GM-CSF Clone 'SPM482 antibody Host Rat
- Known as:
- GM-CSF Clone 'SPM482 (anti-) Host Rat
- Catalog number:
- 'AM11171PU-S
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GM-CSF Clone 'SPM482 antibody Host Rat
Related genes to: GM-CSF Clone 'SPM482 antibody Host Rat
- 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: GM-CSF Clone 'SPM482 antibody Host Rat
Related articles to: GM-CSF Clone 'SPM482 antibody Host Rat
- 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 - Platelet transfusion refractoriness (PTR) is a common and clinically challenging condition with complex underlying mechanisms. Human leukocyte antigen (HLA) alloimmunization is the principal cause of immune PTR (iPTR), whereas non-HLA antibodies (non-HLA Abs) are known to contribute to antibody-mediated rejection, microvascular inflammation, interstitial fibrosis, and graft loss. However, whether non-HLA Abs contribute to the development of PTR and how they are associated with HLA alloimmunization remain unclear. - Source: PubMed
Publication date: 2026/07/30
Qi JunZhu HuachaoWang ManniWang TianjuLi YuhuiShang LixiaChen LeWang XiaofangShao JingMa ChaofengXu Hua - The aim of this study was to generate lentiviral vectors carrying an array of AP-1 motifs driving luciferase gene expression as reporters of Mitogen Activated Protein Kinase (MAPK) activity. We created a series of vectors based on LeGO-iG that were used to generate stably transduced leukaemia cell lines. A vector termed LEGO-AP1 × 6-GM55 containing an array of 6 AP-1 sites linked to the minimal CSF2 promoter was sufficient to support high levels of MAPK-inducible luciferase activity in leukaemic cell lines that was suppressed by MAPK inhibitors. The inclusion of a putative chromatin priming element encompassing RUNX and ETS motifs increased the activity of these vectors. The additional inclusion of the full-length mouse CSF2 promoter, or the human DUSP5 promoter further increased the MAPK-dependent activity of these vectors in leukaemic cells. These vectors support moderate levels of constitutive activity in cells carrying mutations that activate the RAS/RAF/MEK MAPK signalling pathway, and high-level activity after direct activation of MAPK signalling. They also respond to T cell receptor activation via MAPK and Ca2+ signalling pathways. This resource will now make it easier to track receptor or oncogene-inducible MAPK activity in cultured cells, and potentially in tumours, in close to real time. TEASER ABSTRACT: Here we developed a series of lentiviral luciferase reporter vectors activated by RAS/RAF/MAPK signalling to AP-1. These vectors are activated in response to signalling driven by most of the signalling mutations detected in cancer cells or by receptors that control cell growth, differentiation and activation. These vectors have been optimised based on pathways known to activate gene expression in acute myeloid leukaemia or in activated T cells. The regulatory elements tested in these vectors includes an array of 6 AP-1 sites, the CSF2 promoter, the DUSP5 promoter and a chromatin priming element that binds RUNX and ETS factors. - Source: PubMed
Publication date: 2026/08/13
Coleman Danial J LAmes LukeAain HurooulGamble JoannaKoscielniak KingaZhang ZijinLau CherisseJoyce AbigailCockerill Peter N