Recombinant Mouse GM-CSF
- Known as:
- Recombinant Mouse GM-CSF
- Catalog number:
- SJF05-01
- Product Quantity:
- 10jg/vial
- Category:
- -
- Supplier:
- amoytop
- Gene target:
- Recombinant Mouse GM-CSF
Ask about this productRelated genes to: Recombinant Mouse GM-CSF
- 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: Recombinant Mouse GM-CSF
Related articles to: Recombinant Mouse GM-CSF
- Photodynamic therapy (PDT) is a promising treatment for cholangiocarcinoma (CCA), but its efficacy is limited by robust tumor antioxidant defenses and immunosuppressive microenvironment. Disrupting the expression of SLC6A6, a taurine transporter critical for redox homeostasis, represents a promising strategy for sensitizing CCA cells to PDT by disrupting taurine-mediated antioxidant protection. - Source: PubMed
Publication date: 2026/06/02
Zhu JingjinZou TianhaoWang WeiminXu JianjunLi XuanLiu LeiYang BohanSong ZifangGao Yang - Periodontitis is a complex inflammatory disease in which chronic immune activation drives destruction of periodontal soft tissues and alveolar bone. Although early-onset forms show high heritability, much genetic risk remains unresolved. To identify shared genetic signals across early- and later-onset periodontitis, we combined two European genome-wide association study datasets (3183 cases, 10 326 controls) and applied Fisher's combined probability test (FCOMB) and effect-size-based genome-wide association meta-analysis (GWAMA) across > 7 million variants to capture shared signals with either heterogeneous or more concordant effect sizes. We confirmed known associations at SIGLEC5 and DEFA1A3 and identified several additional suggestive loci. Among these, FCOMB highlighted the strongest signal at the long non-coding RNA LINC01541 (rs11876034, P = 1.7 × 10-6). We evaluated the biological relevance of LINC01541 by repressing it in gingival fibroblasts using CRISPR interference. Knockdown led to significant downregulation of inflammatory mediators, including CSF2 and CSF3, regulators of neutrophil recruitment, members of the interleukin (IL) family (IL1B, IL36B, IL36RN), and chemokines (CXCL5, CXCL8, CCL20). Six of the top ten differentially expressed genes belonged to an epithelial keratinization expression cluster. Gene-set enrichment analyses following linc01541 knockdown demonstrated repression of cytokine signaling, with IL-10 signaling most affected (padj = 5.3 × 10-14; AUC = 0.81), alongside activation of cell-cycle pathways (padj = 3.3 × 10-24; AUC = 0.73). We demonstrated the utility of aggregating heterogeneous samples to detect modest but biologically meaningful genetic effects. The convergence of the genetic association at LINC01541 with functional evidence suggests that this lncRNA modulates an upstream mucosal inflammatory axis relevant to periodontal pathogenesis. - Source: PubMed
Richter Gesa MAkinloye Oluwabukunmi MKühnlenz TimWeiner January RdHoltfreter Birtede Coo AliciaDiz-De Almeida SilviaLoos Bruno GJepsen SørenDommisch HenrikBruckmann CorinnaKapferer-Seebacher InesHomuth GeorgKocher ThomasVölzke HenryBerger KlausLaudes MatthiasLieb Wolfgangvan der Velde Nathalievan Schoor Natasja Mde Groot LisetteBlanco JuanCarracedo AngelCruz RaquelDempfle AstridTeumer AlexanderFreitag-Wolf SandraSchaefer Arne S - Allergic asthma and allergic rhinitis (AR) are among the most frequent chronic conditions in the pediatric age. They frequently coexist in children and are sustained by type 2- driven airway inflammation and impaired epithelial-immune interactions. Immunonutritional and postbiotic strategies have been proposed as adjunctive therapeutic approaches for these diseases. - Source: PubMed
Publication date: 2026/05/27
Caldaria ErikaIorio RaffaeleMarziali DarioOglio FrancaCadavere AlessiaMasino AntonioAgizza AlessandraCoppola SerenaCarucci Laura - 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