a functional food and supplement with immunomodulatory properties attributed to its bioactive components. These bioactive components include proteins, fatty acids, polysaccharides, pigments, and antioxidants. Nonetheless, a comprehensive gene-expression profile related to the innate and adaptive immune responses of C. vulgaris supplementation is lacking. This study aimed to evaluate the immunomodulatory effects of C. vulgaris in a mouse model through the oral administration of C. vulgaris biomass into BALB/c mice. Seven days after the oral administration, spleen tissues were analysed via a qPCR array to assess the expression of 84 genes related to the innate and adaptive immune response. Results show a significant upregulation (fold change > 2.0) of seven essential immune genes, such as Irf7, Mpo, Stat1, Tlr6, Tlr7, Tlr9, and Tyk2. In contrast, five immune-related genes, including Ccl5, Ccr6, Csf2, Myd88, and Rorc, were significantly downregulated (fold change <-2.0). These results show a comprehensive immune-gene expression profile elicited following seven days after the oral administration of C. vulgaris in mice. This work offers novel insights into the immunomodulatory properties of C. vulgaris through the immune gene expression profile it exhibited and underscores its known potential as an alternative therapy to boost immunity in various health conditions. - Source: PubMed
Publication date: 2025/11/14
Robben Dexter MillerAmin ZarinaBudiman CahyoKumar Vijay Subbiah - To investigate the role and underlying mechanisms of colony-stimulating factor 2 (CSF2) in the progression of kidney renal clear cell carcinoma (KIRC). - Source: PubMed
Publication date: 2025/10/28
Song YuanSu HusongFan YuHuang JunfengXue Sheng - This study delineates a hierarchical signaling axis driving gastric cancer (GC) progression through integrated transcriptomic and functional analyses. Single-cell sequencing and TCGA data identified CSF2 as a key oncogene, with elevated expression correlating with poor prognosis. Mechanistically, the transcription factor HES1 directly activates IGF2BP2 transcription, as confirmed by chromatin immunoprecipitation and dual-luciferase assays. IGF2BP2 subsequently stabilizes CSF2 mRNA via N6-methyladenosine (mA) modification, validated through RNA immunoprecipitation and mRNA decay kinetics. Functional interrogation revealed that the HES1-IGF2BP2-CSF2 axis promotes GC cell growth, motility, and infiltrative capacity while inhibiting apoptosis. Critically, this axis orchestrates glycolytic reprogramming, evidenced by upregulated HK2/PKM2/LDHA expression, increased lactate/ATP production, and enhanced glycolytic flux. In vivo xenografts demonstrated accelerated tumor growth upon axis activation, with immunohistochemistry showing elevated Ki67 and reduced apoptosis. These results establish a novel signaling cascade wherein HES1 transcriptionally integrates IGF2BP2-mediated mA epitranscriptomics and metabolic rewiring to fuel GC aggressiveness. - Source: PubMed
Publication date: 2025/11/08
Du JunLi LeiChen BanglingChen YuzhongWang QingkangMa Jiachi - Eosinophils play an important role in mediating itch and inflammation in dermatitis. The role of the eosinophil granule protein eosinophil peroxidase (EPX) in mediating inflammation and itch was tested in a dermatitis mouse model. Mice were sensitized to trimellitic anhydride (TMA) and subsequently challenged chronically on the ear to establish dermatitis. Loss of EPX (in EPX (-/-) mice) or blocking EPX with the drug resorcinol significantly reduced dermatitis in mice exposed to TMA. Resorcinol also reduced levels of thymic stromal lymphopoietin protein (TSLP) in skin. Further studies showed that EPX increased different cytokines in keratinocytes in cell culture via two distinct mechanisms. EPX induced TSLP expression requires lysophosphatidic acid signaling while EPX induced expression of TNF-a, CSF2, CSF3, and IL1a required IL-1 signaling. We also showed that blocking IL-1 reduced inflammation in skin following TMA exposure in mice. Thus, EPX is an important mediator of inflammation and itch, that are mediated via at least two pathways. This suggests that both EPX and its signaling pathways may provide novel therapeutic strategies in dermatitis. - Source: PubMed
Publication date: 2025/11/08
Kornfield JamesRoth-Carter Quinn RLuo HuijunOchkur Sergei IJacobsen Elizabeth AFryer Allison DLee James JJacoby David B - , a dematiaceous fungus, causes serious infections such as phaeohyphomycosis. These infections can severely impair patient quality of life and may be life-threatening. Current understanding of host immune defenses against this pathogen remains limited. - Source: PubMed
Publication date: 2025/10/20
Dong QiLu JiejieLiu MengyingWu WeiweiKang YuyingZhang Ruijun