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Blood, 15 December 2005, Vol. 106, No. 13, pp. 4034-4042. Prepublished online as a Blood First Edition Paper on July 28, 2005; DOI 10.1182/blood-2005-04-1622. This Article Full Text (PDF) All Versions of this Article: 2005-04-1622v1 106/13/4034    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by van Wijk, R. Articles by van Solinge, W. W Search for Related Content PubMed PubMed Citation Articles by van Wijk, R. Articles by van Solinge, W. W Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 21, 2005 Accepted July 20, 2005 The energy-less red blood cell is lost - erythrocyte enzyme abnormalities of glycolysis Richard van Wijk and Wouter W van Solinge* Department of Laboratory Medicine, University Medical Center Utrecht, Utrecht, The Netherlands * Corresponding author; email: wsolinge{at}azu.nl. The red blood cell depends solely on the anaerobic conversion of glucose by the Embden-Meyerhof Pathway for the generation and storage of high-energy phosphates, which is necessary for the maintenance of a number of vital functions. Many red blood cell enzymopathies have been described that disturb the erythrocyte's integrity, shorten its cellular survival, and result in hemolytic anemia. By far the majority of these enzymopathies are hereditary in nature. In this review, we summarize the current knowledge regarding the genetic, biochemical, and structural features of clinically relevant red blood cell enzymopathies involved in the Embden-Meyerhof Pathway and the Rapoport-Luebering Shunt. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Bonnefond, M. Vaxillaire, Y. Labrune, C. Lecoeur, J.-C. Chevre, N. Bouatia-Naji, S. Cauchi, B. Balkau, M. Marre, J. Tichet, et al. Genetic Variant in HK1 Is Associated With a Proanemic State and A1C but Not Other Glycemic Control-Related Traits Diabetes, November 1, 2009; 58(11): 2687 - 2697. [Abstract] [Full Text] [PDF] F. Roux-Dalvai, A. Gonzalez de Peredo, C. Simo, L. Guerrier, D. Bouyssie, A. Zanella, A. Citterio, O. Burlet-Schiltz, E. Boschetti, P. G. Righetti, et al. Extensive Analysis of the Cytoplasmic Proteome of Human Erythrocytes Using the Peptide Ligand Library Technology and Advanced Mass Spectrometry Mol. Cell. Proteomics, November 1, 2008; 7(11): 2254 - 2269. [Abstract] [Full Text] [PDF] D.-S. Lee, J. Park, K. A. Kay, N. A. Christakis, Z. N. Oltvai, and A.-L. Barabasi Cozzarelli Prize Winner@;DELIM@;From the Cover: The implications of human metabolic network topology for disease comorbidity PNAS, July 22, 2008; 105(29): 9880 - 9885. [Abstract] [Full Text] [PDF] G. R. Buchanan and M. J. Kahn Hemolytic anemias ASH Self-Assessment Program, January 1, 2007; 2007(1): 102 - 142. [Full Text] [PDF]

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