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RNase L (human) monoclonal antibody (2E9)

 
ALX-804-581-C100 100 µg 151.00 USD
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Product Specification

Alternative Name:Ribonuclease L (2',5'-oligoisoadenylate synthetase-dependent), 2-5A-dependent RNase, Ribonuclease 4
 
Clone:2E9
 
Host:Mouse
 
Isotype:IgG1
 
Immunogen:Recombinant human RNase L.
 
UniProt ID:P34096
 
Species reactivity:Human
 
Crossreactivity:Does not cross-react with mouse RNase L.
 
Applications:ELISA, ICC, IHC (PS), IP, WB
 
Recommended Dilutions/Conditions:Western Blot (Alkaline phosphatase/ECL detection)
Suggested dilutions/conditions may not be available for all applications.
Optimal conditions must be determined individually for each application.
 
Purity Detail:Affinity purified.
 
Formulation:Liquid. In PBS containing 10% glycerol and 0.02% sodium azide.
 
Handling:Avoid freeze/thaw cycles.
 
Shipping:Shipped on Blue Ice
 
Short Term Storage:+4°C
 
Long Term Storage:-20°C
 
Scientific Background: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).
 

Product Literature References

An infectious retrovirus susceptible to an IFN antiviral pathway from human prostate tumors: B. Dong, et al.; PNAS 104, 1655 (2007), Abstract; Full Text
Germline mutations in the ribonuclease L gene in families showing linkage with HPC1: J. Carpten, et al.; Nat. Genet. 30, 181 (2002), Abstract;
Alternative function of a protein kinase homology domain in 2', 5'-oligoadenylate dependent RNase L: B. Dong & R.H. Silverman; Nucleic Acids Res. 27, 439 (1999), Abstract;
2-5A-dependent RNase molecules dimerize during activation by 2-5A: B. Dong & R.H. Silverman; J. Biol. Chem. 270, 4133 (1995), Abstract; Full Text
Elevated levels of 2',5'-linked oligoadenylate-dependent ribonuclease L occur as an early event in colorectal tumorigenesis: L. Wang, et al.; Clin. Cancer Res. 1, 1421 (1995), Abstract;

General Literature References

Effects of RNase L mutations associated with prostate cancer on apoptosis induced by 2',5'-oligoadenylates: Y. Xiang, et al.; Cancer Res. 63, 6795 (2003), Abstract;
Implications for RNase L in prostate cancer biology: R.H. Silverman; Biochemistry 42, 1805 (2003), Review, Abstract;

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