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Exp Hematol. 2017 Jan;45:64-68.e5. doi: 10.1016/j.exphem.2016.09.006. Epub 2016 Sep 22.

The AMP-activated protein kinase beta 1 subunit modulates erythrocyte integrity.

Author information

1
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
2
University of Edinburgh Division of Pathology, Centre for Comparative Pathology, Institute of Genetics & Molecular Medicine, Western General Hospital, Edinburgh, UK.
3
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK. Electronic address: as24@sanger.ac.uk.

Abstract

Failure to maintain a normal in vivo erythrocyte half-life results in the development of hemolytic anemia. Half-life is affected by numerous factors, including energy balance, electrolyte gradients, reactive oxygen species, and membrane plasticity. The heterotrimeric AMP-activated protein kinase (AMPK) is an evolutionarily conserved serine/threonine kinase that acts as a critical regulator of cellular energy balance. Previous roles for the alpha 1 and gamma 1 subunits in the control of erythrocyte survival have been reported. In the work described here, we studied the role of the beta 1 subunit in erythrocytes and observed microcytic anemia with compensatory extramedullary hematopoiesis together with splenomegaly and increased osmotic resistance.

PMID:
27666489
PMCID:
PMC5823972
DOI:
10.1016/j.exphem.2016.09.006
[Indexed for MEDLINE]
Free PMC Article

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