| ALX-804-581-C100 | 100 µg | 124.00 USD | ![]() |
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| Alternative Name: | Ribonuclease L (2',5'-oligoisoadenylate synthetase-dependent), 2-5A-dependent RNase, Ribonuclease 4 |
| Concentration: | 1mg/ml |
| Purity Detail: | Affinity purified. |
| Formulation: | Liquid. In PBS containing 10% glycerol and 0.02% sodium azide. |
| Clone: | 2E9 |
| Isotype: | Mouse IgG1 |
| Immunogen: | Recombinant human RNase L. |
| Specificity: | Recognizes human RNase L. Detects a band of ~83kDa by Western blot. Does not cross-react with mouse RNase L. |
| Application: | ELISA Western Blot (Alkaline phosphatase/ECL detection) Immunoprecipitation Immunocytochemistry Immunohistochemistry (paraffin sections) |
| Short Term Storage: | +4°C |
| Long Term Storage: | -20°C |
| Handling: | Avoid freeze/thaw cycles. |
| Miscellaneous/General: | RNase L is an endoribonuclease regulated by 2-5A synthetase (2-5A). It is a 741 aa cytoplasmic and mitochondrial protein in human. RNase L functions in the antiviral and antiproliferative activities of interferons (IFN) and in multiple apoptotic pathways, standing in the first line of the innate cellular defense mechanism induced by the IFN pathway. In its native state, the N-terminal half of RNase L functions as a repressor of the ribonuclease domain in the C-terminal half. Upon binding with high affinity to 2-5A molecules, the inactive monomeric form of RNase L is induced to dimerize into its catalytically active form. Since mutations in RNase L relate to an increase incidence of prostate cancer, the activation of RNase L directly or indirectly suppresses prostate tumorigenesis and/or metastasis. The 2-5A/RNase L pathway is implicated in mediating apoptosis in response to viral infections and to several types of external stimuli. The fungal ribonuclease, α-sarcin, the RNA modyfing enzyme, ricin A chain, and UV light each lead to ribotoxic stress responses involving damage to the 3-end of the large ribosomal RNA. These treatments activate c-jun N-terminal kinases (JNKs). JNK activation in response to UV irradiation has been linked to apoptosis through Bax (requires caspase 3 activity, appearance of cytosolic cytochrome C indicating involvement of mitochondria). |
