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Granulocyte_Macrophage Colony Stimulating Factor (GM_CSF), Clone CC305, Mab anti_Bovine; ELISA_WB

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[#YSRTMCA1828] Granulocyte_Macrophage Colony Stimulating Factor (GM_CSF), Clone CC305, Mab anti_Bovine; ELISA_WB

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YSRTMCA1828 | Granulocyte_Macrophage Colony Stimulating Factor (GM_CSF), Clone CC305, Mab anti_Bovine; ELISA_WB, 0.5 mg.
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(1) Unusual Presentation of Severe Endobronchial Obstruction Caused by Cryptococcus gattii in a Child: Case Report and Literature Review Severe Endobronchial Cryptococcosis in a Child.[TOP]

Pubmed ID :30339241
Publication Date : //
Disease caused by Cryptococcus gattii typically manifests as meningoencephalitis or pulmonary nodules. Endobronchial lesions are rare, and most cases are caused by Cryptococcus neoformans. We describe here a case of endobronchial disease in a child caused by C gattii. The disease spectrum in this patient was notable for the discovery of anti-granulocyte macrophage colony-stimulating factor autoantibodies.

Authors : Huynh Julie, Saddi Vishal, Cooper Peter, Cheng Alan T, Meyer Weiland, Chen Sharon, Isaacs David,



(2) Heme oxygenase-1 protects airway epithelium against apoptosis by targeting the proinflammatory NLRP3-RXR axis in asthma.[TOP]

Pubmed ID :30333233
Publication Date : //
Asthma is thought to be caused by malfunction of type 2 T helper cell (Th2)-mediated immunity, causing excessive inflammation, mucus overproduction, and apoptosis of airway epithelial cells. Heme oxygenase-1 (HO-1) functions in heme catabolism and is both cytoprotective and anti-inflammatory. We hypothesized that this dual function may be related to asthma's etiology. Using primary airway epithelial cells (pAECs) and an asthma mouse model, we demonstrate that severe lung inflammation is associated with rapid pAEC apoptosis. Surprisingly, NOD-like receptor protein 3 (NLRP3) inhibition, retinoid X receptor (RXR) deficiency, and HO-1 induction were associated with abrogated apoptosis. MCC950, a selective small-molecule inhibitor of canonical and noncanonical NLRP3 activation, reduced RXR expression, leading to decreased pAEC apoptosis that was reversed by the RXR agonist adapalene. Of note, HO-1 induction in a mouse model of ovalbumin-induced eosinophilic asthma suppressed Th2 responses and reduced apoptosis of pulmonary pAECs. In vitro, HO-1 induction desensitized cultured pAECs to ovalbumin-induced apoptosis, confirming the in vivo observations. Critically, the HO-1 products carbon monoxide and bilirubin suppressed the NLRP3-RXR axis in pAECs. Furthermore, HO-1 impaired production of NLRP3-RXR-induced cytokines (interleukin [IL]-25, IL-33, thymic stromal lymphopoietin [TSLP] and granulocyte-macrophage colony-stimulating factor [GM-SCF]) in pAECs and lungs. Finally, we demonstrate that HO-1 binds to the NACHT domain of NLRP3 and the RXRα and RXRβ subunits and that this binding is not reversed by Sn-protoporphyrin. Our findings indicate that HO-1 and its products are essential for pAEC survival to maintain airway epithelium homeostasis during NLRP3-RXR-mediated apoptosis and inflammation.

Authors : Lv Jiajia, Su Wen, Yu Qianying, Zhang Meng, Di Caixia, Lin Xiaoliang, Wu Min, Xia Zhenwei,



(3) Humanized 3F8 Anti-GD2 Monoclonal Antibody Dosing With Granulocyte-Macrophage Colony-Stimulating Factor in Patients With Resistant Neuroblastoma: A Phase 1 Clinical Trial.[TOP]

Pubmed ID :30326045
Publication Date : //
Chimeric and murine anti-GD2 antibodies are active against neuroblastoma, but the development of neutralizing antibodies can compromise efficacy. To decrease immunogenicity, hu3F8, a humanized anti-GD2 antibody, was constructed.

Authors : Kushner Brian H, Cheung Irene Y, Modak Shakeel, Basu Ellen M, Roberts Stephen S, Cheung Nai-Kong,



(4) Involvement and Possible Role of Eosinophils in Asthma Exacerbation.[TOP]

