ArticleCommunicative & integrative biology2013
NAADP/TPC2/Ca(2+) Signaling Inhibits Autophagy.
Article in Communicative & integrative biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Mechanisms of autophagy-lysosome dysfunction in neurodegenerative diseases.Nature reviews. Molecular cell biology · 2024Review
- Structural basis for inhibition of the lysosomal two-pore channel TPC2 by a small molecule antagonist.Structure (London, England : 1993) · 2024Article
- Protein mishandling and impaired lysosomal proteolysis generated through calcium dysregulation in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Lysosomal TPCN (two pore segment channel) inhibition ameliorates beta-amyloid pathology and mitigates memory impairment in Alzheimer disease.Autophagy · 2022Article
- Targeting the two-pore channel 2 in cancer progression and metastasis.Exploration of targeted anti-tumor therapy · 2022Review
- Ion Channels and Transporters in Autophagy.Autophagy · 2022Article
- Review
- NAADP-induced intracellular calcium ion is mediated by the TPCs (two-pore channels) in hypoxia-induced pulmonary arterial hypertension.Journal of cellular and molecular medicine · 2021Article
- Sex-dependent calcium hyperactivity due to lysosomal-related dysfunction in astrocytes from APOE4 versus APOE3 gene targeted replacement mice.Molecular neurodegeneration · 2020Article
- Two-pore channels (TPCs): Novel voltage-gated ion channels with pleiotropic functions.Channels (Austin, Tex.) · 2017Review
- Two-Pore Channels: Catalyzers of Endolysosomal Transport and Function.Frontiers in pharmacology · 2017Review
- The reverse-mode NCX1 activity inhibitor KB-R7943 promotes prostate cancer cell death by activating the JNK pathway and blocking autophagic flux.Oncotarget · 2016Article
- Two-pore channels function in calcium regulation in sea star oocytes and embryos.Development (Cambridge, England) · 2014Article
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Authors and funding
4 authors.
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Abstract
Nicotinic adenine acid dinucleotide phosphate (NAADP) is one of the most potent endogenous Ca(2+) mobilizing messengers. NAADP mobilizes Ca(2+) from an acidic lysosome-related store, which can be subsequently amplified into global Ca(2+) waves by calcium-induced calcium release (CICR) from ER/SR via Ins(1,4,5)P 3 receptors or ryanodine receptors. A body of evidence indicates that 2 pore channel 2 (TPC2), a new member of the superfamily of voltage-gated ion channels containing 12 putative transmembrane segments, is the long sought after NAADP receptor. Activation of NAADP/TPC2/Ca(2+) signaling inhibits the fusion between autophagosome and lysosome by alkalizing the lysosomal pH, thereby arresting autophagic flux. In addition, TPC2 is downregulated during neural differentiation of mouse embryonic stem (ES) cells, and TPC2 downregulation actually facilitates the neural lineage entry of ES cells. Here we propose the mechanism underlying how NAADP-induced Ca(2+) release increases lysosomal pH and discuss the role of TPC2 in neural differentiation of mouse ES cells.
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