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, Vol. 10, 2009, p. 107.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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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 -