Chimpanzee GM-CSF ELISPOT kit, silver staining
- Known as:
- Chimpanzee GM-CSF ELISPOT reagent, silver staining
- Catalog number:
- ct168-pb2
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- U-CyTech biosciences
- Gene target:
- Chimpanzee GM-CSF ELISPOT kit silver staining
Related genes to: Chimpanzee GM-CSF ELISPOT kit, silver staining
- 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: Chimpanzee GM-CSF ELISPOT kit, silver staining
Related articles to: Chimpanzee GM-CSF ELISPOT kit, silver staining
- Palmatine chloride (berbericinine, CHClNO) is a protoberberine alkaloid found in several plants, including Rhizoma Coptidis, Cortex Phellodendri, Rhizoma Corydalis, Guduchi (), and roots. Palmatine chloride (PA) is known as an inhibitor of dopamine generation. However, its effect on endoplasmic reticulum (ER) stress-related macrophage activation caused by endotoxin (lipopolysaccharide) is not yet well known. In this study, the effects of PA on pyroptotic responses of mouse macrophages (RAW 264.7) activated by endotoxin were investigated using Griess reagent assay for nitric oxide (NO) production, fluo-4 assay for cytosolic calcium release, dihydrorhodamine 123 assay for hydrogen peroxide production, multiple cytokine assay for cytokine production, real-time PCR for inflammatory gene transcriptions, and flow cytometry assay for p38 MAPK activation. Preliminary experiments using THP-1 human monocytic cells demonstrated that PA was not cytotoxic and significantly reduced basal NO production. Results revealed that PA significantly reduced excessive production levels of NO, hydrogen peroxide, pro-inflammatory cytokines (such as interleukin (IL)-6, CCL3 (MIP-1α), and CSF2 (GM-CSF)), and cytosolic calcium release in endotoxin-stimulated RAW 264.7, but significantly increased the production of anti-inflammatory cytokine IL-10. PA inhibited endotoxin-induced transcripts of , , , and in activated RAW 264.7. It also decreased p38 MAPK phosphorylation and level of Fas in RAW 264.7 stimulated by endotoxin. To further interpret these findings, a network pharmacology-informed analysis based on large-scale literature mining was performed, supporting the multi-target regulatory role of PA in ER stress-related pathways. Briefly, PA exerts anti-inflammatory effects on endotoxin-stimulated RAW 264.7 via the calcium-CHOP pathway, consequently reducing endotoxin-induced production of pro-inflammatory mediators (NO, cytokines, etc.) and relieving ER stress-related pyroptotic cascade. - Source: PubMed
Publication date: 2026/06/24
Kim Young-JinPark Wansu - Prostate cancer (PCa) exhibits an immune "cold" tumor microenvironment (TME) with significant enrichment of immunosuppressive myeloid-derived suppressor cells (MDSCs), which contribute to tumor progression and poor responses to immune checkpoint blockade (ICB). Although extensively studied, the precise mechanism underlying the tumor-intrinsic signals that educate and sustain the expansion and immunosuppressive function of MDSCs remains unelucidated. Here, we identify a previously unrecognized function of RelB by which nuclear interaction with ILF2 restricts ubiquitin-mediated degradation and sustains nuclear stability of RelB, thereby enhancing RelB-mediated CSF2 transactivation and enhanced GM-CSF (granulocyte-macrophage colony-stimulating factor) production and secretion. The secreted GM-CSF, in turn, promotes RelB nuclear accumulation, forming a feed-forward loop for sustaining GM-CSF generation. In MDSCs, GM-CSF activates STAT3-mediated MDSC expansion and immunosuppression. Disruption of RelB/ILF2 complex attenuates GM-CSF-driven MDSC expansion, restores CD8⁺ T cell-mediated antitumor activity, and inhibits tumor growth. In addition, a RelB-targeting peptide SN52 sensitizes PCa tumors to PD-1 blockade therapy. Collectively, our findings identify the RelB/ILF2-GM-CSF loop as a central regulator of MDSC-mediated immunosuppression, which may be targeted to improve PCa response to ICB. - Source: PubMed
Publication date: 2026/07/11
Xu FanLi MinZhang YuanXu ZhiYin QimingZhang SijiaWu FeiMa YuyanJia ZhangjunWang XiumeiDong JiachenZhou ZiyuLi Jian JianLi XiaoZhang Yanyan - IDH wild-type glioblastoma (IDH-wt GBM) exhibits substantial intratumoral heterogeneity, which contributes to treatment resistance, disease recurrence, and variable clinical outcomes. This study aimed to identify radiomics-based intratumoral heterogeneity (RITH) subtypes in IDH-wt GBM and to assess their prognostic relevance, associated pathomic differences, and transcriptomic associations. - Source: PubMed
Publication date: 2026/07/03
Duan XinNiu WenjuLi XuanLi ZehuiLiang QianYang XiangliTan YanZhang Hui - Ischemic heart disease (IHD) remains the leading cause of mortality worldwide, and the long-term benefits conferred by revascularization are limited. Cardiac shock wave therapy (CSWT) can promote neovascularization and attenuate myocardial injury, and has been applied in the treatment of IHD; its mechanism may involve Circulating Angiogenic cells (CACs) and their key proteins. This study aimed to explore the potential mechanism by which CSWT exerts effects on angiogenesis and attenuates structural damage following Acute Myocardial Infarction (AMI). Using and experiments combined with Olink proteomics, three core regulatory proteins involved in angiogenesis, namely S100A4, CSF2, and FOXO1, were screened. , optimized CSWT enhanced the migration and tube formation of rat bone marrow-derived CACs, as well as the expression of pro-angiogenic factors such as VEGF and HGF. , CSWT after AMI reduced infarct size, elevated the levels of CACs (CD34/CD133) and vascular markers (CD31/-SMA), and modulated 18 differentially expressed proteins. Key regulatory factors S100A4, CSF2, and FOXO1 were identified by Olink proteomics. The expression levels of these proteins were verified by dual qPCR experiments and . The results reveal that CSWT modulates the S100A4/CSF2/FOXO1 network and activates CACs in AMI, suggesting a mechanistic basis for further translational evaluation of CSWT as a potential adjuvant therapy for IHD. - Source: PubMed
Publication date: 2026/06/12
Li YangLi HaoLiu ChenZeng XiaoyingTian XinHu WenwenWang LuqiaoHua BaotongYang Ping - Expression of the Csf1r gene is regulated by a conserved enhancer, the fms-intronic regulatory element (FIRE). In mice with a germ-line deletion of FIRE (Fireko), CSF1R expression is undetectable in bone marrow progenitors and classical monocytes, but monocytopoiesis and non-classical monocyte maturation are unaffected. The loss of CSF1R is overcome in part by CSF2 in vitro and inflammatory recruitment in vivo. Fireko mice lack microglia and subpopulations of tissue-resident macrophages in peritoneum, kidney, heart, adipose, liver, skeletal muscle, pancreas, pituitary, adrenal and gonads. Heterozygous mutation impacts CSF1-induced proliferation and postnatal expansion of tissue macrophages. Physiological functions of the heart and kidney were not affected by the absence of macrophages. In a model of renal injury, macrophage recruitment and histopathology in wild-type and Fireko mice were indistinguishable, but there was a male-specific increase in serum creatinine and urea in the Fireko mice. Tissue-resident macrophages depleted in Fireko mice, including microglia, were replaced by donor-derived cells following intraperitoneal transfer of wild-type bone marrow at weaning. The Fireko mouse provides a platform to dissect functions of tissue-resident macrophages in development, homeostasis and pathology. - Source: PubMed
Publication date: 2026/07/13
Liu YajunJacquelin SebastienTaylor IsisGreen Emma KPatkar Omkar LKeshvari SaharRanpura GinellO'Brien Conan J OJessen ElineMaxwell EmmaAllavena RachelGallerand AlexandreIvanov StoyanAdamson AntonyHumphreys Neil ESummers Kim MIrvine Katharine MHume David A