Pyridine nucleotide metabolites stimulate calcium release from sea urchin egg microsomes desensitized to inositol trisphosphate.

Clapper, D. L.; Walseth, Timothy F.; Dargie, P J; Lee, Hon Cheung

doi:10.1016/s0021-9258(18)47970-7

Cited by 528 publications

(167 citation statements)

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“…The egg homogenate system contained Ca 2+ pumps that were able to pump Ca 2+ into vesicles in an ATP-dependent manner and IP 3 receptors that would release Ca 2+ from the vesicles in response to the addition of IP 3 . Two important observations using the sea urchin egg homogenate system were made in 1987 ( 9 ). The first was that nicotinamide adenine dinucleotide (NAD) was able to release Ca 2+ , but only after a lag of several minutes.…”

Section: Naadp: Discovery In Sea Urchin Egg Homogenatementioning

confidence: 99%

“…The lag in the response to NAD was due to the conversion of NAD to cADPR by ADP-ribosyl cyclases. The second observation was that nicotinamide adenine dinucleotide (NADP) caused an immediate and robust release of Ca 2+ from the egg homogenate ( 9 ). Further examination of the NADP-induced Ca 2+ release revealed that the release was not due to NADP itself, but a contaminant in commercial sources of NADP that could be resolved chromatographically from NADP ( 1 ).…”

Section: Naadp: Discovery In Sea Urchin Egg Homogenatementioning

confidence: 99%

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NAADP: From Discovery to Mechanism

Walseth

Guse

2021

Front. Immunol.

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Nicotinic acid adenine dinucleotide 2’-phosphate (NAADP) is a naturally occurring nucleotide that has been shown to be involved in the release of Ca2+ from intracellular stores in a wide variety of cell types, tissues and organisms. Current evidence suggests that NAADP may function as a trigger to initiate a Ca2+ signal that is then amplified by other Ca2+ release mechanisms. A fundamental question that remains unanswered is the identity of the NAADP receptor. Our recent studies have identified HN1L/JPT2 as a high affinity NAADP binding protein that is essential for the modulation of Ca2+ channels.

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Section: Naadp: Discovery In Sea Urchin Egg Homogenatementioning

confidence: 99%

Section: Naadp: Discovery In Sea Urchin Egg Homogenatementioning

confidence: 99%

NAADP: From Discovery to Mechanism

Walseth

Guse

2021

Front. Immunol.

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“…Sea urchin eggs were the material with which two new second messengers were discovered. The story began with the demonstration that pyridine nucleotide derivatives could release calcium from the egg's stores independently of InsP 3 (Clapper et al 1987). The first of these derivatives to be purified was cyclic ADPribose (cADPr; Lee et al 1989) and the second was nicotinic acid adenine dinucleotide phosphate (NAADP; .…”

Section: Fertilization Second Messengersmentioning

confidence: 99%

Calcium signalling in early embryos

Whitaker

2008

Phil. Trans. R. Soc. B

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The onset of development in most species studied is triggered by one of the largest and longest calcium transients known to us. It is the most studied and best understood aspect of the calcium signals that accompany and control development. Its properties and mechanisms demonstrate what embryos are capable of and thus how the less-understood calcium signals later in development may be generated. The downstream targets of the fertilization calcium signal have also been identified, providing some pointers to the probable targets of calcium signals further on in the process of development.In one species or another, the fertilization calcium signal involves all the known calcium-releasing second messengers and many of the known calcium-signalling mechanisms. These calcium signals also usually take the form of a propagating calcium wave or waves.Fertilization causes the cell cycle to resume, and therefore fertilization signals are cell-cycle signals. In some early embryonic cell cycles, calcium signals also control the progress through each cell cycle, controlling mitosis.Studies of these early embryonic calcium-signalling mechanisms provide a background to the calcium-signalling events discussed in the articles in this issue.

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“…A recent study showed that NAD breakdown products signal degeneration following activation of plant TIR domains (Wan et al, 2019), suggesting excess cADPR and ADPR production can contribute to a degenerative process. cADPR is a calcium mobilizing agent that potentiates calcium-induced calcium release in sea urchin egg homogenate (Clapper et al, 1987;Lee, 1993;Lee et al, 1989), and in other cell types, including T-lymphocytes (Guse et al, 1999), cardiac myocytes (Rakovic et al, 1996), and neurons (Currie et al, 1992;Higashida et al, 2001). Studies using pharmacological approaches or in vitro reconstitution of channels have shown that cADPR modulates intracellular calcium release through ryanodine receptor channels (RyRs) but not inositol 1,4,5-trisphosphate receptors (IP 3 Rs) (Clapper et al, 1987;Dargie et al, 1990;Meszaros et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

“…cADPR is a calcium mobilizing agent that potentiates calcium-induced calcium release in sea urchin egg homogenate (Clapper et al, 1987;Lee, 1993;Lee et al, 1989), and in other cell types, including T-lymphocytes (Guse et al, 1999), cardiac myocytes (Rakovic et al, 1996), and neurons (Currie et al, 1992;Higashida et al, 2001). Studies using pharmacological approaches or in vitro reconstitution of channels have shown that cADPR modulates intracellular calcium release through ryanodine receptor channels (RyRs) but not inositol 1,4,5-trisphosphate receptors (IP 3 Rs) (Clapper et al, 1987;Dargie et al, 1990;Meszaros et al, 1993). Moreover, both cADPR and ADPR activate TRPM2, a calcium permeable non-specific cation channel located predominantly on the plasma membrane (Kolisek et al, 2005;Yu et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Activation of Sarm1 produces cADPR to increase intra-axonal calcium and promote axon degeneration in CIPN

Avizonis

et al. 2021

Preprint

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Cancer patients frequently develop chemotherapy-induced peripheral neuropathy (CIPN), a painful and long-lasting disorder with profound somatosensory deficits. There are no effective therapies to prevent or treat this disorder. Pathologically, CIPN is characterized by a dying-back axonopathy that begins at intra-epidermal nerve terminals of sensory neurons and progresses in a retrograde fashion. Calcium dysregulation constitutes a critical event in CIPN, but it is not known how chemotherapies such as paclitaxel alter intra-axonal calcium and cause degeneration. Here, we demonstrate that paclitaxel triggers Sarm1-dependent cADPR production in distal axons, promoting intra-axonal calcium flux from both intracellular and extracellular calcium stores. Genetic or pharmacologic antagonists of cADPR signaling prevent paclitaxel-induced axon degeneration and allodynia symptoms, without mitigating the anti-neoplastic efficacy of paclitaxel. Our data demonstrate that cADPR is a calcium modulating factor that promotes paclitaxel-induced axon degeneration and suggest that targeting cADPR signaling provides a potential therapeutic approach for treating CIPN.

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Pyridine nucleotide metabolites stimulate calcium release from sea urchin egg microsomes desensitized to inositol trisphosphate.

Cited by 528 publications

References 24 publications

NAADP: From Discovery to Mechanism

NAADP: From Discovery to Mechanism

Calcium signalling in early embryos

Activation of Sarm1 produces cADPR to increase intra-axonal calcium and promote axon degeneration in CIPN

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