Aminopeptidases

Publication Title: 
Nature

The lengths of human telomeres, which protect chromosome ends from degradation and end fusions, are crucial determinants of cell lifespan. During embryogenesis and in cancer, the telomerase enzyme counteracts telomeric DNA shortening. As shown in cancer cells, human telomerase binds the shelterin component TPP1 at telomeres during the S phase of the cell cycle, and adds ~60 nucleotides in a single round of extension, after which telomerase is turned off by unknown mechanisms.

Author(s): 
Chen, Liuh-Yow
Redon, Sophie
Lingner, Joachim
Publication Title: 
Nature

The lengths of human telomeres, which protect chromosome ends from degradation and end fusions, are crucial determinants of cell lifespan. During embryogenesis and in cancer, the telomerase enzyme counteracts telomeric DNA shortening. As shown in cancer cells, human telomerase binds the shelterin component TPP1 at telomeres during the S phase of the cell cycle, and adds ~60 nucleotides in a single round of extension, after which telomerase is turned off by unknown mechanisms.

Author(s): 
Chen, Liuh-Yow
Redon, Sophie
Lingner, Joachim
Publication Title: 
Proceedings of the National Academy of Sciences of the United States of America

With >1 million deaths annually, mostly among children in sub-Saharan Africa, malaria poses one of the most critical challenges in medicine today. Although introduction of the artemisinin class of antimalarial drugs has offered a temporary solution to the problem of drug resistance, new antimalarial drugs are needed to ensure effective control of the disease in the future. Herein, we have investigated members of the methionine aminopeptidase family as potential antimalarial targets.

Author(s): 
Chen, Xiaochun
Chong, Curtis R.
Shi, Lirong
Yoshimoto, Tadashi
Sullivan, David J.
Liu, Jun O.
Publication Title: 
The Journal of Biological Chemistry

The classical late infantile neuronal ceroid lipofuscinosis (LINCLs) is an autosomal recessive disease, where the defective gene is Cln2, encoding tripeptidyl-peptidase I (TPP1). At the molecular level, LINCL is caused by accumulation of autofluorescent storage materials in neurons and other cell types. Currently, there is no established treatment for this fatal disease. This study reveals a novel use of gemfibrozil and fenofibrate, Food and Drug Administration-approved lipid-lowering drugs, in up-regulating TPP1 in brain cells.

Author(s): 
Ghosh, Arunava
Corbett, Grant T.
Gonzalez, Frank J.
Pahan, Kalipada
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