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Ribonuclease L
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'''Ribonuclease L''' or '''RNase L''' is a latent enzyme that cleaves the components of [[RNA]]. Its increased production is activated by [[interferon]] which, in turn, causes the destruction of all RNA within the cell, both cellular and [[virus|viral]]. It is a key component of the intracellular [[immune system|immune]] response to viral pathogens. RNase L is present in small quantities during the normal cell cycle. When interferon binds to receptors on the cell membrane, it triggers the production of more RNase L along with [[2'-5' Oligodenylate Synthetase]] (OAS). OAS converts [[ATP]] to [[pyrophosphate]] and [[2'-5'linked oligoadenylates]]. The 2-5 A molecules bind to RNase L and activates it. The activated RNaseL destroys all cellular and viral RNA, which triggers [[autophagy]] and programmed cell death. Several abnormalities of the 2-5A/RNaseL pathways have been documented in [[chronic fatigue syndrome]] patients and previously had been suggested a potential [[diagnostic biomarker]]. Studies of [[Peripheral blood mononuclear cell|peripheral blood mononuclear cells]] have found that the RNase L and 2-5 A pathways are dysregulated,<ref>{{Cite journal | last = Roelens | first = Simon | author-link = | last2 = Herst | first2 = C. Vincent | author-link2 = | last3 = D'Haese | first3=Anne | authorlink3 = | last4 = Smet | first4=Karen De | authorlink4 = | last5 = Frémont | first5 = Marc | authorlink5 = | last6 = De Meirleir | first6 = Kenny | authorlink6 = Kenny De Meirleir | last7 = Englebienne | first7 = Patrick | last8 = Patrick Englebienne | first8 = | date = Jan 2001| title = G-Actin Cleavage Parallels 2-5A-Dependent RNase L Cleavage in Peripheral Blood Mononuclear Cells—Relevance to a Possible Serum-Based Screening Test for Dysregulations in the 2-5A Pathway|url=http://www.tandfonline.com/doi/full/10.1300/J092v08n03_07|journal=Journal of Chronic Fatigue Syndrome|language=en|volume=8|issue=3-4 | pages = 63–82|doi=10.1300/J092v08n03_07|issn=1057-3321|pmc=|pmid=|access-date=|quote=|via=}}</ref> with abnormally high levels of the active form of 2-5 A.<ref>{{Cite journal | last = Suhadolnik | first = R.J. | authorlink = | last2 = Reichenbach | first2 = N.L. | author-link2 = | last3 = Hitzges | first3=P. | authorlink3 = | last4 = Sobol | first4 = R.W. | authorlink4 = | last5 = Peterson | first5 = D. L. | authorlink5 = | last6 = Henry | first6 = B. | authorlink6 = | last7 = Ablashi | first7 = D.V. | last8 = Müller | first8 = W.E. | last9 = Schröder | first9 = H.C. | date = Jan 1994| title = Upregulation of the 2-5A synthetase/RNase L antiviral pathway associated with chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/8148461|journal=Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America|volume=18 | issue = Suppl 1|pages=S96–104|doi=10.1093/clinids/18.supplement_1.s96|issn=1058-4838|pmc=|pmid=8148461|access-date=|quote=|via=}}</ref> RNase L proteins of the molecular weights 80, 42 and 37 kDa have also been found.<ref>[[Robert Suhadolnik|Suhadolnik RJ]], Peterson DL, O'Brien K, Cheney PR, Herst CV, Reichenbach NL, Kon N, Horvath SE, Iacono KT, Adelson ME, et al. [https://www.researchgate.net/publication/13977271_Biochemical_Evidence_for_a_Novel_Low_Molecular_Weight_2-5A-Dependent_RNase_L_in_Chronic_Fatigue_Syndrome Biochemical evidence for a novel low molecular weight 2-5A-dependent RNase L in chronic fatigue syndrome.] J Interferon Cytokine Res. 1997 Jul;17(7):377-85. [[doi:]][https://www.liebertpub.com/doi/abs/10.1089/jir.1997.17.377 10.1089/jir.1997.17.377] [[PubMed Identifier|PMID]]: [[pubmed:9243369|9243369]]</ref> RNaseL activity and concentrations of bioactive 2-5 A are correlated with physical function.<ref>Snell CR, Vanness JM, Strayer DR, Stevens SR. [https://www.researchgate.net/publication/11300688_Physical_performance_and_prediction_of_2-5A_synthetaseRNase_L_antiviral_pathway_activity_in_patients_with_Chronic_Fatigue_Syndrome Physical performance and prediction of 2-5A synthetase/RNase L antiviral pathway activity in patients with chronic fatigue syndrome.] In Vivo. 2002 Mar-Apr;16(2):107-9. [[PubMed Identifier|PMID]]: [[pubmed:12073768|12073768]]</ref> ==Notable studies == *2001, G-Actin Cleavage Parallels 2-5A-Dependent RNase L Cleavage in Peripheral Blood Mononuclear Cells—Relevance to a Possible Serum-Based Screening Test for Dysregulations in the 2-5A Pathway<ref>Simon Roelens, C. Vincent Herst, Anne D'Haese, Karen De Smet, Marc Frémont, Kenny De Meirleir & Patrick Englebienne. (2001). G-Actin Cleavage Parallels 2-5A-Dependent RNase L Cleavage in Peripheral Blood Mononuclear Cells—Relevance to a Possible Serum-Based Screening Test for Dysregulations in the 2-5A Pathway. ''Journal of Chronic Fatigue Syndrome'', Vol. 8, Iss. 3-4, pp. 63-82. http://dx.doi.org/10.1300/J092v08n03_07</ref> - [http://dx.doi.org/10.1300/J092v08n03_07 (Abstract)] *2001, Interactions Between Rnase L Ankyrin-Like Domain and ABC Transporters as a Possible Origin for Pain, Ion Transport, CNS and Immune Disorders of [[Chronic Fatigue Immune Dysfunction Syndrome]]<ref>Patrick Englebienne, C. Vincent Herst, Karen De Smet, Anne D'Haese & Kenny De Meirleir. (2001). Interactions Between Rnase L Ankyrin-Like Domain and ABC Transporters as a Possible Origin for Pain, Ion Transport, CNS and Immune Disorders of Chronic Fatigue Immune Dysfunction Syndrome. ''Journal of Chronic Fatigue Syndrome'', Vol. 8, Iss. 3-4, pp. 83-102. http://dx.doi.org/10.1300/J092v08n03_08</ref> - [http://dx.doi.org/10.1300/J092v08n03_08 (Abstract)] ==See also== *[[Ampligen]] == References == {{Reflist}} [[Category:Body systems]] [[Category:Enzymes]]
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