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
- BackgroundSystemic inflammation has been implicated in cognitive aging and neurodegeneration; however, inflammatory biomarkers are expressed in coordinated patterns rather than as isolated markers.ObjectiveTo identify latent inflammatory biomarker groupings and evaluate their associations with cognitive performance among midlife and older adults.MethodsThis cross-sectional study included 334 participants from the Aging Research Characterizing Health Exposome via Social Drivers (ARCHES) study. Cognitive performance was assessed using the Preclinical Alzheimer Cognitive Composite (PACC). Plasma inflammatory biomarkers were quantified using the NuLISA™ multiplex immunoassay platform. Exploratory factor analysis (EFA) (minimum residual extraction, oblimin rotation) identified latent inflammatory factors, retaining biomarkers with loadings ≥0.40. Factor scores were evaluated in multivariable linear regression models adjusted for age, sex, education, and genotype status; sensitivity analyses adjusted for socioeconomic context, medication use, BMI, lifestyle factors, and clinical diagnoses. Age-stratified and nonlinear spline analyses were conducted.Results27 of 43 biomarkers formed an eight-factor structure explaining 43% of variance. Two factors were significantly associated with cognitive performance after FDR correction. Factor 4 (CCL4, CXCL1, S100A12) and Factor 5 (IL2, IL5, IL13, IL10, CSF2) were inversely associated with PACC scores. These associations remained consistent across sensitivity analyses. Age-stratified analyses showed that several inflammatory factors were associated with cognitive performance among participants aged 45-<65 years, whereas no factors remained significant among participants aged ≥65 years after FDR correction. Nonlinear modeling indicated a non-linear age-cognitive performance relationship.ConclusionsEFA identified clusters of correlated inflammatory biomarkers associated with cognitive performance in this cohort of midlife and older adults. - Source: PubMed
Publication date: 2026/09/02
Singh Ramkrishna KBekena SemereWalker Alexis I BTaylor KaylinZhu YiqiPal SubrataMohamed Essa ATrani Jean-FrancoisKaplan IanBabulal Ganesh M - IL-17-producing Type 17 T (T17) cells are central drivers of inflammation in both psoriasis and hidradenitis suppurativa (HS), as evidenced by the clinical efficacy of IL-17-targeting therapies. However, therapeutic responses differ substantially between diseases, raising the possibility that the composition and regulation of T17 states are disease context dependent. - Source: PubMed
Publication date: 2026/08/14
Park NayoungLee JongeunKim DayeonRambhia DarshnaKim JaebumZhou WeiCao JunyueKrueger James GKo YounheeKim Jaehwan - Chronic exposure to endocrine-disrupting chemicals has been increasingly recognized as a potential contributor to cancer progression. Monobutyl phthalate (MBP), a major metabolite of dibutyl phthalate, is widely detected in human biological samples, yet its long-term impact on anaplastic thyroid cancer (ATC) has not been systematically investigated. CAL-62 cells were continuously exposed to an environmentally relevant concentration of MBP (10 nM) over 3 months to establish a chronic exposure model that mimics long-term environmental exposure. Transcriptomic profiling was integrated with network toxicology to identify key molecular pathways and hub genes, followed by molecular docking and Western blot validation. Chronic MBP exposure significantly enhanced cell viability, proliferation, colony formation, and tumorsphere formation, indicating promotion of malignant phenotypes. Transcriptomic profiling revealed extensive molecular remodeling characterized by activation of inflammation-associated pathways, including cytokine-cytokine receptor interaction, IL-17, TNF, and JAK-STAT signaling, accompanied by suppression of p53- and mTOR-related pathways. Integrated analysis identified 57 overlapping KEGG pathways, with IL6 and CSF2 emerging as central hub genes. Molecular docking demonstrated favorable binding affinities between MBP and representative target proteins, including IL6, TP53, CASP3, BCL2, and PPARG. Western blot analysis further confirmed increased IL6 and BCL2 expression together with decreased TP53, CASP3, and PPARG expression following chronic MBP exposure. Chronic environmentally relevant MBP exposure promotes ATC malignant progression through coordinated inflammation-associated molecular network remodeling accompanied by suppression of apoptosis-related signaling. Integrating network toxicology with transcriptomic profiling provides an effective systems-level strategy for identifying biologically relevant molecular networks underlying chronic environmental toxicant exposure. - Source: PubMed
Publication date: 2026/08/04
Deng YuTan SongweiWei JinlanGuo XingyueHu LongqingQu XincaiZhou Jing - Porcine reproductive and respiratory syndrome virus (PRRSV) infection often causes severe immunosuppression in pigs. However, the mechanisms by which PRRSV antagonizes host antiviral immune responses remain incompletely understood. We found that granulocyte-macrophage colony-stimulating factor (CSF2) was significantly upregulated in porcine alveolar macrophages (PAMs) upon PRRSV infection. CSF2 upregulation inhibits PRRSV replication by promoting IL15 expression, and Fos-related antigen 1 (FRA1) enhances the antiviral activity of the CSF2-IL15 axis via transcriptional regulation. Further investigation revealed that the PRRSV N protein directly interacts with HSPA1B and activates HSPA1B-mediated chaperone-mediated autophagy (CMA) to degrade FRA1, thereby antagonizing host antiviral immunity. Our study reveals that the PRRSV N protein promotes FRA1 autophagic degradation by upregulating heat shock protein HSPA1B, thereby suppressing the host CSF2-IL15 antiviral pathway. This study provides new insights into the arms race between PRRSV and the host, as well as novel perspectives for the development of anti-PRRSV infection strategies. - Source: PubMed
Publication date: 2026/08/21
Liu XiaoZhang JianwuYan XiaoyangMeng YinanWang HaozheLv FangPeng BoZheng ZifangLi YangFeng YingtongXu LeleXiao Shuqi - Platelet-rich plasma (PRP) has emerged as a promising therapy for post-viral olfactory dysfunction (PVOD) though its biological mechanisms remain unclear. This study evaluated clinical outcomes and targeted proteomic changes following PRP for refractory PVOD. - Source: PubMed
Publication date: 2026/08/14
Li Vivienne MLee Jennifer SKurabi ArwaZhou ThomasFaraji FarhoudYan Carol H