Search results for: Recombinant Human IL-16 [+His] Proteins
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[Recombinant human IL-16 inhibits proliferation and induces apoptosis in MT-4 cells].To investigate the effects of recombinant human IL-16 (rhIL-16) on the proliferation and apoptosis of MT-4 cells.
1731 related Products with: [Recombinant human IL-16 inhibits proliferation and induces apoptosis in MT-4 cells].Macrophage Colony Stimula Macrophage Colony Stimula Recombinant Human Interle Recombinant Human Inhibin Recombinant Human p16-INK Recombinant Human Interle Recombinant Human Involuc Recombinant Human Inhibin Apoptosis (Human) Antibod Recombinant Human HGF [fr Human Small Intestine Mic Recombinant Human Interle
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[Cloning and prokaryotic expression of human secreted IL-16 gene].To clone human secreted IL-16 cDNA, construct its prokaryotic expression vector and express it in E.coli DH5α.
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Role of interleukin 16 in multiple myeloma.Multiple myeloma is a malignancy characterized by the expansion of a plasma cell clone that localizes to the human bone marrow. Myeloma cells and bone marrow stromal cells produce soluble factors that promote the survival and progression of multiple myeloma. Interleukin 16 (IL-16) is involved in regulating the migration and proliferation of normal leukocytes. However, the role of IL-16 in human cancers, including multiple myeloma, is unclear.
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Increased expression of S100 calcium binding protein A8 in GM-CSF-stimulated neutrophils leads to the increased expressions of IL-8 and IL-16.In our previous proteomic surveillance, we found that at least 11 proteins in neutrophils were increased more than 2.5-fold by the stimulation of GM-CSF. In this paper, focusing on one of the 11 proteins, S100 calcium binding protein A8 (S100A8), we tried to elucidate the effect of S100A8 and the cooperative effect of S100A8 and GM-CSF on production and secretion of cytokines of neutrophils.
2280 related Products with: Increased expression of S100 calcium binding protein A8 in GM-CSF-stimulated neutrophils leads to the increased expressions of IL-8 and IL-16.Human S100 Calcium Bindin Recombinant Human S100B C Chicken S100 calcium bind S100 alpha - Rabbit polyc ELISA kit Calcyclin,Chick calcium binding protein P Native Influenza HA (A To FIV Core Ag, recombinant Rabbit Anti-Human Toll In Rat monoclonal anti mouse FDA Standard Frozen Tissu Rat intestinal fatty acid
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Down-regulation of interleukin-16 in human mast cells HMC-1 by Clostridium difficile toxins A and B.Toxin A (TcdA) and toxin B (TcdB) are the major virulence factors of Clostridium difficile and are the causative agents for clinical symptoms, such as secretory diarrhoea and pseudomembranous colitis. Mast cells are essentially involved in the toxin-induced colonic inflammatory processes. To study the direct effects of these toxins on the expression of inflammatory genes, a DNA microarray containing evaluated probes of 90 selected inflammatory genes was applied to the immature mast cell line HMC-1. TcdA and TcdB induced up-regulation of only a limited number of genes within the early phase of cell treatment. Interleukin-8 (IL-8), transcription factor c-jun and heme oxygenase-1 messenger RNA (mRNA) increased more than 2-fold. In contrast, IL-16, known as a CD4(+) T-cell chemoattractant factor and the chemokine receptor cKit were down-regulated. Stimulation of HMC-1 cells with IL-8 had no effect on IL-16 mRNA level, indicating that both cytokines were independently affected by the toxins. Regulation of both cytokines, however, depended on glucosylation of Rho GTPases as tested by application of enzyme-deficient TcdA or TcdB. Down-regulation of total and secreted IL-16 protein was checked by enzyme-linked immunosorbent assay. The data implicate that TcdA and TcdB affect lymphocyte migration by modulating release of the chemoattractant factor IL-16 from mast cells. In addition, this is the first report showing that Rho GTPases are involved in the regulation of IL-16 expression.
