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Full-Text Articles in Medicine and Health Sciences
Abnormal Erythroid Maturation Leads To Microcytic Anemia In The Tsap6/Steap3 Null Mouse Model, L. Blanc, J. Papoin, G. Debnath, M. Vidal, R. Amson, A. Telerman, X. L. An, N. Mohandas
Abnormal Erythroid Maturation Leads To Microcytic Anemia In The Tsap6/Steap3 Null Mouse Model, L. Blanc, J. Papoin, G. Debnath, M. Vidal, R. Amson, A. Telerman, X. L. An, N. Mohandas
Journal Articles
Genetic ablation of the ferrireductase STEAP3, also known as TSAP6, leads to severe microcytic and hypochromic red cells with moderate anemia in the mouse. However, the mechanism leading to anemia is poorly understood. Previous results indicate that TSAP6/Steap3 is a regulator of exosome secretion. Using TSAP6/Steap3 knockout mice, we first undertook a comprehensive hematologic characterization of the red cell compartment, and confirmed a dramatic decrease in the volume and hemoglobin content of these erythrocytes. We observed marked anisocytosis as well as the presence of fragmenting erythrocytes. Consistent with these observations, we found by ektacytometry decreased membrane mechanical stability of knockout …
Calhm1 Ion Channel Elicits Amyloid-Beta Clearance By Insulin-Degrading Enzyme In Cell Lines And In Vivo In The Mouse Brain, V. Vingtdeux, P. Chandakkar, H. Zhao, L. Blanc, S. Ruiz, P. Marambaud
Calhm1 Ion Channel Elicits Amyloid-Beta Clearance By Insulin-Degrading Enzyme In Cell Lines And In Vivo In The Mouse Brain, V. Vingtdeux, P. Chandakkar, H. Zhao, L. Blanc, S. Ruiz, P. Marambaud
Journal Articles
Alzheimer's disease is characterized by amyloid-beta (Abeta) peptide accumulation in the brain. CALHM1, a cell-surface Ca(2+) channel expressed in brain neurons, has anti-amyloidogenic properties in cell cultures. Here, we show that CALHM1 controls Abeta levels in vivo in the mouse brain through a previously unrecognized mechanism of regulation of Abeta clearance. Using pharmacological and genetic approaches in cell lines, we found that CALHM1 ion permeability and extracellular Ca(2+) were required for the Abeta-lowering effect of CALHM1. Abeta level reduction by CALHM1 could be explained by an increase in extracellular Abeta degradation by insulin-degrading enzyme (IDE), extracellular secretion of which was …