GLYCOGEN SYNTHASE KINASE 3Β PREDICTION AS PRIMARY CELLULAR TARGET TO MEDIATE ANTI-HEPATITIS C EFFECT OF NITAZOXANIDE
Journal Title: International Research Journal of Pharmacy (IRJP) - Year 2013, Vol 4, Issue 11
Abstract
Hepatitis C is a major healthcare problem that launched the quest and the interest of scientists to search for solutions that alleviate its risks. New groups of drugs are developed and repurposed for this reason. One of the drugs that recently repurposed to be used as an anti-HCV drug is Nitazoxanide (NTZ). NTZ is mainly a thiazolide antiparasitic drug that is mainly used for the treatment of cryptosporidiosis and giardiasis. Tizoxanide (TIZ), which is the active metabolite of NTZ, was recently reported to be active against some viruses including hepatitis C virus (HCV). The anti- HCV mode of action of Nitazoxanide is the overproduction of the hyperphosphorylated HCV non-structural protein 5 A (NS5A). However, the exact mechanism of action is not so clear. Some previous works suggested one member of the CMGC Serine/Threonine protein kinase family to be the primary cellular target of NTZ. A more recent work revealed that NS5A is a direct substrate of casein kinase I (CKI). However, no direct effect of NTZ or TIZ was reported on CKI in enzymatic assays. In this work, starting with the chemical structure of NTZ and TIZ, some in-silico approaches were applied to hypothesize the human primary cellular target for NTZ. Accordingly, glycogen synthase kinase 3 (GSK3), a member of CMGC Serine/Threonine protein kinase family, was retrieved as a proposed target of NTZ that is likely mediating its anti-HCV effect.
Authors and Affiliations
M. Ahmad , Alaa Hemeida, Amal Hussein, Medhat Hashem
Keywords
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- EP ID EP136284
- DOI 10.7897/2230-8407.041109
- Views 100
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