| 產品詳情 |
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| Antigenic Specificity | TNF-RI, Mouse |
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| Clone | HM14 |
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| Host Species | Rat |
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| Reactive Species | mouse |
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| Isotype | IgG2a |
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| Format | unconjugated |
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| Size | 100 μg |
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| Concentration | 100 μg/ml |
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| Applications | frozen sections, FC, immunoassay, IP |
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| Reviews / Ratings | If you have used this antibody, please help fellow researchers by submitting reviews to pAbmAbs and antYbuddY. |
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| Description | The monoclonal antibody HM104 recognizes the extracellular part of the Tumor Necrosis Factor Receptor type I (TNF-RI) of the membrane-bound as well as the soluble receptor. TNF-RI (~55-60 kDa) is present on most cell types and is considered to play a prominent role in cell stimulation by TNF-alpha. TNF-alpha activates inflammatory responses, induces apoptosis, regulates cellular proliferation, and may even promote cancer progression. The effects of TNF-alpha are mediated by TNF-RI and TNF-RII, which have both distinct and overlapping downstream signaling cascades. Induction of cytotoxicity and other functions are mediated largely via TNF-RI. TNF-RI is equally well activated by both the 17 kDa soluble and 26 kDa membrane-bound form, whereas TNF-RII is efficiently activated only by the membrane bound form of TNF-alpha. TNF-RI signaling is initiated when trimeric TNF-alpha binds TNF-RI receptors. Subsequent TNF-RI trimerization promotes the recruitment of a proximal signaling complex composed of TNF Receptor Associated protein with a Death Domain (TRADD), Receptor Interacting Protein (RIP), cellular Inhibitor of Apoptosis Protein 1 (cIAP1), TNF Receptor Associated Factor 2 (TRAF2), and likely TRAF5. Studies with TNF-RI-deficient mice indicate that TNF-RI mediates most of the proliferation, pro-inflammatory, and apoptosis-activating pathways. |
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| Immunogen | n/a |
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| Other Names | CD120a, Tumor necrosis factor receptor superfamily member 1A, p55/p60, TNF-RI |
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| Gene, Accession # | n/a |
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| Catalog # | HM1009 |
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| Price | |
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| Order / More Info | TNF-RI, Mouse Antibody from HYCULT BIOTECH |
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| Product Specific References | n/a |
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