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Nuclear factor I-A represses expression of the cell adhesion molecule L1.

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Nuclear factor I-A represses expression of the cell adhesion molecule L1. / Schneegans, Tanja; Borgmeyer, Uwe; Hentschke, Moritz; Gronostajski, Richard M; Schachner, Melitta; Tilling, Thomas.

in: BMC MOL BIOL, Jahrgang 10, 2009, S. 107.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Schneegans, T, Borgmeyer, U, Hentschke, M, Gronostajski, RM, Schachner, M & Tilling, T 2009, 'Nuclear factor I-A represses expression of the cell adhesion molecule L1.', BMC MOL BIOL, Jg. 10, S. 107. https://doi.org/10.1186/1471-2199-10-107

APA

Schneegans, T., Borgmeyer, U., Hentschke, M., Gronostajski, R. M., Schachner, M., & Tilling, T. (2009). Nuclear factor I-A represses expression of the cell adhesion molecule L1. BMC MOL BIOL, 10, 107. https://doi.org/10.1186/1471-2199-10-107

Vancouver

Schneegans T, Borgmeyer U, Hentschke M, Gronostajski RM, Schachner M, Tilling T. Nuclear factor I-A represses expression of the cell adhesion molecule L1. BMC MOL BIOL. 2009;10:107. https://doi.org/10.1186/1471-2199-10-107

Bibtex

@article{104a4b7ab6f441c0823f1e53fc8fd5a1,
title = "Nuclear factor I-A represses expression of the cell adhesion molecule L1.",
abstract = "BACKGROUND: The neural cell adhesion molecule L1 plays a crucial role in development and plasticity of the nervous system. Neural cells thus require precise control of L1 expression. RESULTS: We identified a full binding site for nuclear factor I (NFI) transcription factors in the regulatory region of the mouse L1 gene. Electrophoretic mobility shift assay (EMSA) showed binding of nuclear factor I-A (NFI-A) to this site. Moreover, for a brain-specific isoform of NFI-A (NFI-A bs), we confirmed the interaction in vivo using chromatin immunoprecipitation (ChIP). Reporter gene assays showed that in neuroblastoma cells, overexpression of NFI-A bs repressed L1 expression threefold. CONCLUSION: Our findings suggest that NFI-A, in particular its brain-specific isoform, represses L1 gene expression, and might act as a second silencer of L1 in addition to the neural restrictive silencer factor (NRSF).",
author = "Tanja Schneegans and Uwe Borgmeyer and Moritz Hentschke and Gronostajski, {Richard M} and Melitta Schachner and Thomas Tilling",
year = "2009",
doi = "10.1186/1471-2199-10-107",
language = "Deutsch",
volume = "10",
pages = "107",
journal = "BMC MOL BIOL",
issn = "1471-2199",
publisher = "BioMed Central Ltd.",

}

RIS

TY - JOUR

T1 - Nuclear factor I-A represses expression of the cell adhesion molecule L1.

AU - Schneegans, Tanja

AU - Borgmeyer, Uwe

AU - Hentschke, Moritz

AU - Gronostajski, Richard M

AU - Schachner, Melitta

AU - Tilling, Thomas

PY - 2009

Y1 - 2009

N2 - BACKGROUND: The neural cell adhesion molecule L1 plays a crucial role in development and plasticity of the nervous system. Neural cells thus require precise control of L1 expression. RESULTS: We identified a full binding site for nuclear factor I (NFI) transcription factors in the regulatory region of the mouse L1 gene. Electrophoretic mobility shift assay (EMSA) showed binding of nuclear factor I-A (NFI-A) to this site. Moreover, for a brain-specific isoform of NFI-A (NFI-A bs), we confirmed the interaction in vivo using chromatin immunoprecipitation (ChIP). Reporter gene assays showed that in neuroblastoma cells, overexpression of NFI-A bs repressed L1 expression threefold. CONCLUSION: Our findings suggest that NFI-A, in particular its brain-specific isoform, represses L1 gene expression, and might act as a second silencer of L1 in addition to the neural restrictive silencer factor (NRSF).

AB - BACKGROUND: The neural cell adhesion molecule L1 plays a crucial role in development and plasticity of the nervous system. Neural cells thus require precise control of L1 expression. RESULTS: We identified a full binding site for nuclear factor I (NFI) transcription factors in the regulatory region of the mouse L1 gene. Electrophoretic mobility shift assay (EMSA) showed binding of nuclear factor I-A (NFI-A) to this site. Moreover, for a brain-specific isoform of NFI-A (NFI-A bs), we confirmed the interaction in vivo using chromatin immunoprecipitation (ChIP). Reporter gene assays showed that in neuroblastoma cells, overexpression of NFI-A bs repressed L1 expression threefold. CONCLUSION: Our findings suggest that NFI-A, in particular its brain-specific isoform, represses L1 gene expression, and might act as a second silencer of L1 in addition to the neural restrictive silencer factor (NRSF).

U2 - 10.1186/1471-2199-10-107

DO - 10.1186/1471-2199-10-107

M3 - SCORING: Zeitschriftenaufsatz

VL - 10

SP - 107

JO - BMC MOL BIOL

JF - BMC MOL BIOL

SN - 1471-2199

ER -