Abstract
The best of both: SIRT1/2 inhibitors were developed by combining chemical features of selisistat (SIRT1-selective inhibitor; blue) and carprofen (anti-inflammatory drug; red). The most potent compound (shown) increased acetyl-p53 and acetyl-α-tubulin levels, and induced slight apoptosis at 50 μM in U937 cells, differently from selisistat and carprofen.
Keywords:
SIRT1/2; apoptosis; histone deacetylases; inhibitors; sirtuins.
Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylation / drug effects
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Anti-Inflammatory Agents, Non-Steroidal / chemistry
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology
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Antineoplastic Agents / chemistry
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Antineoplastic Agents / pharmacology
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Apoptosis / drug effects
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Carbazoles / chemistry*
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Carbazoles / pharmacology*
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Cell Line, Tumor
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Histone Deacetylase Inhibitors / chemistry*
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Histone Deacetylase Inhibitors / pharmacology*
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Humans
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Neoplasms / drug therapy
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Neoplasms / enzymology*
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Sirtuin 1 / antagonists & inhibitors*
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Sirtuin 1 / metabolism
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Sirtuin 2 / antagonists & inhibitors*
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Sirtuin 2 / metabolism
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Tubulin / metabolism
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Tumor Suppressor Protein p53 / metabolism
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Antineoplastic Agents
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Carbazoles
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Histone Deacetylase Inhibitors
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Tubulin
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Tumor Suppressor Protein p53
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Sirtuin 1
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Sirtuin 2
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carprofen