M-CSF Receptor (Phospho-Tyr809) Antibody
- Known as:
- M-CSF Receptor (Phospho-Tyr809) Antibody
- Catalog number:
- 11906
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- M-CSF Receptor (Phospho-Tyr809) Antibody
Related genes to: M-CSF Receptor (Phospho-Tyr809) Antibody
- 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: M-CSF Receptor (Phospho-Tyr809) Antibody
Related articles to: M-CSF Receptor (Phospho-Tyr809) Antibody
- Cassava-based fufu is widely consumed but nutritionally limited, particularly in micronutrients. Incorporation of orange-fleshed sweet potato (OFSP) may enhance its nutritional value. This study evaluated the nutrient composition, microbial safety, functional properties and contribution to recommended dietary allowance (RDA) of cassava-orange-fleshed sweet potato composite fufu flour for adults and children. Four blends were formulated: CONTROL (100% CF, Control), CSF1 (90% CF:10% OFSPF), CSF2 (80% CF:20% OFSPF), and CSF3 (70% CF:30% OFSPF). Nutrient composition, functional properties, microbial safety, pasting behavior, carotene content, and sensory attributes were analyzed using standard methods. Moisture (5.54-6.41%), ash (1.05-2.10%), crude fiber (0.23-1.91%), fat (1.80-9.96%), protein (2.02-7.82%), and carbohydrates (77.60-87.32%) varied significantly (p < 0.05) across blends. Pasting properties revealed: peak time (46.4 -5.63 s), pasting temperature (74.47-77.53 °C). Peak viscosity (26.0-44.6 RVU), minimum viscosity (12.67-14.83RVU), Ultimate viscosity (18.1-31.5 RVU), Attenuation value (142.5-354.5 RVU), and regeneration value (63.0-208 BVU). These results indicate that the inclusion of OFSPF modifies starch gelatinization behavior and improves paste stability. Microbial counts remained within safe limits during storage, with sample CSF2 (80% CF:20% OFSPF) and CSF1 (90% CF:10% OFSPF) having no fungal growth at 35 days. Although CSF3 exhibited the highest carotene (276.87 µg/g) and protein contents (7.82%), CSF2 provided a more balanced combination of nutrient enhancement and functional properties, and was therefore considered the most suitable formulation. This product has potential as a food-based strategy to combat micronutrient deficiencies in vulnerable populations. - Source: PubMed
Publication date: 2026/07/23
Elemuo G KUdemba C ONjuwa E GOnwuzuruike U AEmetole J M - 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 - 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