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lüll Role of ubiquitination in Na,K-ATPase regulation during lung injury Helenius IT; Dada LA; Sznajder JIProc Am Thorac Soc 2010[Feb]; 7 (1): 65-70During acute lung injury edema accumulates in the alveolar space, resulting in hypoxemia due to intrapulmonary shunt. The alveolar Na,K-ATPase, by effecting active Na(+) transport, is essential for removing edema from the alveolar spaces. However, during hypoxia it is endocytosed and degraded, which results in decreased Na,K-ATPase function and impaired lung edema clearance. Na,K-ATPase endocytosis and degradation require the phosphorylation and subsequent ubiquitination of the Na,K-ATPase. These events are the results of cross-talk between post-translational modifications, and how ubiquitination of a specific protein can result from injurious extracellular stimuli. Here, we review current knowledge on the regulation of Na,K-ATPase activity during lung injury, focusing on the role of Na,K-ATPase ubiquitination during hypoxia. A better understanding of these signaling pathways can be of relevance for the design of novel treatments to ameliorate the deleterious effects of acute lung injury.|Animals[MESH]|Down-Regulation[MESH]|Humans[MESH]|Lysosomes/enzymology[MESH]|Phosphorylation[MESH]|Pulmonary Alveoli/enzymology[MESH]|Pulmonary Edema/*enzymology/pathology[MESH]|Respiratory Distress Syndrome/*enzymology/metabolism[MESH]|Respiratory Mucosa/*enzymology/pathology[MESH]|Signal Transduction[MESH]|Sodium-Potassium-Exchanging ATPase/*metabolism[MESH]|Ubiquitin/*metabolism[MESH]|Ubiquitination/*physiology[MESH] |