Cytokines & Chemokines

Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) was initially characterized as a growth factor that can support the in vitro colony formation of granulocyte-macrophage progenitors. Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) is produced by a number of different cell types, including activated T cells, B cells, macrophages, mast cells, endothelial cells, and fibroblasts, in response to cytokine of immune and inflammatory stimuli. Besides granulocyte-macrophage progenitors, Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) is a growth factor for erythroid, megakaryocyte, and eosinophil progenitors. On mature hematopoietic, monocytes/macrophages and eosinophils. Human Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) can induce human endothelial cells to migrate and proliferate. Additionally, Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) can stimulate the proliferation of a number of tumor cell lines, including osteogenic sarcoma, carcin

Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) was initially characterized as a growth factor that can support the in vitro colony formation of granulocyte-macrophage progenitors. Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) is produced by a number of different cell types, including activated T cells, B cells, macrophages, mast cells, endothelial cells, and fibroblasts, in response to cytokine of immune and inflammatory stimuli. Besides granulocyte-macrophage progenitors, Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) is a growth factor for erythroid, megakaryocyte, and eosinophil progenitors. On mature hematopoietic, monocytes/macrophages and eosinophils. Human Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) can induce human endothelial cells to migrate and proliferate. Additionally, Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) can stimulate the proliferation of a number of tumor cell lines, including osteogenic sarcoma, carcin

Fibroblast Growth Factor-4 (FGF-4) also known as K-FGF is a heparin-binding growth factor of the FGF family.It was identified by its oncogenic transforming activity. FGF-4 and FGF-3 are located closely on chromosome 11. FGF-4 and its receptors (FGF R1c, 2c, 3c and 4) play an important role in the regulation of embryonic development, cell proliferation, and cell differentiation. FGF-4 is required for normal limb and cardiac valve development during embryogenesis.

Fibroblast Growth Factor-4 (FGF-4) also known as K-FGF is a heparin-binding growth factor of the FGF family.It was identified by its oncogenic transforming activity. FGF-4 and FGF-3 are located closely on chromosome 11. FGF-4 and its receptors (FGF R1c, 2c, 3c and 4) play an important role in the regulation of embryonic development, cell proliferation, and cell differentiation. FGF-4 is required for normal limb and cardiac valve development during embryogenesis.

Fibroblast Growth Factor-4 (FGF-4) also known as K-FGF is a heparin-binding growth factor of the FGF family.It was identified by its oncogenic transforming activity. FGF-4 and FGF-3 are located closely on chromosome 11. FGF-4 and its receptors (FGF R1c, 2c, 3c and 4) play an important role in the regulation of embryonic development, cell proliferation, and cell differentiation. FGF-4 is required for normal limb and cardiac valve development during embryogenesis.

Interleukin-1 Beta (IL-1β) is a proinflammatory cytokine produced in a variety of cells including monocytes, tissue macrophages, keratinocytes and other epithelial cells. Both IL-1 alpha and IL-1 beta binds to the same receptor and has similar if not identical biological properties. These cytokines have a broad range of activities including, stimulation of thymocyte proliferation, by inducing IL-2 release, B-cell maturation and proliferation, mitogenic FGF-like activity and the ability to stimulate the release of prostaglandin and collagenase from synovial cells. However, whereas IL-1 beta is a secreted cytokine, IL-1 alpha is predominantly a cell-associated cytokine.

Interleukin-1 Beta (IL-1β) is a proinflammatory cytokine produced in a variety of cells including monocytes, tissue macrophages, keratinocytes and other epithelial cells. Both IL-1 alpha and IL-1 beta binds to the same receptor and has similar if not identical biological properties. These cytokines have a broad range of activities including, stimulation of thymocyte proliferation, by inducing IL-2 release, B-cell maturation and proliferation, mitogenic FGF-like activity and the ability to stimulate the release of prostaglandin and collagenase from synovial cells. However, whereas IL-1 beta is a secreted cytokine, IL-1 alpha is predominantly a cell-associated cytokine.

Interleukin-1 Beta (IL-1β) is a proinflammatory cytokine produced in a variety of cells including monocytes, tissue macrophages, keratinocytes and other epithelial cells. Both IL-1 alpha and IL-1 beta binds to the same receptor and has similar if not identical biological properties. These cytokines have a broad range of activities including, stimulation of thymocyte proliferation, by inducing IL-2 release, B-cell maturation and proliferation, mitogenic FGF-like activity and the ability to stimulate the release of prostaglandin and collagenase from synovial cells. However, whereas IL-1 beta is a secreted cytokine, IL-1 alpha is predominantly a cell-associated cytokine.

Human Interferon gamma (hIFN-γ) is amacrophage-activating factor and the lone member of Interferon type II. The active form of IFN-γ is an antiparallel dimer that interacts with the receptor IFN-γR1 and sets off IFN-γ/JAK/STAT pathway. IFN-γ signaling does diverse biological functions primarily related to host defense and immune regulation, including antiviral and antibacterial defense, apoptosis, inflammation, and innate and acquired immunity. While IFN-γ–induced inflammatory cascade summons a variety of immune-related cell types, such as macrophages, natural killer (NK) cells and cytotoxic T lymphocytes (CTLs), IFN-γ is also implicated in resistance to NK cell and CTL responses and in immune escape in a variety of cancers.