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Mol. Cells 2009; 28(6): 559-563

Published online November 19, 2009

https://doi.org/10.1007/s10059-009-0151-7

© The Korean Society for Molecular and Cellular Biology

Glyceraldehyde-3-Phosphate, a Glycolytic
Intermediate, Plays a Key Role in Controlling Cell
Fate Via Inhibition of Caspase Activity

Mi Jang, Hyo Jin Kang, Sun Young Lee, Sang J. Chung, Sunghyun Kang, Seung Wook Chi, Sayeon Cho, Sang Chul Lee, Chong-Kil Lee, Byoung Chul Park, Kwang-Hee Bae, and Sung Goo Park

Received: August 19, 2009; Revised: September 14, 2009; Accepted: September 17, 2009

Abstract

Glyceraldehyde-3-phosphate is a key intermediate in several central metabolic pathways of all organisms. Aldolase and glyceraldehyde-3-phosphate dehydrogenase are involved in the production or elimination of glyceraldehyde-3-phosphate during glycolysis or gluconeogenesis, and are differentially expressed under various physiological conditions, including cancer, hypoxia, and apoptosis. In this study, we examine the effects of glyceraldehyde-3-phosphate on cell survival and apoptosis. Overexpression of aldolase protected cells against apoptosis, and addition of glyceraldehyde-3-phosphate to cells delayed apoptosis. Additionally, delayed apoptotic phenomena were observed when glyceraldehyde-3-phosphate was added to a cell-free system, in which artificial apoptotic process was induced by adding dATP and cytochrome c. Surprisingly, glyceraldehyde-3-phosphate directly suppressed caspase-3 activity in a reversible noncompetitive mode, preventing caspase-dependent proteolysis. Based on these results, we suggest that glyceraldehyde-3-phosphate, a key molecule in several central metabolic pathways, functions as a molecule switch between cell survival and apoptosis.

Keywords aldolase, apoptosis, caspase-3, GAPDH, glyceraldehyde-3-phosphate

Article

Research Article

Mol. Cells 2009; 28(6): 559-563

Published online December 31, 2009 https://doi.org/10.1007/s10059-009-0151-7

Copyright © The Korean Society for Molecular and Cellular Biology.

Glyceraldehyde-3-Phosphate, a Glycolytic
Intermediate, Plays a Key Role in Controlling Cell
Fate Via Inhibition of Caspase Activity

Mi Jang, Hyo Jin Kang, Sun Young Lee, Sang J. Chung, Sunghyun Kang, Seung Wook Chi, Sayeon Cho, Sang Chul Lee, Chong-Kil Lee, Byoung Chul Park, Kwang-Hee Bae, and Sung Goo Park

Received: August 19, 2009; Revised: September 14, 2009; Accepted: September 17, 2009

Abstract

Glyceraldehyde-3-phosphate is a key intermediate in several central metabolic pathways of all organisms. Aldolase and glyceraldehyde-3-phosphate dehydrogenase are involved in the production or elimination of glyceraldehyde-3-phosphate during glycolysis or gluconeogenesis, and are differentially expressed under various physiological conditions, including cancer, hypoxia, and apoptosis. In this study, we examine the effects of glyceraldehyde-3-phosphate on cell survival and apoptosis. Overexpression of aldolase protected cells against apoptosis, and addition of glyceraldehyde-3-phosphate to cells delayed apoptosis. Additionally, delayed apoptotic phenomena were observed when glyceraldehyde-3-phosphate was added to a cell-free system, in which artificial apoptotic process was induced by adding dATP and cytochrome c. Surprisingly, glyceraldehyde-3-phosphate directly suppressed caspase-3 activity in a reversible noncompetitive mode, preventing caspase-dependent proteolysis. Based on these results, we suggest that glyceraldehyde-3-phosphate, a key molecule in several central metabolic pathways, functions as a molecule switch between cell survival and apoptosis.

Keywords: aldolase, apoptosis, caspase-3, GAPDH, glyceraldehyde-3-phosphate

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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