Literature DB >> 18693757

Trafficking and intracellular ATPase activity of human ecto-nucleotidase NTPDase3 and the effect of ER-targeted NTPDase3 on protein folding.

Vasily V Ivanenkov1, Jean Sévigny, Terence L Kirley.   

Abstract

Ecto-nucleoside triphosphate diphosphohydrolases, NTPDase1 (CD39) and NTPDase3, are integral plasma membrane proteins that hydrolyze extracellular nucleotides, thereby modulating the function of purinergic receptors. During processing in the secretory pathway, the active sites of ecto-nucleotidases are located in the lumen of vesicular compartments, thus raising the question whether the ecto-nucleotidases affect the ATP-dependent processes in these compartments, including protein folding in the endoplasmic reticulum (ER). It has been reported (J. Biol. Chem. (2001) 276, 41518-41525) that CD39 is not active until it reaches the plasma membrane, suggesting that terminal glycosylation in Golgi is critical for its activity. To investigate the subcellular location and the mechanism of ecto-nucleotidase activation, we expressed human NTPDase3 in COS-1 cells and blocked the secretory transport with monensin or brefeldin A, or by targeting to ER with a signal peptide. Cell surface biotinylation, sensitivity to glycosidases, and fluorescence microscopy analyses suggest that, in contrast to the previous report on CD39, NTPDase3 becomes catalytically active in the ER or in the ER-Golgi intermediate compartment, and that terminal glycosylation in Golgi is not essential for activity. Moreover, ER-targeted NTPDase3, but not wild-type NTPDase3 or ER-targeted inactive G221A mutant, significantly diminished the folding efficiency and the transport to the plasma membrane of coexpressed CD39 used as a reporter protein. These data suggest that ER-targeted NTPDase3 significantly depletes ATP in ER, whereas wild-type NTPDase3 is likely to acquire ATPase activity in a post-ER, but pre-Golgi, compartment, thus avoiding unproductive ATP hydrolysis and interference with protein folding in the ER. ER-targeted NTPDase3 may be a useful experimental tool to study the effects of ER ATP depletion on ER function under normal and stress conditions.

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Year:  2008        PMID: 18693757      PMCID: PMC2562647          DOI: 10.1021/bi800402q

Source DB:  PubMed          Journal:  Biochemistry        ISSN: 0006-2960            Impact factor:   3.162


  49 in total

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3.  Characterization of disulfide bonds in human nucleoside triphosphate diphosphohydrolase 3 (NTPDase3): implications for NTPDase structural modeling.

Authors:  Vasily V Ivanenkov; Jarek Meller; Terence L Kirley
Journal:  Biochemistry       Date:  2005-06-28       Impact factor: 3.162

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  5 in total

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Journal:  Purinergic Signal       Date:  2017-09-27       Impact factor: 3.765

2.  The GDA1_CD39 superfamily: NTPDases with diverse functions.

Authors:  Aileen F Knowles
Journal:  Purinergic Signal       Date:  2011-01-21       Impact factor: 3.765

3.  Rat submandibular glands secrete nanovesicles with NTPDase and 5'-nucleotidase activities.

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Journal:  Purinergic Signal       Date:  2014-12-19       Impact factor: 3.765

Review 4.  Cellular function and molecular structure of ecto-nucleotidases.

Authors:  Herbert Zimmermann; Matthias Zebisch; Norbert Sträter
Journal:  Purinergic Signal       Date:  2012-05-04       Impact factor: 3.765

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  5 in total

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