2163 related Products with: Down-regulation of interleukin-16 in human mast cells HMC-1 by Clostridium difficile toxins A and B.Interleukin-24 antibody S interleukin 17 receptor C ELISA Human , Interleukin Rabbit Anti-Human Inhibin Anti-human C1 Esterase In MID1 interacting G12-like Inhibin beta-A antibody S Rabbit Anti-intestinal FA Protease Inhibitor 15 ant Astra Blue 6GLL, Stain fo Rat monoclonal anti mouse Interferon alpha-6 antibo
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[Serum cytokine profiling of prostate cancer and benign prostatic hyperplasia using recombinant antibody microarray].To identify the differential expressions of serum cytokines between prostate cancer (PCa) and benign prostatic hyperplasia (BPH), and provide proteomic evidence for the early diagnosis of PCa.
2724 related Products with: [Serum cytokine profiling of prostate cancer and benign prostatic hyperplasia using recombinant antibody microarray].Anti-Human Benign Prostat Prostate cancer, PIN (pro Anti-Human Benign Prostat Top 4 types of cancer (co Prostate cancer and hyper Prostate cancer, hyperpla Tissue microarray of top Prostate cancer and hyper Top 4 types of cancer (co Prostate cancer and hyper Prostate cancer, hyperpla Prostate cancer, hyperpla
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Immunomodulation of caprine lentiviral infection by interleukin-16.Interleukin-16 (IL-16) is a proinflammatory cytokine produced by a variety of cells including lymphocytes, macrophages, mast cells, and eosinophils. We have shown in our previous studies increased expression of IL-16 mRNA and protein in caprine arthritis-encephalitis virus (CAEV)-infected goats blood. In this study, we determined the immunomodulatory effects of IL-16 in vitro using cells derived from CAEV infected and uninfected goats. Human recombinant IL-16 (rhIL-16) significantly increased chemotaxis of peripheral blood mononuclear cells (PBMCs) of both control and CAEV-infected goats. Pretreatment of PBMC with anti-goat CD4 monoclonal antibody inhibited IL-16-induced chemotaxis of PBMC of control and infected goats suggesting that IL-16 exerts its action in goats primarily by binding to CD4. The CAEV proviral DNA was less in caprine monocytes treated with rhIL-16 infected in vitro with CAEV. These data suggest inhibitory effect of IL-16 on viral integration. Flow cytometric studies indicated a trend toward IL-16-induced increased expression of lymphocyte activation markers. Combined with our previously reported data, these experiments suggest that increased IL-16 expression during CAEV infection may inhibit viral integration.
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IL-16 signaling specifically induces STAT6 activation through CD4.Biologic activities of IL-16 have been well described (e.g., chemotaxis of CD4+ cells, CD25 upregulation, secretion of IL-1b, IL-4 and TNF-a secretion) but very few signaling events have been described. To gain a better understanding of how the biologic activities of IL-16 are regulated following receptor engagement (CD4) we have analyzed the activation state of numerous STAT proteins in primary human peripheral blood mononuclear cells (PBMCs) and the human monocytic cell line THP-1 following IL-16 stimulation. Of the four STAT proteins tested, only STAT6 was activated (phosphorylated) in a dose-dependant manner by IL-16. The activation of STAT6 was completely abolished when IL-16 was pre-incubated with soluble CD4 (the IL-16 cell surface receptor), demonstrating the need for CD4 engagement in STAT6 activation. These results are the first to demonstrate a link between IL-16 and STAT6 activation.
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Interleukin-16 inhibits immunoglobulin e production by B lymphocytes.The increased production of IgE is a hallmark of atopic disorders. CD4+ T cells regulate the production of Immunoglobulin (Ig) E by B cells. Interleukin (IL) 16, a CD4+ specific cytokine, is highly expressed at sites of allergic inflammation. Our aim was to determine the effect of IL-16 on IgE production in atopic subjects.
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