a-Thalassemia trait caused by frameshift mutations in exon 2 of the a2-globin gene: HBA2:c.131delT and HBA2:c.143delA

We describe two frameshift mutations associated with an a-thalassemia (a-thal) phenotype, identified in three unrelated individuals investigated for persistent microcytosis. The first mutation, HBA2:c.131delT, is located in codon 43, and the second, HBA2:c.143delA, is located in codon 47. Both are d...

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Main Authors: Finlayson, J., Ghassemifar, Reza, Holmes, P., Grey, D., Newbound, C., Pell, N., Jennens, M., Greenwood, L., Beilby, J.
Format: Journal Article
Published: 2012
Online Access:http://hdl.handle.net/20.500.11937/47879
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author Finlayson, J.
Ghassemifar, Reza
Holmes, P.
Grey, D.
Newbound, C.
Pell, N.
Jennens, M.
Greenwood, L.
Beilby, J.
author_facet Finlayson, J.
Ghassemifar, Reza
Holmes, P.
Grey, D.
Newbound, C.
Pell, N.
Jennens, M.
Greenwood, L.
Beilby, J.
author_sort Finlayson, J.
building Curtin Institutional Repository
collection Online Access
description We describe two frameshift mutations associated with an a-thalassemia (a-thal) phenotype, identified in three unrelated individuals investigated for persistent microcytosis. The first mutation, HBA2:c.131delT, is located in codon 43, and the second, HBA2:c.143delA, is located in codon 47. Both are due to single base pair deletions that cause a frameshift and a premature termination codon (PTC) at positions 48/49. The presence of a PTC at this position has been documented to result in nonsense mediated mRNA decay that would account for the thalassemic phenotype.
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institution Curtin University Malaysia
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last_indexed 2025-11-14T09:36:19Z
publishDate 2012
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spelling curtin-20.500.11937-478792017-09-13T14:18:22Z a-Thalassemia trait caused by frameshift mutations in exon 2 of the a2-globin gene: HBA2:c.131delT and HBA2:c.143delA Finlayson, J. Ghassemifar, Reza Holmes, P. Grey, D. Newbound, C. Pell, N. Jennens, M. Greenwood, L. Beilby, J. We describe two frameshift mutations associated with an a-thalassemia (a-thal) phenotype, identified in three unrelated individuals investigated for persistent microcytosis. The first mutation, HBA2:c.131delT, is located in codon 43, and the second, HBA2:c.143delA, is located in codon 47. Both are due to single base pair deletions that cause a frameshift and a premature termination codon (PTC) at positions 48/49. The presence of a PTC at this position has been documented to result in nonsense mediated mRNA decay that would account for the thalassemic phenotype. 2012 Journal Article http://hdl.handle.net/20.500.11937/47879 10.3109/03630269.2012.717053 restricted
spellingShingle Finlayson, J.
Ghassemifar, Reza
Holmes, P.
Grey, D.
Newbound, C.
Pell, N.
Jennens, M.
Greenwood, L.
Beilby, J.
a-Thalassemia trait caused by frameshift mutations in exon 2 of the a2-globin gene: HBA2:c.131delT and HBA2:c.143delA
title a-Thalassemia trait caused by frameshift mutations in exon 2 of the a2-globin gene: HBA2:c.131delT and HBA2:c.143delA
title_full a-Thalassemia trait caused by frameshift mutations in exon 2 of the a2-globin gene: HBA2:c.131delT and HBA2:c.143delA
title_fullStr a-Thalassemia trait caused by frameshift mutations in exon 2 of the a2-globin gene: HBA2:c.131delT and HBA2:c.143delA
title_full_unstemmed a-Thalassemia trait caused by frameshift mutations in exon 2 of the a2-globin gene: HBA2:c.131delT and HBA2:c.143delA
title_short a-Thalassemia trait caused by frameshift mutations in exon 2 of the a2-globin gene: HBA2:c.131delT and HBA2:c.143delA
title_sort a-thalassemia trait caused by frameshift mutations in exon 2 of the a2-globin gene: hba2:c.131delt and hba2:c.143dela
url http://hdl.handle.net/20.500.11937/47879