The gain-of-function enhancement of IP3-receptor channel gating by familial Alzheimer's disease-linked presenilin mutants increases the open probability of mitochondrial permeability transition pore.

doi:10.1016/j.ceca.2016.05.002

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Article

The gain-of-function enhancement of IP3-receptor channel gating by familial Alzheimer's disease-linked presenilin mutants increases the open probability of mitochondrial permeability transition pore.

Cell calcium - 1 Jul 2016

Toglia Patrick, Ullah Ghanim

Abstract excerpt

Mutants in presenilins (PS1 or PS2) are the major cause of familial Alzheimer's disease (FAD). They affect intracellular Ca(2+) homeostasis by increasing the open probability (Po) of inositol 1,4,5-trisposphate (IP3) receptor (IP3R) Ca(2+) release channel located on the endoplasmic reticulum (ER)...

Topics

Alzheimer Disease
Calcium
Humans
Hydrogen-Ion Concentration
Inositol 1,4,5-Trisphosphate Receptors
Ion Channel Gating
Mitochondria
Mitochondrial Membrane Transport Proteins
Mitochondrial Permeability Transition Pore
Mutation
Presenilins
Probability
Sodium-Calcium Exchanger
Time Factors

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PMID: 27184076
DOI: 10.1016/j.ceca.2016.05.002

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026. Prepared record publication-27184076-2026-08-30.1. Manifest publication-graph-cohort-2026-08-30.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 30 Aug 2026.

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