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- Volume 5, Issue 2, 2009
Current Enzyme Inhibition - Volume 5, Issue 2, 2009
Volume 5, Issue 2, 2009
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Post-Wortmannin Era: Novel Phosphoinositide 3-Kinase Inhibitors with Potential Therapeutic Applications
Authors: Laura Braccini, Fulvio Morello, Alessia Perino and Emilio HirschPhosphoinositide 3-kinases (PI3Ks) are a family of enzymes extensively involved in cell signaling, acting downstream of tyrosine kinase and G-protein coupled receptors. Based on structural and substrate specificity, mammalian PI3Ks include class I (A, B), class II and class III enzymes. Several lines of evidence have shown that PI3Ks participate in the regulation of fundamental cellular functions such as cell growth, apop Read More
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Engineered Protein Protease Inhibitors
Authors: Malini Viswanathan, Stephen R. Comeau and Robert C. LadnerProteases are a class of proteins that degrade other proteins. There are several classes of proteases and these are defined by the chemical nature of the catalytic sites. The process of proteolysis is a vital function that is exquisitely regulated. Many diseases involve deregulation of proteolysis due to over-expression of one or more proteases or endogenous protease inhibitors being faulty or missing. Engineered protease inhibitors t Read More
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Poly(ADP-Ribosylation): Beneficial Effects of Its Inhibition
Authors: V. Giansanti, F. Dona and A. I. ScovassiPoly(ADP-ribosylation) is a post-translational modification of proteins which plays a crucial role in basic cellular processes, including DNA repair and replication, transcription and cell death. The biochemical reaction of poly(ADPribosylation) consists of the conversion of ß-NAD+ into ADP-ribose, and the further formation of polymers of variable length and structure bound to nuclear protein acceptors. Polymer synthesis and degra Read More
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Serine Protease Inhibitor Kazal Type 1 (SPINK1): Beyond the Trypsin Inhibitor
Authors: Masaki Ohmuraya, Nobuyuki Ozaki, Masahiko Hirota, Hideo Baba and Ken-ichi YamamuraSerine protease inhibitor Kazal type 1 (SPINK1) was originally identified as a trypsin inhibitor in the pancreatic acinar cells in 1948. Recent studies showed an association of mutations in SPINK1 gene and hereditary chronic pancreatitis. Thus, a lack of SPINK1 may result in the premature conversion of trypsinogen into active trypsin in acinar cells, leading to pancreatitis. However, we found that mice deficient for Spink3, a Read More
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Volumes & issues
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Volume 20 (2024)
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Volume 19 (2023)
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Volume 18 (2022)
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Volume 17 (2021)
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Volume 16 (2020)
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Volume 15 (2019)
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Volume 14 (2018)
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Volume 13 (2017)
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Volume 12 (2016)
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Volume 11 (2015)
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Volume 10 (2014)
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Volume 9 (2013)
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Volume 8 (2012)
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Volume 7 (2011)
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Volume 6 (2010)
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Volume 5 (2009)
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Volume 4 (2008)
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Volume 3 (2007)
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Volume 2 (2006)
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Volume 1 (2005)
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