Lewis(x) and alpha2,3-sialyl glycans and their receptors TAG-1, Contactin, and L1 mediate CD24-dependent neurite outgrowth.

Standard

Lewis(x) and alpha2,3-sialyl glycans and their receptors TAG-1, Contactin, and L1 mediate CD24-dependent neurite outgrowth. / Lieberoth, Annika; Splittstoesser, Frauke; Katagihallimath, Nainesh; Jakovcevski, Igor; Loers, Gabriele; Ranscht, Barbara; Karagogeos, Domna; Schachner, Melitta; Kleene, Ralf.

in: J NEUROSCI, Jahrgang 29, Nr. 20, 20, 2009, S. 6677-6690.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Lieberoth, A, Splittstoesser, F, Katagihallimath, N, Jakovcevski, I, Loers, G, Ranscht, B, Karagogeos, D, Schachner, M & Kleene, R 2009, 'Lewis(x) and alpha2,3-sialyl glycans and their receptors TAG-1, Contactin, and L1 mediate CD24-dependent neurite outgrowth.', J NEUROSCI, Jg. 29, Nr. 20, 20, S. 6677-6690. <http://www.ncbi.nlm.nih.gov/pubmed/19458237?dopt=Citation>

APA

Lieberoth, A., Splittstoesser, F., Katagihallimath, N., Jakovcevski, I., Loers, G., Ranscht, B., Karagogeos, D., Schachner, M., & Kleene, R. (2009). Lewis(x) and alpha2,3-sialyl glycans and their receptors TAG-1, Contactin, and L1 mediate CD24-dependent neurite outgrowth. J NEUROSCI, 29(20), 6677-6690. [20]. http://www.ncbi.nlm.nih.gov/pubmed/19458237?dopt=Citation

Vancouver

Lieberoth A, Splittstoesser F, Katagihallimath N, Jakovcevski I, Loers G, Ranscht B et al. Lewis(x) and alpha2,3-sialyl glycans and their receptors TAG-1, Contactin, and L1 mediate CD24-dependent neurite outgrowth. J NEUROSCI. 2009;29(20):6677-6690. 20.

Bibtex

@article{0365ce39e98f4f5290e48a01276b3927,
title = "Lewis(x) and alpha2,3-sialyl glycans and their receptors TAG-1, Contactin, and L1 mediate CD24-dependent neurite outgrowth.",
abstract = "Although carbohydrates have been implicated in cell interactions in the nervous system, the molecular bases of their functions have remained largely obscure. Here, we show that promotion or inhibition of neurite outgrowth of cerebellar or dorsal root ganglion neurons, respectively, induced by the mucin-type adhesion molecule CD24 depends on alpha2,3-linked sialic acid and Lewis(x) present on glia-specific CD24 glycoforms. Alpha2,3-sialyl residues of CD24 bind to a structural motif in the first fibronectin type III domain of the adhesion molecule L1. Following the observation that the adhesion molecules TAG-1 and Contactin show sequence homologies with fucose-specific lectins, we obtained evidence that TAG-1 and Contactin mediate Lewis(x)-dependent CD24-induced effects on neurite outgrowth. Thus, L1, TAG-1, and Contactin function as lectin-like neuronal receptors. Their cis interactions with neighboring adhesion molecules, e.g., Caspr1 and Caspr2, and with their triggered signal transduction pathways elicit cell type-specific promotion or inhibition of neurite outgrowth induced by glial CD24 in a glycan-dependent trans interaction.",
author = "Annika Lieberoth and Frauke Splittstoesser and Nainesh Katagihallimath and Igor Jakovcevski and Gabriele Loers and Barbara Ranscht and Domna Karagogeos and Melitta Schachner and Ralf Kleene",
year = "2009",
language = "Deutsch",
volume = "29",
pages = "6677--6690",
journal = "J NEUROSCI",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "20",

}

RIS

TY - JOUR

T1 - Lewis(x) and alpha2,3-sialyl glycans and their receptors TAG-1, Contactin, and L1 mediate CD24-dependent neurite outgrowth.

AU - Lieberoth, Annika

AU - Splittstoesser, Frauke

AU - Katagihallimath, Nainesh

AU - Jakovcevski, Igor

AU - Loers, Gabriele

AU - Ranscht, Barbara

AU - Karagogeos, Domna

AU - Schachner, Melitta

AU - Kleene, Ralf

PY - 2009

Y1 - 2009

N2 - Although carbohydrates have been implicated in cell interactions in the nervous system, the molecular bases of their functions have remained largely obscure. Here, we show that promotion or inhibition of neurite outgrowth of cerebellar or dorsal root ganglion neurons, respectively, induced by the mucin-type adhesion molecule CD24 depends on alpha2,3-linked sialic acid and Lewis(x) present on glia-specific CD24 glycoforms. Alpha2,3-sialyl residues of CD24 bind to a structural motif in the first fibronectin type III domain of the adhesion molecule L1. Following the observation that the adhesion molecules TAG-1 and Contactin show sequence homologies with fucose-specific lectins, we obtained evidence that TAG-1 and Contactin mediate Lewis(x)-dependent CD24-induced effects on neurite outgrowth. Thus, L1, TAG-1, and Contactin function as lectin-like neuronal receptors. Their cis interactions with neighboring adhesion molecules, e.g., Caspr1 and Caspr2, and with their triggered signal transduction pathways elicit cell type-specific promotion or inhibition of neurite outgrowth induced by glial CD24 in a glycan-dependent trans interaction.

AB - Although carbohydrates have been implicated in cell interactions in the nervous system, the molecular bases of their functions have remained largely obscure. Here, we show that promotion or inhibition of neurite outgrowth of cerebellar or dorsal root ganglion neurons, respectively, induced by the mucin-type adhesion molecule CD24 depends on alpha2,3-linked sialic acid and Lewis(x) present on glia-specific CD24 glycoforms. Alpha2,3-sialyl residues of CD24 bind to a structural motif in the first fibronectin type III domain of the adhesion molecule L1. Following the observation that the adhesion molecules TAG-1 and Contactin show sequence homologies with fucose-specific lectins, we obtained evidence that TAG-1 and Contactin mediate Lewis(x)-dependent CD24-induced effects on neurite outgrowth. Thus, L1, TAG-1, and Contactin function as lectin-like neuronal receptors. Their cis interactions with neighboring adhesion molecules, e.g., Caspr1 and Caspr2, and with their triggered signal transduction pathways elicit cell type-specific promotion or inhibition of neurite outgrowth induced by glial CD24 in a glycan-dependent trans interaction.

M3 - SCORING: Zeitschriftenaufsatz

VL - 29

SP - 6677

EP - 6690

JO - J NEUROSCI

JF - J NEUROSCI

SN - 0270-6474

IS - 20

M1 - 20

ER -