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Inositol trisphosphate receptor Ca2+ release channels.
The inositol 1,4,5-trisphosphate (InsP3) receptors (InsP3Rs) are a family of Ca2+ release channels localized predominately in the endoplasmic reticulum of all cell types. They function to releaseExpand
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Essential Regulation of Cell Bioenergetics by Constitutive InsP3 Receptor Ca2+ Transfer to Mitochondria
Mechanisms that regulate cellular metabolism are a fundamental requirement of all cells. Most eukaryotic cells rely on aerobic mitochondrial metabolism to generate ATP. Nevertheless, regulation ofExpand
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Mechanism of Ca2+ Disruption in Alzheimer's Disease by Presenilin Regulation of InsP3 Receptor Channel Gating
Mutations in presenilins (PS) are the major cause of familial Alzheimer's disease (FAD) and have been associated with calcium (Ca2+) signaling abnormalities. Here, we demonstrate that FAD mutant PS1Expand
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Gain-of-Function Enhancement of IP3 Receptor Modal Gating by Familial Alzheimer’s Disease–Linked Presenilin Mutants in Human Cells and Mouse Neurons
By altering IP3 receptor gating, presenilin mutations associated with familial Alzheimer’s disease increase Ca2+ release from the endoplasmic reticulum. Opening the Calcium Floodgates? Alzheimer’sExpand
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Mode Switching Is the Major Mechanism of Ligand Regulation of InsP3 Receptor Calcium Release Channels
The inositol 1,4,5-trisphosphate (InsP3) receptor (InsP3R) plays a critical role in generation of complex Ca2+ signals in many cell types. In patch clamp recordings of isolated nuclei from insect Sf9Expand
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Familial Alzheimer’s disease–associated presenilin 1 mutants promote γ-secretase cleavage of STIM1 to impair store-operated Ca2+ entry
Excess cleavage of STIM1 may underlie calcium homeostasis defects that contribute to memory loss in Alzheimer’s disease. Cleaving toward memory loss The senile dementia that occurs in Alzheimer’sExpand
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Constitutive cAMP response element binding protein (CREB) activation by Alzheimer's disease presenilin-driven inositol trisphosphate receptor (InsP3R) Ca2+ signaling
Mutations in presenilins (PS) account for most early-onset familial Alzheimer's disease (FAD). Accumulating evidence suggests that disrupted Ca2+ signaling may play a proximal role in FADExpand
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Graded recruitment and inactivation of single InsP3 receptor Ca2+‐release channels: implications for quartal Ca2+release
Modulation of cytoplasmic free Ca2+ concentration ([Ca2+]i) by receptor‐mediated generation of inositol 1,4,5‐trisphosphate (InsP3) and activation of its receptor (InsP3R), a Ca2+‐release channel inExpand
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The Presenilin-2 Loop Peptide Perturbs Intracellular Ca2+ Homeostasis and Accelerates Apoptosis*
In cells undergoing apoptosis, a 22-amino-acid presenilin-2-loop peptide (PS2-LP, amino acids 308–329 in presenilin-2) is generated through cleavage of the carboxyl-terminal fragment of presenilin-2Expand
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Calpain-cleaved Type 1 Inositol 1,4,5-Trisphosphate Receptor (InsP3R1) Has InsP3-independent Gating and Disrupts Intracellular Ca2+ Homeostasis*
The type 1 inositol 1,4,5-trisphosphate receptor (InsP3R1) is a ubiquitous intracellular Ca2+ release channel that is vital to intracellular Ca2+ signaling. InsP3R1 is a proteolytic target ofExpand
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