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 PMID:27666489  

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

Emma L Cambridge | Zoe McIntyre | Simon Clare | Mark J Arends | David Goulding | Christopher Isherwood | Susana S Caetano | Carmen Ballesteros Reviriego | Agnieszka Swiatkowska | Leanne Kane | Katherine Harcourt | Sanger Mouse Genetics Project | David J Adams | Jacqueline K White | Anneliese O Speak
Experimental hematology | 2017

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.

Pubmed ID: 27666489

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Associated grants

  • Agency: Wellcome Trust, United Kingdom
  • Agency: Cancer Research UK, United Kingdom
    Id: 13031

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International Mouse Phenotyping Consortium (IMPC) (tool)

RRID:SCR_006158

Center that produces knockout mice and carries out high-throughput phenotyping of each line in order to determine function of every gene in mouse genome. These mice will be preserved in repositories and made available to scientific community representing valuable resource for basic scientific research as well as generating new models for human diseases.

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