Mouse Rnasel Antibody (N-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q05921 |
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Clone Names | 110328064 |
Gene ID | 24014 |
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Other Names | 2-5A-dependent ribonuclease, 2-5A-dependent RNase, 3126-, Ribonuclease 4, Ribonuclease L, RNase L, Rnasel, Rns4 |
Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
Name | Rnasel |
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Synonyms | Rns4 |
Function | Endoribonuclease that functions in the interferon (IFN) antiviral response. In INF treated and virus infected cells, RNASEL probably mediates its antiviral effects through a combination of direct cleavage of single-stranded viral RNAs, inhibition of protein synthesis through the degradation of rRNA, induction of apoptosis, and induction of other antiviral genes. RNASEL mediated apoptosis is the result of a JNK-dependent stress-response pathway leading to cytochrome c release from mitochondria and caspase-dependent apoptosis. Therefore, activation of RNASEL could lead to elimination of virus infected cells under some circumstances. In the crosstalk between autophagy and apoptosis proposed to induce autophagy as an early stress response to small double-stranded RNA and at later stages of prolonged stress to activate caspase-dependent proteolytic cleavage of BECN1 to terminate autophagy and promote apoptosis. Might play a central role in the regulation of mRNA turnover (By similarity). Cleaves 3' of UpNp dimers, with preference for UU and UA sequences, to sets of discrete products ranging from between 4 and 22 nucleotides in length (By similarity). |
Cellular Location | Cytoplasm. Mitochondrion |
Tissue Location | Expressed in spleen, thymus, lung, testis, kidney, liver and heart |
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Background
Endoribonuclease that functions in the interferon (IFN) antiviral response. In INF treated and virus infected cells, RNASEL probably mediates its antiviral effects through a combination of direct cleavage of single-stranded viral RNAs, inhibition of protein synthesis through the degradation of rRNA, induction of apoptosis, and induction of other antiviral genes. RNASEL mediated apoptosis is the result of a JNK-dependent stress-response pathway leading to cytochrome c release from mitochondria and caspase-dependent apoptosis. Therefore, activation of RNASEL could lead to elimination of virus infected cells under some circumstances. Might play a central role in the regulation of mRNA turnover (By similarity).
References
Ireland, D.D., et al. PLoS Pathog. 5 (10), E1000602 (2009) :Andersen, J.B., et al. RNA Biol 6(3):305-315(2009)Salehzada, T., et al. PLoS ONE 4 (10), E7563 (2009) :Li, X.L., et al. Proc. Natl. Acad. Sci. U.S.A. 105(52):20816-20821(2008)Malathi, K., et al. Nature 448(7155):816-819(2007)
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