Alzheimer ’ s disease-associated peptide A β 42 mobilizes ER Ca 2 + via InsP 3 R-dependent and-independent mechanisms

@inproceedings{Jensen2013AlzheimerS,
  title={Alzheimer ’ s disease-associated peptide A β 42 mobilizes ER Ca 2 + via InsP 3 R-dependent and-independent mechanisms},
  author={Laura E. Jensen and Geert Bultynck and Tomas Luyten and Hozeefa Amijee and Martin D Bootman and H Llewelyn Roderick},
  year={2013}
}
*Correspondence: H. Llewelyn Roderick, Babraham Institute, Babraham, Cambridge, CB22 3AT, UK e-mail: llewelyn.roderick@ babraham.ac.uk †Present address: Martin D. Bootman, Department of Life, Health and Chemical Sciences, The Open University, Milton Keynes, UK Dysregulation of Ca2+ homeostasis is considered to contribute to the toxic action of the Alzheimer’s disease (AD)-associated amyloid-β-peptide (Aβ). Ca2+ fluxes across the plasma membrane and release from intracellular stores have both… CONTINUE READING
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Alzheimer’s disease-associated peptide Aβ42 mobilizes ER Ca2+ via InsP3Rdependent and -independent mechanisms

  • LE Citation Jensen, G Bultynck, T Luyten, H Amijee, MD Bootman, HL Roderick
  • 2013

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums

  • Jensen, Bultynck, Luyten, Amijee, Bootman, Roderick
  • 2013

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