Photoaffinity Labeling of Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) Targets in Mammalian Cells*

Lin-Moshier, Yaping; Walseth, Timothy F.; Churamani, Dev; Davidson, Sean M.; Slama, James T.; Hooper, Robert; Brailoiu, Eugene; Patel, Sandip; Marchant, Jonathan S.

doi:10.1074/jbc.m111.305813

Cited by 154 publications

(172 citation statements)

References 32 publications

(53 reference statements)

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“…Third, whereas the intracellular target of InsP3 has long been recognized, the selective receptor of the two newly discovered second messengers, cADPr and NAADP, has recently been questioned. Indeed, a couple of recent investigations demonstrated that the genetic suppression of TPC1-2 does not prevent cell labeling by NAADP [415,416] . Conversely, the same studies suggested that a 22-and 23-kDa pair of accessory proteins might serve as NAADP receptors and regulate the activity of its target channels, including TPC1-2 in ECs and RyRs in the immune system.…”

Section: Resultsmentioning

confidence: 99%

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Moccia

Berra‐Romani²,

Tanzi³

2012

WJBC

110

192

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A monolayer of endothelial cells (ECs) lines the lumen of blood vessels and forms a multifunctional transducing organ that mediates a plethora of cardiovascular processes. The activation of ECs from as state of quiescence is, therefore, regarded among the early events leading to the onset and progression of potentially lethal diseases, such as hypertension, myocardial infarction, brain stroke, and tumor. Intracellular Ca 2+ signals have long been know to play a central role in the complex network of signaling pathways regulating the endothelial functions. Notably, recent work has outlined how any change in the pattern of expression of endothelial channels, transporters and pumps involved in the modulation of intracellular Ca 2+ levels may dramatically affect whole body homeostasis. Vascular ECs may react to both mechanical and chemical stimuli by generating a variety of intracellular Ca 2+ signals, ranging from brief, localized Ca 2+ pulses to prolonged Ca 2+ oscillations engulfing the whole cytoplasm. The well-defined spatiotemporal profile of the subcellular Ca 2+ signals elicited in ECs by specific extracellular inputs depends on the interaction between Ca 2+ releasing channels, which are located both on the plasma membrane and in a number of intracellular organelles, and Ca 2+ removing systems. The present article aims to summarize both the past and recent literature in the field to provide a clear-cut picture of our current knowledge on the molecular nature and the role played by the components of the Ca 2+ machinery in vascular ECs under both physiological and pathological conditions.

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Section: Resultsmentioning

confidence: 99%

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Moccia

Berra‐Romani²,

Tanzi³

2012

WJBC

110

192

View full text Add to dashboard Cite

show abstract

“…Literature suggest proton-permeable ion channels activated by NAADP or Ca 2C ; 18 although photoaffinity labeling studies suggest that NAADP does not directly bind TPCs. 19,20 However other studies indicate Na C -selective channels regulated by phosphoinositide-3,5-bisphosphate (PI(3,5)P 2 ) and ATP. 21,22 Further studies may still be needed to account for both sets of data.…”

Section: Introductionmentioning

confidence: 99%

Two-pore channel 1 interacts with citron kinase, regulating completion of cytokinesis

et al. 2015

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Two-pore channels (TPC1, 2, and 3) are recently identified endolysosmal ion channels, but remain poorly characterized. In this study, we show for the first time a role for TPC1 in cytokinesis, the final step in cell division. HEK 293 T-REx cells inducibly overexpressing TPC1 demonstrated a lack of proliferation accompanied by multinucleation and an increase in G2/M cycling cells. Increased TPC1 was associated with a concomitant accumulation of active RhoGTP and a decrease in phosphorylated myosin light chain (MLC). Finally, we demonstrated a novel interaction between TPC1 and citron kinase (CIT). These results identify TPC1 as a central component of cytokinetic control, specifically during abscission, and introduce a means by which the endolysosomal system may play an active role in this process.

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“…One piece of evidence supporting this idea is the preservation of photolabeling in TPC knockout mice (11). For example, as shown in Fig.…”

mentioning

confidence: 69%

“…Photolabeling studies using a radioactive NAADP-derived probe (5N 3 -[ 32 P]NAADP) have suggested that NAADP may not directly bind to TPCs but may stimulate channel activity via small NAADP-binding proteins (ϳ23 kDa) associated with the TPC complex (11)(12)(13)(14). One piece of evidence supporting this idea is the preservation of photolabeling in TPC knockout mice (11).…”

mentioning

confidence: 80%

TPC1 Knockout Knocks Out TPC1

Hooper

Churamani

Davidson

et al. 2015

Molecular and Cellular Biology

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Photoaffinity Labeling of Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) Targets in Mammalian Cells*

Cited by 154 publications

References 32 publications

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Two-pore channel 1 interacts with citron kinase, regulating completion of cytokinesis

TPC1 Knockout Knocks Out TPC1

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Photoaffinity Labeling of Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) Targets in Mammalian Cells*

Cited by 154 publications

References 32 publications

Update on vascular endothelial Ca2+signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca2+signalling: A tale of ion channels, pumps and transporters

Two-pore channel 1 interacts with citron kinase, regulating completion of cytokinesis

TPC1 Knockout Knocks Out TPC1

Contact Info

Product

Resources

About

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters