rHu MCSF
- Known as:
- rHu MCSF
- Catalog number:
- AK8238-1000
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- Akro
- Gene target:
- rHu MCSF
Related genes to: rHu MCSF
- Gene:
- CSF1 NIH gene
- Name:
- colony stimulating factor 1
- Previous symbol:
- -
- Synonyms:
- M-CSF, MCSF, MGC31930
- Chromosome:
- 1p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-01-14
- 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: rHu MCSF
Related articles to: rHu MCSF
- 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 heart and kidney were not affected by the absence of macrophages. In a model of renal injury macrophage recruitment and histopathology in WT and Fireko mice were indistinguishable but there was a male-specific increase in serum creatinine and urea in the Fireko. 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: 2026/06/26
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 - Murine and human immune systems differ significantly, particularly within the myeloid lineage. Humanized mice, generated by transplanting human hematopoietic stem, progenitor cells into genetically modified mice, are invaluable to study human immune development and function in vivo. However, a major limitation of current models is suboptimal myelopoiesis, particularly lack of functional human neutrophils, hampering the modeling of human immune responses and chronic diseases. Here, we describe a humanized mouse model, named MaGIC for genes replaced, in the strain, which improves human myelopoiesis and enables development of functional human neutrophils. In MaGIC mice, human cytokines M-CSF/CSF1(M), GM-CSF/CSF2(G) and IL-6(I) are knocked-in replacing mouse genes and murine (a) are deleted. Human THPO in these mice supports human hematopoiesis. More importantly, insertion of human CD47 (C) under the control of endogenous mouse CD47 promoter enables xenotransplantation and human neutrophil development. MaGIC mice support all human neutrophil subsets found in human bone marrow and blood, a major improvement. This is achieved by creating a niche postirradiation for human granulocyte-macrophage progenitors via reduced murine CD47 and physiological levels of human CD47. These mice also have mature human monocytes, tissue macrophages, alveolar macrophages, dendritic cells, and NK cells, enabled by humanized M-CSF and GM-CSF. Human neutrophils in MaGIC mice are fully functional in chemotaxis, phagocytosis, reactive oxygen species production, and neutrophil extracellular trap formation in response to inflammation. MaGIC mice address critical gaps in current models and enable incisive translational research on human neutrophils, advancing studies in infectious, autoimmune, and inflammatory diseases. - Source: PubMed
Publication date: 2025/09/16
Sefik EsenPhilbrick WilliamZhang FengruiAgrawal KritiVan Lee BrianSam JohannesKaratepe KutayZheng YunjiangLiang KaixinPeng SophiaMirza HarisRangavajhula AthreyaSimon PerrineArun NehaBabu PriyankaEynon ElizabethChiorazzi MichaelShan LiangHalene StephanieLuo Hongbo RRongvaux AnthonyKluger YuvalFlavell Richard A - Head and neck squamous cell carcinoma (HNSCC) is the seventh most prevalent cancer worldwide. Despite intensive treatments, the prognosis is unfavorable. Recently, immunotherapy has emerged as a novel therapeutic strategy, and several immune-checkpoint blockade blockers provide clinical benefits to patients. However, the response rates of these antibodies are limited, and there is a pressing need to increase the efficacy of immunotherapy for HNSCC patients. Epigenetic treatment is emerging as a promising combination approach able to change immune-related gene signatures in tumors and potentially increase the efficacy of immunotherapy. In this study, we sought to elucidate further immune-related gene signatures altered through epigenetic treatment and explored whether epigenetic drugs can increase the efficacy of anti PD-L1 treatment in HNSCC. - Source: PubMed
Publication date: 2025/07/23
Fukumoto ChonjiSadhukhan PritamShibata MasahiroUgurlu Muhammed TGoldberg RachelSidransky DavidMarchionni LuigiSillé Fenna C MHoque Mohammad Obaidul - Blockade of immune checkpoints, such as programmed death-ligand 1 (PD-L1), has shown promise in cancer treatment; however, clinical response remains limited in many cancer types. Our previous research demonstrated that p300/CBP mediates the acetylation of the PD-L1 promoter, regulating PD-L1 expression. In this study, we further investigated the role of the p300/CBP bromodomain in regulating PD-L1 expression using CCS1477, a selective bromodomain inhibitor developed by our team. We found that the p300/CBP bromodomain is essential for H3K27 acetylation at PD-L1 enhancers. Inhibiting this modification significantly reduced enhancer activity and PD-L1 transcription, including exosomal PD-L1, which has been implicated as key contributors to resistance against PD-L1 blockade therapy in various cancers. Furthermore, CCS1477 treatment resulted in a marked reduction of myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME) by inhibiting key cytokines such as IL6, CSF1, and CSF2, which are crucial for MDSC differentiation and recruitment. By reducing PD-L1 expression and modulating the immunosuppressive TME, CCS1477 creates a more favorable environment for tumor-infiltrating lymphocytes, significantly enhancing the efficacy of immune checkpoint blockade (ICB) therapy. Notably, these effects were observed in both prostate cancer and melanoma models, underscoring the broad therapeutic potential of p300/CBP bromodomain inhibition in improving ICB outcomes. - Source: PubMed
Publication date: 2025/04/21
Liu JinghuiWang XinyiHe DahengMaasoumyhaghighi HamedNouri MansourehWu MengPeng JiaRao XiongjianWang RuixinWu SaiWang JianlinBrooks NigelPegg NeilFrese KrisLi ZhiguoLiu Xiaoqi - In inflammation, osteopontin (OPN) acts as both a stone matrix component for calcium oxalate (CaOx) crystal formation and an inflammatory mediator. While previous studies have demonstrated the individual roles of OPN and macrophages (Mφ) in renal CaOx stone formation during inflammation, their interaction remains poorly understood. This study aimed to elucidate the role of OPN in modulating Mφ function during crystal formation, using an ex vivo model. Bone marrow-derived macrophages (BMDM) were isolated from eight-week-old male C57BL/6J wild-type and OPN knockout mice. BMDMs from OPN-positive (BMDM) and OPN-negative (BMDM) mice were co-cultured with fluorescently labeled CaOx monohydrate (COM) crystals for phagocytosis assays and analyzed using the IN Cell Analyzer 6000. We further performed real-time quantitative reverse transcription PCR and RNA sequencing to identify gene expression profiles and clarify the role of OPN in Mφ function. The assay analysis demonstrated that phagocytosis rates were significantly higher in BMDM than in BMDM. Inflammatory markers, such as IL-6, TNF, CD44, were upregulated following COM exposure, and IL-6 expression was significantly lower in BMDM than in BMDM. RNA sequencing revealed that BMDM exhibited a less pro-inflammatory and more anti-inflammatory phenotype (Csf2, Irf5, Itgax, Csf1, Cd163), resembling M2-like Mφs. Further functional analysis indicated that OPN knockdown in Mφs increased the S100 family and CREB signaling, which enhanced the M2-like phenotype shift and phagosome formation. In conclusion, OPN plays a critical role in enhancing pro-inflammatory Mφ function, potentially limiting COM phagocytosis. Modulating OPN expression in circulating Mφs may represent a therapeutic approach for kidney stone disease. - Source: PubMed
Publication date: 2025/03/25
Hattori TatsuyaTaguchi KazumiChaya RyosukeHamamoto ShuzoOkada AtsushiYasui Takahiro