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Adenosine triphosphate secretion (ATP secretion)

Target
ATP secretion
Molecular classification
Other (ATP is a small molecule nucleotide; "secretion" is a process, not a molecular target)
01

Overview

Adenosine triphosphate (ATP) secretion refers to the active process by which cells export intracellular ATP into the extracellular space. This process is not itself a single molecular target but rather a cellular event involving multiple proteins and pathways. Extracellular ATP acts as an important signaling molecule in various physiological contexts including neurotransmission, immune responses, and inflammation. Mechanistically, ATP can be secreted via several routes, such as exocytosis of secretory vesicles containing high concentrations of ATP—mediated by the vesicular nucleotide transporter (VNUT)—or through plasma membrane channels like pannexin 1 during processes such as immunogenic cell death[6][7]. During cancer therapy-induced immunogenic cell death, for example, dying tumor cells secrete large amounts of ATP via mechanisms requiring autophagy-related lysosomal exocytosis and caspase-dependent activation of both Rho-associated kinase 1 (ROCK1) and myosin II-driven blebbing. Pannexin 1 channels are also involved in this regulated release pathway[6]. Extracellularly released ATP functions as a danger signal, activating purinergic receptors on immune cells to stimulate anti-tumor immunity or modulate inflammation. Dysregulation or excessive extracellular accumulation can contribute to pathological conditions such as chronic inflammation or neuropathic pain. Because "ATP secretion" describes a biological process rather than an individual protein or receptor target—and involves multiple molecules—it is not considered an actionable therapeutic target itself but rather an outcome influenced by targeting specific transporters/channels or upstream regulators involved in its control[6][7].

Other names
ATP releaseextracellular ATP releasepurinergic signaling (context-dependent)
02

Mechanism of action

Inhibition of vesicular nucleotide transporter to reduce vesicular/extracellular ATP[7] Induction of immunogenic cell death leading to caspase-dependent and pannexin 1 channel-mediated ATP secretion[6]

03

Biological functions

Signal transductionImmune responseNeurotransmissionCell-to-cell communication
04

Disease associations

Cancer (immunogenic cell death)InflammationNeurological disorders
05

Interacting drugs

DIDS (4,4'-diisothiocyano-2,2'-disulphonic stilbene acid; inhibits vesicular nucleotide transporter VNUT)[7]

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