Modulation of the homophilic interaction between the first and second Ig modules of neural cell adhesion molecule by heparin

Nikolaj Kulahin; Olga Rudenko; V. Kiselyov; Flemming M. Poulsen; Vladimir Berezin; Elisabeth Marianne Bock

doi:10.1111/j.1471-4159.2005.03338.x

Modulation of the homophilic interaction between the first and second Ig modules of neural cell adhesion molecule by heparin

Nikolaj Kulahin, Olga Rudenko, V. Kiselyov, Flemming M. Poulsen, Vladimir Berezin, Elisabeth Marianne Bock

Eyepath Lab

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

21 Citationer (Scopus)

Abstract

Udgivelsesdato: October 2005

Originalsprog	Engelsk
Tidsskrift	Journal of Neurochemistry
Vol/bind	95
Udgave nummer	1
Sider (fra-til)	46-55
ISSN	0022-3042
DOI	https://doi.org/10.1111/j.1471-4159.2005.03338.x
Status	Udgivet - 2005

Bibliografisk note

KEYWORDS
chondroitin sulfate • heparan sulfate • heparin • homophilic binding • NCAM

Adgang til dokumentet

10.1111/j.1471-4159.2005.03338.x

Citationsformater

@article{0746bdf06c3711dcbee902004c4f4f50,

title = "Modulation of the homophilic interaction between the first and second Ig modules of neural cell adhesion molecule by heparin",

abstract = "The second Ig module (IgII) of the neural cell adhesion molecule (NCAM) is known to bind to the first Ig module (IgI) of NCAM (so-called homophilic binding) and to interact with heparan sulfate and chondroitin sulfate glycoconjugates. We here show by NMR that the heparin and chondroitin sulfate-binding sites (HBS and CBS, respectively) in IgII coincide, and that this site overlaps with the homophilic binding site. Using NMR and surface plasmon resonance (SPR) analyses we demonstrate that interaction between IgII and heparin indeed interferes with the homophilic interaction between IgI and IgII. Accordingly, we show that treatment of cerebellar granule neurons (CGNs) with heparin inhibits NCAM-mediated outgrowth. In contrast, treatment with heparinase III or chondroitinase ABC abrogates NCAM-mediated neurite outgrowth in CGNs emphasizing the importance of the presence of heparan/chondroitin sulfates for proper NCAM function. Finally, a peptide encompassing HBS in IgII, termed the heparin-binding peptide (HBP), is shown to promote neurite outgrowth in CGNs. These observations indicate that neuronal differentiation induced by homophilic NCAM interaction is modulated by interactions with heparan/chondroitin sulfates.",

author = "Nikolaj Kulahin and Olga Rudenko and V. Kiselyov and Poulsen, {Flemming M.} and Vladimir Berezin and Bock, {Elisabeth Marianne}",

note = "KEYWORDS chondroitin sulfate • heparan sulfate • heparin • homophilic binding • NCAM",

year = "2005",

doi = "10.1111/j.1471-4159.2005.03338.x",

language = "English",

volume = "95",

pages = "46--55",

journal = "Journal of Neurochemistry",

issn = "0022-3042",

publisher = "Wiley-Blackwell",

number = "1",

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TY - JOUR

T1 - Modulation of the homophilic interaction between the first and second Ig modules of neural cell adhesion molecule by heparin

AU - Kulahin, Nikolaj

AU - Rudenko, Olga

AU - Kiselyov, V.

AU - Poulsen, Flemming M.

AU - Berezin, Vladimir

AU - Bock, Elisabeth Marianne

N1 - KEYWORDS chondroitin sulfate • heparan sulfate • heparin • homophilic binding • NCAM

PY - 2005

Y1 - 2005

N2 - The second Ig module (IgII) of the neural cell adhesion molecule (NCAM) is known to bind to the first Ig module (IgI) of NCAM (so-called homophilic binding) and to interact with heparan sulfate and chondroitin sulfate glycoconjugates. We here show by NMR that the heparin and chondroitin sulfate-binding sites (HBS and CBS, respectively) in IgII coincide, and that this site overlaps with the homophilic binding site. Using NMR and surface plasmon resonance (SPR) analyses we demonstrate that interaction between IgII and heparin indeed interferes with the homophilic interaction between IgI and IgII. Accordingly, we show that treatment of cerebellar granule neurons (CGNs) with heparin inhibits NCAM-mediated outgrowth. In contrast, treatment with heparinase III or chondroitinase ABC abrogates NCAM-mediated neurite outgrowth in CGNs emphasizing the importance of the presence of heparan/chondroitin sulfates for proper NCAM function. Finally, a peptide encompassing HBS in IgII, termed the heparin-binding peptide (HBP), is shown to promote neurite outgrowth in CGNs. These observations indicate that neuronal differentiation induced by homophilic NCAM interaction is modulated by interactions with heparan/chondroitin sulfates.

AB - The second Ig module (IgII) of the neural cell adhesion molecule (NCAM) is known to bind to the first Ig module (IgI) of NCAM (so-called homophilic binding) and to interact with heparan sulfate and chondroitin sulfate glycoconjugates. We here show by NMR that the heparin and chondroitin sulfate-binding sites (HBS and CBS, respectively) in IgII coincide, and that this site overlaps with the homophilic binding site. Using NMR and surface plasmon resonance (SPR) analyses we demonstrate that interaction between IgII and heparin indeed interferes with the homophilic interaction between IgI and IgII. Accordingly, we show that treatment of cerebellar granule neurons (CGNs) with heparin inhibits NCAM-mediated outgrowth. In contrast, treatment with heparinase III or chondroitinase ABC abrogates NCAM-mediated neurite outgrowth in CGNs emphasizing the importance of the presence of heparan/chondroitin sulfates for proper NCAM function. Finally, a peptide encompassing HBS in IgII, termed the heparin-binding peptide (HBP), is shown to promote neurite outgrowth in CGNs. These observations indicate that neuronal differentiation induced by homophilic NCAM interaction is modulated by interactions with heparan/chondroitin sulfates.

U2 - 10.1111/j.1471-4159.2005.03338.x

DO - 10.1111/j.1471-4159.2005.03338.x

M3 - Journal article

C2 - 16181411

SN - 0022-3042

VL - 95

SP - 46

EP - 55

JO - Journal of Neurochemistry

JF - Journal of Neurochemistry

IS - 1

ER -