Orphan receptor COUP-TF I antagonizes retinoic acid-induced neuronal differentiation

Chicken ovalbumin upstream promoter‐transcription factors (COUP‐TF) are expressed in the developing nervous system and interact with nuclear hormone receptors to regulate expression of different genes. The role of COUP‐TF orphan receptors in neurogenesis is virtually unknown. To study the possible f...

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Veröffentlicht in:Journal of neuroscience research 1995-05, Vol.41 (1), p.39-48
Hauptverfasser: Neuman, K., Soosaar, A., Nornes, H. O., Neuman, Toomas
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container_title Journal of neuroscience research
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creator Neuman, K.
Soosaar, A.
Nornes, H. O.
Neuman, Toomas
description Chicken ovalbumin upstream promoter‐transcription factors (COUP‐TF) are expressed in the developing nervous system and interact with nuclear hormone receptors to regulate expression of different genes. The role of COUP‐TF orphan receptors in neurogenesis is virtually unknown. To study the possible function of COUP‐TF I during neuronal differentiation, we generated COUP‐TF I overexpressing teratocarcinoma PCC7 cell lines and analyzed retinoic acid (RA)‐induced neuronal differentiation of these cells. COUP‐TF I overexpression results in the blockade of morphological differentiation after induction to differentiate. COUP‐TF I represses expression of micro‐tubule‐associated protein 2 (MAP2) gene and delays induction of growth‐associated protein 43 (GAP43) gene expression. In contrast, expression of the neurofilament light subunit (NF‐L) gene is not affected by COUP‐TF I overexpression during neuronal differentiation. Also, cells overexpressing COUP‐TF I do not stop proliferating after RA and dBcAMP treatment and possess suppressed transcriptional activation from different RA response elements. These results suggest that COUP‐TF I plays an important role in regulating RA‐induced neuronal differentiation.© 1995 Wiley‐Liss, Inc.
doi_str_mv 10.1002/jnr.490410106
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In contrast, expression of the neurofilament light subunit (NF‐L) gene is not affected by COUP‐TF I overexpression during neuronal differentiation. Also, cells overexpressing COUP‐TF I do not stop proliferating after RA and dBcAMP treatment and possess suppressed transcriptional activation from different RA response elements. 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subjects Animals
Base Sequence
Biomarkers
Bucladesine - pharmacology
Cell Cycle - drug effects
Cell Cycle - genetics
Cell Differentiation - drug effects
Cell Differentiation - physiology
COUP Transcription Factor I
DNA-Binding Proteins - genetics
DNA-Binding Proteins - pharmacology
Enhancer Elements, Genetic - genetics
GAP-43 Protein
GAP43
gene expression
Gene Expression - physiology
MAP2
Membrane Glycoproteins - genetics
Mice
Microtubule-Associated Proteins - genetics
Molecular Sequence Data
Nerve Tissue Proteins - genetics
neurofilament
Neurofilament Proteins - genetics
nuclear hormone receptors
Receptors, Glucocorticoid - physiology
teratocarcinoma
Teratocarcinoma - pathology
Teratocarcinoma - physiopathology
Transcription Factors - genetics
Transcription Factors - pharmacology
Tretinoin - pharmacology
Tumor Cells, Cultured - cytology
title Orphan receptor COUP-TF I antagonizes retinoic acid-induced neuronal differentiation
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