Publication: Analysis of protein profiling studies of β-thalassemia/Hb E disease
Issued Date
2016-11-01
Resource Type
ISSN
18628354
18628346
18628346
Other identifier(s)
2-s2.0-84987665859
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Proteomics - Clinical Applications. Vol.10, No.11 (2016), 1093-1102
Suggested Citation
Pathrapol Lithanatudom, Duncan R. Smith Analysis of protein profiling studies of β-thalassemia/Hb E disease. Proteomics - Clinical Applications. Vol.10, No.11 (2016), 1093-1102. doi:10.1002/prca.201600086 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/42859
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Analysis of protein profiling studies of β-thalassemia/Hb E disease
Author(s)
Other Contributor(s)
Abstract
© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim A number of studies have used global protein profiling technologies on a range of patient samples to detect proteins that are differentially expressed in β-thalassemia/Hb E as an aid for understanding the physiopathology of this disease. Seven studies have identified a total of 111 unique, differentially expressed proteins. Seven proteins (prothrombin, alpha-1-antichymotrypsin, fibrinogen beta chain, hemoglobin beta, selenium-binding protein, microtubule-actin cross-linking factor and adenomatous polyposis coli protein 2) have been identified in two independent studies, whereas two proteins (carbonic anhydrase 1 and peroxiredoxin-2) have been identified in three independent studies. Both of these latter two proteins were consistently upregulated in the studies that identified them. Ontological analysis of all differentially regulated proteins identified “response to inorganic substances” as the most significant functional annotation cluster, which is consistent with iron overload being a major pathological consequence of this disease. Despite the range of samples investigated and the relatively small number of studies undertaken, a coherent picture of the mediators of the pathological consequences of β-thalassemia/Hb E disease is starting to emerge.