ArticlePflugers Archiv : European journal of physiology2003
Regulation of K-Cl cotransport by Syk and Src protein tyrosine kinases in deoxygenated sickle cells.
Article in Pflugers Archiv : European journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Inhibition of Band 3 tyrosine phosphorylation: a new mechanism for treatment of sickle cell disease.British journal of haematology · 2020Article
- Oxidation Impacts the Intracellular Signaling Machinery in Hematological Disorders.Antioxidants (Basel, Switzerland) · 2020Review
- The role of WNK in modulation of KCl cotransport activity in red cells from normal individuals and patients with sickle cell anaemia.Pflugers Archiv : European journal of physiology · 2019Article
- Global transformation of erythrocyte properties via engagement of an SH2-like sequence in band 3.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Fluorescence assay of the interaction between hemoglobin and the cytoplasmic domain of erythrocyte membrane band 3.Blood cells, molecules & diseases · 2015Article
- Article
- Pathophysiological insights in sickle cell disease.The Indian journal of medical research · 2011Review
- Regulation of K-Cl cotransport in erythrocytes of frog Rana temporaria by commonly used protein kinase and protein phosphatase inhibitors.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2010Article
- Urea stimulation of KCl cotransport induces abnormal volume reduction in sickle reticulocytes.Blood · 2007Article
- Regulation of K-Cl cotransport by protein phosphatase 1alpha in mouse erythrocytes.Pflugers Archiv : European journal of physiology · 2006Article
- Regulation of K-Cl cotransport: from function to genes.The Journal of membrane biology · 2004Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Protein tyrosine kinases (PTK) of the Src family are thought to suppress K-Cl cotransport (KCC) activity via negative regulation of protein phosphatases. However, some PTK inhibitors reduce KCC activity, suggesting opposite regulation by different PTK families. We have reported previously that deoxygenation of sickle cells stimulates KCC and activates Syk (a Syk family PTK), but not Lyn (an Src family PTK). In this study the same results were obtained when PTK activities were measured under the conditions used to measure KCC activity and which prevent any change in intracellular [Mg(2+)]. Methyl-2,5-dihydroxycinnamate (DHC), a PTK inhibitor, was more selective for Syk than Lyn, while staurosporine (ST), a broad-specificity protein kinase inhibitor, inhibited Lyn more than Syk. Deoxygenation or 4-amino-5-(4-chlorophenyl)-7-( t-butyl)pyrazolo[3,4- d] pyrimidine (pp2, a specific Src inhibitor) stimulated KCC independently. These effects were not additive and were inhibited by DHC. In contrast, ST-induced KCC activation was resistant to DHC, suggesting a different pathway of activation. Overall, these data indicate that Syk activity is required for KCC activation, either induced by deoxygenation of sickle cells, or mediated by Src inhibition in oxygenated cells, and that Syk and Src PTKs exert opposing and interconnected regulatory effects on the activity of the transporter.
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