The Role of ATP in the Regulation of NCAM Function

Martin Hübschmann; Galina Skladchikova

doi:10.1007/s11064-008-9769-7

The Role of ATP in the Regulation of NCAM Function

Abstract

Extracellular ATP is an abundant signaling molecule that has a number of functions in the nervous system. It is released by both neurons and glial cells, activates purinergic receptors and acts as a trophic factor as well as a neurotransmitter. In this review, we summarize the evidence for a direct ATP-NCAM interaction and discuss its functional implications. The ectodomain of NCAM contains the ATP binding Walker motif A and has intrinsic ATPase activity, which could modulate NCAM-dependent signaling processes. NCAM interacts directly with and signals through FGFR. The NCAM binding site to ATP overlaps with the site of NCAM-FGFR interaction, and ATP is capable of disrupting NCAM-FGFR binding. This implies that NCAM signaling through FGFR can be regulated by ATP, which is supported by the observation that ATP can abrogate NCAM-induced neurite outgrowth. Finally, ATP can induce NCAM ectodomain shedding, possibly affecting the structural plasticity associated with learning and memory.

Original language	English
Journal	Neurochemical Research
ISSN	0364-3190
DOIs	https://doi.org/10.1007/s11064-008-9769-7
Publication status	Published - 2008

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title = "The Role of ATP in the Regulation of NCAM Function",

abstract = "Extracellular ATP is an abundant signaling molecule that has a number of functions in the nervous system. It is released by both neurons and glial cells, activates purinergic receptors and acts as a trophic factor as well as a neurotransmitter. In this review, we summarize the evidence for a direct ATP-NCAM interaction and discuss its functional implications. The ectodomain of NCAM contains the ATP binding Walker motif A and has intrinsic ATPase activity, which could modulate NCAM-dependent signaling processes. NCAM interacts directly with and signals through FGFR. The NCAM binding site to ATP overlaps with the site of NCAM-FGFR interaction, and ATP is capable of disrupting NCAM-FGFR binding. This implies that NCAM signaling through FGFR can be regulated by ATP, which is supported by the observation that ATP can abrogate NCAM-induced neurite outgrowth. Finally, ATP can induce NCAM ectodomain shedding, possibly affecting the structural plasticity associated with learning and memory.",

author = "Martin H{\"u}bschmann and Galina Skladchikova",

year = "2008",

doi = "10.1007/s11064-008-9769-7",

language = "English",

journal = "Neurochemical Research",

issn = "0364-3190",

publisher = "Springer",

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T1 - The Role of ATP in the Regulation of NCAM Function

AU - Hübschmann, Martin

AU - Skladchikova, Galina

PY - 2008

Y1 - 2008

N2 - Extracellular ATP is an abundant signaling molecule that has a number of functions in the nervous system. It is released by both neurons and glial cells, activates purinergic receptors and acts as a trophic factor as well as a neurotransmitter. In this review, we summarize the evidence for a direct ATP-NCAM interaction and discuss its functional implications. The ectodomain of NCAM contains the ATP binding Walker motif A and has intrinsic ATPase activity, which could modulate NCAM-dependent signaling processes. NCAM interacts directly with and signals through FGFR. The NCAM binding site to ATP overlaps with the site of NCAM-FGFR interaction, and ATP is capable of disrupting NCAM-FGFR binding. This implies that NCAM signaling through FGFR can be regulated by ATP, which is supported by the observation that ATP can abrogate NCAM-induced neurite outgrowth. Finally, ATP can induce NCAM ectodomain shedding, possibly affecting the structural plasticity associated with learning and memory.

AB - Extracellular ATP is an abundant signaling molecule that has a number of functions in the nervous system. It is released by both neurons and glial cells, activates purinergic receptors and acts as a trophic factor as well as a neurotransmitter. In this review, we summarize the evidence for a direct ATP-NCAM interaction and discuss its functional implications. The ectodomain of NCAM contains the ATP binding Walker motif A and has intrinsic ATPase activity, which could modulate NCAM-dependent signaling processes. NCAM interacts directly with and signals through FGFR. The NCAM binding site to ATP overlaps with the site of NCAM-FGFR interaction, and ATP is capable of disrupting NCAM-FGFR binding. This implies that NCAM signaling through FGFR can be regulated by ATP, which is supported by the observation that ATP can abrogate NCAM-induced neurite outgrowth. Finally, ATP can induce NCAM ectodomain shedding, possibly affecting the structural plasticity associated with learning and memory.

U2 - 10.1007/s11064-008-9769-7

DO - 10.1007/s11064-008-9769-7

M3 - Journal article

C2 - 18607723

SN - 0364-3190

JO - Neurochemical Research

JF - Neurochemical Research

ER -

The Role of ATP in the Regulation of NCAM Function

Abstract

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