Cytokines & Chemokines

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune diseasesuch as Crohn's disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune disease including Crohn's disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune disease including Crohn's disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune disease. Besides inducing hemorrhagic necrosis of tumors, TNF has been found to be involved in tumorigenesis, tumor metastasis, viral replication, septic shock, fever, inflammation, and autoimmune disease including Crohn's disease, rheumatoid arthritis and graft-versus-host disease. TNF alpha-1a is a potent lymphoid factor that exerts cytotoxic effects on a wide range of tumor cells and certain other target cells.

Chemokine (C-X-C motif) ligand 9 (CXCL9), also known as monokine induced by interferon gamma (MIG), is a small cytokine belonging to the CXC chemokine family.The CXCL9 gene is induced in macrophages and in primary glialcells of the central nervous systemin response to IFN­γ. CXCL9 has been shown to be achemo attractant for activated Th1lymphocytes and tumor-infiltrating leukocytes (TILs) but not for neutrophils or monocytes. CXCL is also involved in other cellular activities including inhibition of tumor growth, angiogenesis, and inhibition of colony formation of hematopoietic progenitors. CXCL9 is closely related to two other CXC chemokines, CXCL10 and CXCL11.CXCL9, CXCL10 and CXCL11 all elicit their chemotactic functions by interacting with the chemokine receptor CXCR3.

Chemokine (C-X-C motif) ligand 9 (CXCL9), also known as monokine induced by interferon gamma (MIG), is a small cytokine belonging to the CXC chemokine family.The CXCL9 gene is induced in macrophages and in primary glialcells of the central nervous systemin response to IFN­γ. CXCL9 has been shown to be achemo attractant for activated Th1lymphocytes and tumor-infiltrating leukocytes (TILs) but not for neutrophils or monocytes. CXCL is also involved in other cellular activities including inhibition of tumor growth, angiogenesis, and inhibition of colony formation of hematopoietic progenitors. CXCL9 is closely related to two other CXC chemokines, CXCL10 and CXCL11.CXCL9, CXCL10 and CXCL11 all elicit their chemotactic functions by interacting with the chemokine receptor CXCR3.

Chemokine (C-X-C motif) ligand 9 (CXCL9), also known as monokine induced by interferon gamma (MIG), is a small cytokine belonging to the CXC chemokine family.The CXCL9 gene is induced in macrophages and in primary glialcells of the central nervous systemin response to IFN­γ. CXCL9 has been shown to be achemo attractant for activated Th1lymphocytes and tumor-infiltrating leukocytes (TILs) but not for neutrophils or monocytes. CXCL is also involved in other cellular activities including inhibition of tumor growth, angiogenesis, and inhibition of colony formation of hematopoietic progenitors. CXCL9 is closely related to two other CXC chemokines, CXCL10 and CXCL11.CXCL9, CXCL10 and CXCL11 all elicit their chemotactic functions by interacting with the chemokine receptor CXCR3.

Vascular Endothelial Growth Factor (VEGF) was initially purified from media conditioned by normal bovine pituitary folliculo-stellate cells and by a variety of transformed cell lines as a mitogen specific for vascular endothelial cells. It was subsequently found to be identical to an independently discovered vascular permeability factor (VPF), which was previously identified in media conditioned by tumor cell lines based on its ability to increase the permeability of capillary blood vessels. Three mouse cDNA clones, which arise through alternative splicing and which encode mature mouse monomeric VEGF having 120, 164, or 188, amino acids, respectively, have been identified. Two receptor tyrosine kinases (RTKs), Flt-1 and Flk-1 (the mouse homologue of human KDR), both members of the type III subclass of RTKs containing seven immunoglobulin-like repeats in their extracellular domains, have been shown to bind VEGF with high affinity. The roles of the homodimers of KDR, Flt, and the heterod

Vascular Endothelial Growth Factor (VEGF) was initially purified from media conditioned by normal bovine pituitary folliculo-stellate cells and by a variety of transformed cell lines as a mitogen specific for vascular endothelial cells. It was subsequently found to be identical to an independently discovered vascular permeability factor (VPF), which was previously identified in media conditioned by tumor cell lines based on its ability to increase the permeability of capillary blood vessels. Three mouse cDNA clones, which arise through alternative splicing and which encode mature mouse monomeric VEGF having 120, 164, or 188, amino acids, respectively, have been identified. Two receptor tyrosine kinases (RTKs), Flt-1 and Flk-1 (the mouse homologue of human KDR), both members of the type III subclass of RTKs containing seven immunoglobulin-like repeats in their extracellular domains, have been shown to bind VEGF with high affinity. The roles of the homodimers of KDR, Flt, and the heterod