The AMP-activated protein kinase beta 1 subunit modulates erythrocyte integrity.
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.
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
Emma L
EL
Cambridge
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
Zoe
Z
McIntyre
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
Simon
S
Clare
University of Edinburgh Division of Pathology, Centre for Comparative Pathology, Institute of Genetics & Molecular Medicine, Western General Hospital, Edinburgh, UK.
Mark J
MJ
Arends
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
David
D
Goulding
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
Christopher
C
Isherwood
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
Susana S
SS
Caetano
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
Carmen Ballesteros
CB
Reviriego
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
Agnieszka
A
Swiatkowska
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
Leanne
L
Kane
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
Katherine
K
Harcourt
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
David J
DJ
Adams
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK.
Jacqueline K
JK
White
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, UK. Electronic address: as24@sanger.ac.uk.
Anneliese O
AO
Speak
D055372:AMP-Activated Protein Kinases / Q000235:genetics* / Q000378:metabolism*; D000747:Anemia, Hypochromic / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000818:Animals; D004912:Erythrocytes / Q000166:cytology / Q000378:metabolism* / Q000473:pathology / Q000648:ultrastructure; D004920:Erythropoiesis / Q000235:genetics; D005260:Female; D015870:Gene Expression; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D020033:Protein Isoforms; D013154:Spleen / Q000378:metabolism / Q000473:pathology
D020033:Protein Isoforms; C554549:Prkab1 protein, mouse; D055372:AMP-Activated Protein Kinases
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