Carboxyl-terminal peptide of beta-amyloid precursor protein blocks inositol 1,4,5-trisphosphate-sensitive Ca2+ release in Xenopus laevis oocytes

The Journal of Biological Chemistry
Joung-Hun KimYoo-Hun Suh

Abstract

The effects of Alzheimer's disease-related amyloidogenic peptides on inositol 1,4,5-trisphosphate receptor-mediated Ca(2+) mobilization were examined in Xenopus laevis oocytes. Intracellular Ca(2+) was monitored by electrophysiological measurement of the endogenous Ca(2+)-activated Cl(-) current. Application of a hyperpolarizing pulse released intracellular Ca(2+) in oocytes primed by pre-injection of a non-metabolizable inositol 1,4,5-trisphosphate analogue. The carboxyl terminus of the amyloid precursor protein inhibited inositol 1,4,5-trisphosphate receptor-mediated intracellular Ca(2+) release in a dose-dependent manner. Equimolar beta-amyloid peptides Abeta(1-40) or Abeta(1-42) had no effect, and whereas a truncated carboxyl terminus lacking the Abeta domain was equipotent to the full-length one, a carboxyl terminus fragment lacking the NPTY sequence was less effective than the full-length fragment. The inhibition induced by the carboxyl terminus was not associated with the block of the Ca(2+)-dependent Cl(-) channel itself or compromised Ca(2+) influx. We conclude that the carboxyl terminus of the amyloid precursor protein inhibits inositol 1,4,5-trisphosphate-sensitive Ca(2+) release and could thus disrupt Ca(2+) homeost...Continue Reading

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Citations

Oct 23, 2002·Journal of Neuroscience Research·Cheol Hyoung ParkYoo-Hun Suh
Mar 21, 2017·Biochemical and Biophysical Research Communications·Jun Ki JangIck Young Kim
Mar 25, 2005·Physiological Reviews·Anant B Parekh, James W Putney
Feb 10, 2006·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Yun Ha JeongYoo-Hun Suh
Jul 21, 2009·Biochimica Et Biophysica Acta·Heng Du, Shirley ShiDu Yan
Jan 25, 2011·Medical Hypotheses·Wenfei HanJiansheng Su

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