Pubmed ID :30323811
Publication Date : //
Eosinophils are involved in the development of asthma exacerbation. Recent studies have suggested that sputum and blood eosinophil counts are important factors for predicting asthma exacerbation. In severe eosinophilic asthma, anti-interleukin (IL)-5 monoclonal antibody decreases blood eosinophil count and asthma exacerbation frequency. However, even in the absence of IL-5, eosinophilic airway inflammation can be sufficiently maintained by the T helper (Th) 2 network, which comprises a cascade of vascular cell adhesion molecule-1/CC chemokines/eosinophil growth factors, including granulocyte-macrophage colony-stimulating factor (GM-CSF). Periostin, an extracellular matrix protein and a biomarker of the Th2 immune response in asthma, directly activates eosinophils . A major cause of asthma exacerbation is viral infection, especially rhinovirus (RV) infection. The expression of intercellular adhesion molecule (ICAM)-1, a cellular receptor for the majority of RVs, on epithelial cells is increased after RV infection, and adhesion of eosinophils to ICAM-1 can upregulate the functions of eosinophils. The expressions of cysteinyl leukotrienes (cysLTs) and CXCL10 are upregulated in virus-induced asthma. CysLTs can directly provoke eosinophilic infiltration and activate eosinophils . Furthermore, eosinophils express the CXC chemokine receptor 3, and CXCL10 activates eosinophils . Both eosinophils and neutrophils contribute to the development of severe asthma or asthma exacerbation. IL-8, which is an important chemoattractant for neutrophils, is upregulated in some cases of severe asthma. Lipopolysaccharide (LPS), which induces IL-8 from epithelial cells, is also increased in the lower airways of corticosteroid-resistant asthma. IL-8 or LPS-stimulated neutrophils increase the transbasement membrane migration of eosinophils, even in the absence of chemoattractants for eosinophils. Therefore, eosinophils are likely to contribute to the development of asthma exacerbation through several mechanisms, including activation by Th2 cytokines, such as IL-5 or GM-CSF or by virus infection-related proteins, such as CXCL10, and interaction with other cells, such as neutrophils.

Authors : Nakagome Kazuyuki, Nagata Makoto,



(5) Pathologic Fibroblasts in Idiopathic Subglottic Stenosis Amplify Local Inflammatory Signals.[TOP]

Pubmed ID :30322354
Publication Date : //
Objective To characterize the phenotype and function of fibroblasts derived from airway scar in idiopathic subglottic stenosis (iSGS) and to explore scar fibroblast response to interleukin 17A (IL-17A). Study Design Basic science. Setting Laboratory. Subjects and Methods Primary fibroblast cell lines from iSGS subjects, idiopathic pulmonary fibrosis subjects, and normal control airways were utilized for analysis. Protein, molecular, and flow cytometric techniques were applied in vitro to assess the phenotype and functional response of disease fibroblasts to IL-17A. Results Mechanistically, IL-17A drives iSGS scar fibroblast proliferation ( P < .01), synergizes with transforming growth factor ß1 to promote extracellular matrix production (collagen and fibronectin; P = .04), and directly stimulates scar fibroblasts to produce chemokines (chemokine ligand 2) and cytokines (IL-6 and granulocyte-macrophage colony-stimulating factor) critical to the recruitment and differentiation of myeloid cells ( P < .01). Glucocorticoids abrogated IL-17A-dependent iSGS scar fibroblast production of granulocyte-macrophage colony-stimulating factor ( P = .02). Conclusion IL-17A directly drives iSGS scar fibroblast proliferation, synergizes with transforming growth factor ß1 to promote extracellular matrix production, and amplifies local inflammatory signaling. Glucocorticoids appear to partially abrogate fibroblast-dependent inflammatory signaling. These results offer mechanistic support for future translational study of clinical reagents for manipulation of the IL-17A pathway in iSGS patients.

Authors : Morrison Robert J, Katsantonis Nicolas-George, Motz Kevin M, Hillel Alexander T, Garrett C Gaelyn, Netterville James L, Wootten Christopher T, Majka Susan M, Blackwell Timothy S, Drake Wonder P, Gelbard Alexander,



(6) The role of IL-3 in bone.[TOP]

Pubmed ID :30320936
Publication Date : //
In the recent past, there has been a burgeoning interest in targeting cytokines such as IL-3 for specific disease conditions of bone such as rheumatoid arthritis and multiple myeloma. Unlike other cytokines, IL-3 is a cytokine with a multilineage potential and broad spectrum of target cells and it plays a vital role in hematopoiesis. Due to its common receptor subunit, the action of IL-3 shows functional redundancy with other cytokines such as the granulocyte-macrophage colony-stimulating factor and IL-5. IL-3 has been successfully used in ameliorating radiation-induced bone marrow aplasia and similar conditions. However, the role of IL-3 in bone cells has not been fully unraveled yet; therefore, the aim of this overview is to present the effects of IL-3 in bone with a special emphasis on osteoclasts and osteoblasts in a concise manner.

