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Updated: Jan 23, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

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Published on: June 7, 2016

NAADP Receptors.

Antony Galione¹

¹Department of Pharmacology, University of Oxford, Oxford OX1 3QT, United Kingdom.

Cold Spring Harbor Perspectives in Biology

|June 12, 2019

Summary

This summary is machine-generated.

Nicotinic acid adenine dinucleotide phosphate (NAADP) triggers calcium release from acidic organelles via two-pore channels (TPCs). This signaling pathway plays diverse roles in cellular functions, including vesicular trafficking and plasma membrane excitability.

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Area of Science:

Cellular Biology
Biochemistry
Physiology

Background:

Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent calcium (Ca2+) mobilizing messenger.
Two-pore channels (TPCs) are emerging as key regulators of Ca2+ release.
Endolysosomes are recognized as important sites for Ca2+ signaling.

Purpose of the Study:

To review the role of NAADP-mediated Ca2+ release from endolysosomal stores.
To discuss the function of TPCs in intracellular calcium signaling.
To highlight the significance of lysosomes in Ca2+ signaling.

Main Methods:

Literature review of recent studies on NAADP and TPCs.
Analysis of the identified roles of TPCs in Ca2+ signaling.
Discussion of the localization and function of TPCs at endolysosomes.

Main Results:

NAADP elicits Ca2+ release from endolysosomal stores, often indirectly via TPCs.
TPCs mediate local Ca2+ release influencing vesicular fusion and trafficking.
TPCs can trigger global Ca2+ release and regulate plasma membrane excitability.

Conclusions:

NAADP-mediated Ca2+ release through TPCs is a widespread trigger for intracellular calcium signaling.
TPCs highlight the crucial role of lysosomes in cellular Ca2+ dynamics.
Further understanding of TPCs enhances insights into lysosomal function in Ca2+ signaling.