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TNF Receptor Type I, is also known as TNF R-p55/p60 and TNFRSF1A. It is a type I transmembrane protein member of the TNF receptor superfamily. It is expressed in most cell types. Binding of either TNF-α or TNF-β to TNF-R1 initiates a signal transduction pathway that results in the activation of the transcription factor NF-κB, whose target genes are involved in the regulation of inflammatory responses, and, in certain cells, induce apoptosis. TNF-R1 is essential for proper development of lymph node germinal centers and Peyer’s patches and for combating intracellular pathogens such as Listeria. It is stored in the Golgi and translocates to the cell surface following proinflammatory stimuli.

TNF Receptor Type I, is also known as TNF R-p55/p60 and TNFRSF1A. It is a type I transmembrane protein member of the TNF receptor superfamily. It is expressed in most cell types. Binding of either TNF-α or TNF-β to TNF-R1 initiates a signal transduction pathway that results in the activation of the transcription factor NF-κB, whose target genes are involved in the regulation of inflammatory responses, and, in certain cells, induce apoptosis. TNF-R1 is essential for proper development of lymph node germinal centers and Peyer’s patches and for combating intracellular pathogens such as Listeria. It is stored in the Golgi and translocates to the cell surface following proinflammatory stimuli.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. 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 diseases including Crohn’s disease, and rheumatoid arthritis as well as 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 diseases. 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 diseases including Crohn’s disease, and rheumatoid arthritis as well as 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 diseases. 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 diseases including Crohn’s disease, and rheumatoid arthritis as well as 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-a) is a homotrimer with a subunit molecular mass of 17.3 kDa. Tumor Necrosis Factor-alpha(TNF-a) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases; and in viral, bacterial, fungal, and parasitic infections. 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 diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease.

Tumor Necrosis Factor-alpha (TNF-a) is a homotrimer with a subunit molecular mass of 17.3 kDa. Tumor Necrosis Factor-alpha(TNF-a) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases; and in viral, bacterial, fungal, and parasitic infections. 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 diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease.

Tumor Necrosis Factor-alpha (TNF-a) is a homotrimer with a subunit molecular mass of 17.3 kDa. Tumor Necrosis Factor-alpha(TNF-a) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases; and in viral, bacterial, fungal, and parasitic infections. 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 diseases including Crohn’s disease, and rheumatoid arthritis as well as graft-versus-host disease.

Tumor Necrosis Factor-Alpha (TNF-alpha) plays a major role in growth regulation, differentiation, inflammation, viral replication, tumorigenesis, and autoimmune diseases. 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 diseases including Crohn’s disease, and rheumatoid arthritis as well as 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 diseases. 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 diseases including Crohn’s disease, and rheumatoid arthritis as well as 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 diseases. 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 diseases including Crohn’s disease, and rheumatoid arthritis as well as 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-α) is produced by neutrophils, activated lymphocytes, macrophages, NK cells, LAK cells, astrocytes endothelial cells, smooth muscle cells and some transformed cells. Mouse TNF-α occurs as a membrane-anchored form. The naturally-occurring form of TNF-α is glycosylated, but non-glycosylated recombinant TNF-α has comparable biological activity. The biologically active native form of TNF-α is reportedly a trimer. Human and mouse TNF-α show approximately 79% homology at the amino acid level and crossreactivity between the two species.

Tumor necrosis factor alpha (TNF-α) is produced by neutrophils, activated lymphocytes, macrophages, NK cells, LAK cells, astrocytes endothelial cells, smooth muscle cells and some transformed cells. Mouse TNF-α occurs as a membrane-anchored form. The naturally-occurring form of TNF-α is glycosylated, but non-glycosylated recombinant TNF-α has comparable biological activity. The biologically active native form of TNF-α is reportedly a trimer. Human and mouse TNF-α show approximately 79% homology at the amino acid level and crossreactivity between the two species.

Tumor necrosis factor alpha (TNF-α) is produced by neutrophils, activated lymphocytes, macrophages, NK cells, LAK cells, astrocytes endothelial cells, smooth muscle cells and some transformed cells. Mouse TNF-α occurs as a membrane-anchored form. The naturally-occurring form of TNF-α is glycosylated, but non-glycosylated recombinant TNF-α has comparable biological activity. The biologically active native form of TNF-α is reportedly a trimer. Human and mouse TNF-α show approximately 79% homology at the amino acid level and crossreactivity between the two species.

Tumor necrosis factor alpha (TNF-α) is produced by neutrophils, activated lymphocytes, macrophages, NK cells, LAK cells, astrocytes endothelial cells, smooth muscle cells and some transformed cells. Mouse TNF-α occurs as a membrane-anchored form. The naturally-occurring form of TNF-α is glycosylated, but non-glycosylated recombinant TNF-α has comparable biological activity. The biologically active native form of TNF-α is reportedly a trimer. Human and mouse TNF-α show approximately 79% homology at the amino acid level and crossreactivity between the two species.

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.