Authors : Soysa Niroshani Surangika, Alles Neil,



(7) Lung Single-Cell Signaling Interaction Map Reveals Basophil Role in Macrophage Imprinting.[TOP]

Pubmed ID :30318149
Publication Date : //
Lung development and function arises from the interactions between diverse cell types and lineages. Using single-cell RNA sequencing (RNA-seq), we characterize the cellular composition of the lung during development and identify vast dynamics in cell composition and their molecular characteristics. Analyzing 818 ligand-receptor interaction pairs within and between cell lineages, we identify broadly interacting cells, including AT2, innate lymphocytes (ILCs), and basophils. Using interleukin (IL)-33 receptor knockout mice and in vitro experiments, we show that basophils establish a lung-specific function imprinted by IL-33 and granulocyte-macrophage colony-stimulating factor (GM-CSF), characterized by unique signaling of cytokines and growth factors important for stromal, epithelial, and myeloid cell fates. Antibody-depletion strategies, diphtheria toxin-mediated selective depletion of basophils, and co-culture studies show that lung resident basophils are important regulators of alveolar macrophage development and function. Together, our study demonstrates how whole-tissue signaling interaction map on the single-cell level can broaden our understanding of cellular networks in health and disease.

Authors : Cohen Merav, Giladi Amir, Gorki Anna-Dorothea, Solodkin Dikla Gelbard, Zada Mor, Hladik Anastasiya, Miklosi Andras, Salame Tomer-Meir, Halpern Keren Bahar, David Eyal, Itzkovitz Shalev, Harkany Tibor, Knapp Sylvia, Amit Ido,



(8) Targeting MAPK (p38, ERK, JNK) and inflammatory CK (GDF-15, GM-CSF) in UVB-Activated Human Skin Cells with Vitis vinifera Seed Extract.[TOP]

Pubmed ID :30317975
Publication Date : //
Ultraviolet B radiation (UVB) activates mitogen-activated protein kinases (MAPK): p38, extracellular signal regulated (ERK), and c-Jun N-terminal (JNK) kinases in human skin cells. Human keratinocytes (KC) exposed to UVB secrete several cytokines (CK), among which the growth differentiation factor-15 (GDF-15) is augmented in inflammatory and aging processes and the granulocyte macrophage-colony stimulating factor (GM-CSF) is involved in cell proliferation, differentiation, and survival, and both CK have implications in skin carcinogenesis. We assessed p38, ERK, JNK, GDF-15, and GM-CSF in UVB-exposed skin cells and a red grape (Vitis vinifera) seed extract's (GSE) capacities to regulate these pathways in UVB-exposed KC. Two concentrations of the GSE extract were selected: GSE1 (37.5 μgEqGA/mL) and GSE2 (75 μgEqGA/mL) and a UVB dose (100 mJ/cm2) within the physiological range. Molecules were assessed with ELISA, semiquantitative results being confirmed by Western blot. UVB triggered the signaling molecules' phosphorylation and the concentrations of CK. All molecules but GM-CSF increased early, at 2 h, from UVB exposure while GM-CSF increased later (at 8 h). MAPK and GDF-15 were regulated by GSE1; GM-CSF, by the higher concentration, GSE2. The amplitude and kinetics of the responses were diverse according to time point, molecules, and the extract's concentration. GSE exerted beneficial effects on MAPK and CK triggered by UVB in human skin cells: reduction of phosphorylation of the assessed signaling molecules and anti-inflammatory effects. Targeting MAPK and specific inflammatory mediators such as GDF-15 and GM-CSF with GSE in UVB-induced skin cells represents a novel and a promising starting point for future photoprotection strategies.

Authors : Decean Hana Petra, Brie Ioana Carmen, Tatomir Corina Bianca, Perde-Schrepler Maria, Fischer-Fodor Eva, Virag Piroska,



(9) Hematopoietic growth factors and tumor angiogenesis.[TOP]

Pubmed ID :30312730
Publication Date : //
Angiogenesis is regulated by numerous "classic" factors such as vascular endothelial growth factor (VEGF) and many other endogenous "non-classic"peptides, including erythropoietin (Epo), and granulocyte-/granulocyte macrophage colony stimulating factor (G-/GM-CSF). The latter play an important regulatory role in angiogenesis, especially under pathological conditions and constitute a crosslink between angiogenesis and hematopoiesis. This article reviews studies on the ability of hematopoietic cytokines to affect several endothelial cell functions in tumor angiogenesis. These findings in all these studies support the hypothesis formulated at the beginning of this century that a common ancestral cell, the hemangioblast, gives rise to cells of both the endothelial and the hematopoietic lineages.

Authors : Ribatti Domenico, Tamma Roberto,



(10) Block of Granulocyte-Macrophage Colony-Stimulating Factor Prevents Inflammation-Induced Preterm Birth in a Mouse Model for Parturition.[TOP]

Pubmed ID :30296925
Publication Date : //
A multitude of factors promotes inflammation in the reproductive tract leading to preterm birth. Macrophages peak in the cervix prior to birth and their numbers are increased by the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF). We hypothesize GM-CSF is produced from multiple sites in the genital tract and is a key mediator in preterm birth.

Authors : Nold Christopher, Stone Julie, O'Hara Kathleen, Davis Patricia, Kiveliyk Vladislav, Blanchard Vanessa, Yellon Steven M, Vella Anthony T,