dc.creatorTerra, H T
dc.creatorSaad, M J
dc.creatorCarvalho, C R
dc.creatorVicentin, D L
dc.creatorCosta, F F
dc.creatorSaad, S T
dc.date1998-Jul
dc.date2015-11-27T12:19:15Z
dc.date2015-11-27T12:19:15Z
dc.date.accessioned2018-03-29T00:52:50Z
dc.date.available2018-03-29T00:52:50Z
dc.identifierAmerican Journal Of Hematology. v. 58, n. 3, p. 224-30, 1998-Jul.
dc.identifier0361-8609
dc.identifier
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/9662275
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/194187
dc.identifier9662275
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1294420
dc.descriptionIn order to investigate the tyrosine phosphorylation of band 3, we performed immunoblotting of intact red cells using anti-phosphotyrosine antibody of 21 patients with sickle cell disorders (11 SS, 5 Sbeta, 5 SC), 7 patients with beta thalassemias (5 beta thal intermedia, 2 deltabeta thal), 10 normal controls, and 1 patient with hereditary spherocytosis. They had not received transfusion for the last 4 months and all were clinically stable. Our results showed an increased tyrosine phosphorylation of two proteins, in the 100 and 80 kD regions, in sickle cell and beta-thalassemic red cells when compared to the normal controls and to the patient with hereditary spherocytosis. Immunoprecipitation of the lysed red cells with anti-band 3 antibody and immunoblotting with anti-phosphotyrosine antibody confirmed that the 100 kD tyrosine phosphorylated protein was band 3. In the sickle cell disease group, the band 3 tyrosine phosphorylation varied from 2- to 10-fold increase compared to control (x +/- SD; SS = 7.8- +/- 2.7-fold; SC = 3.8- +/- 1.3-fold; Sbeta = 5.2- +/- 2.0-fold). It was also higher in the beta-thalassemic group (beta-thal = 4.3- +/- 3.7-fold). There was no significant difference in tyrosine phosphorylation among the various groups tested, except when we compared the phosphorylation in intact red cells of patients with sickle cell anemia and hemoglobinopathy SC (U = 6, P < 0.02). The tyrosine phosphorylation of band 3 was increased in hemoglobinopathies even in the absence of high reticulocyte count. At least two mechanisms might be involved in the increased tyrosine phosphorylation of band 3 in these hemoglobin disorders, probably related to the endogenous reactive oxygen intermediates generated by the abnormal erythrocyte: an inhibition of protein tyrosine phosphatase activity or an activation of the protein tyrosine kinase p72syk.
dc.description58
dc.description224-30
dc.languageeng
dc.relationAmerican Journal Of Hematology
dc.relationAm. J. Hematol.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAdolescent
dc.subjectAdult
dc.subjectAnemia, Sickle Cell
dc.subjectAnion Exchange Protein 1, Erythrocyte
dc.subjectAntibodies
dc.subjectErythrocyte Count
dc.subjectErythrocytes
dc.subjectHemoglobin Sc Disease
dc.subjectHemoglobinopathies
dc.subjectHumans
dc.subjectImmunoblotting
dc.subjectPhosphorylation
dc.subjectPhosphotyrosine
dc.subjectProtein-tyrosine Kinases
dc.subjectReticulocytes
dc.subjectTyrosine
dc.subjectVanadates
dc.subjectBeta-thalassemia
dc.titleIncreased Tyrosine Phosphorylation Of Band 3 In Hemoglobinopathies.
dc.typeArtículos de revistas


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