scholarly journals Copper is Required for Retinoic Acid Receptor-Dependent Transcription and Neuronal Differentiation in P19 Embryonal Carcinoma Cells

2006 ◽  
Vol 52 (5) ◽  
pp. 540-548
Author(s):  
Masaki Watanabe ◽  
Masakatsu Tezuka
Keyword(s):  
Retinoic Acid ◽  
Neuronal Differentiation ◽  
Embryonal Carcinoma ◽  
Retinoic Acid Receptor ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Acid Receptor ◽  
P19 Embryonal Carcinoma Cells

Aggregation and cell cycle dependent retinoic acid receptor mRNA expression in P19 embryonal carcinoma cells

1992 ◽  
Vol 36 (3) ◽  
pp. 165-172 ◽  
Author(s):  
Luigi J.C. Jonk ◽  
Marjolijn E.J. de Jonge ◽  
Frank A.E. Kruyt ◽  
Christine L. Mummery ◽  
Paul T. van der Saag ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Retinoic Acid ◽  
Mrna Expression ◽  
Embryonal Carcinoma ◽  
Retinoic Acid Receptor ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Receptor Mrna ◽  
P19 Embryonal Carcinoma Cells ◽  
Cycle Dependent

scholarly journals Induction and repression of mammalian achaete-scute homologue (MASH) gene expression during neuronal differentiation of P19 embryonal carcinoma cells

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 75-87 ◽  
Author(s):  
J.E. Johnson ◽  
K. Zimmerman ◽  
T. Saito ◽  
D.J. Anderson
Keyword(s):  
Retinoic Acid ◽  
Neuronal Differentiation ◽  
Embryonal Carcinoma ◽  
Model System ◽  
Neuronal Morphology ◽  
Carcinoma Cells ◽  
P19 Cells ◽  
Embryonal Carcinoma Cells ◽  
Bhlh Genes ◽  
P19 Embryonal Carcinoma Cells

MASH1 and MASH2, mammalian homologues of the Drosophila neural determination genes achaete-scute, are members of the basic helix-loop-helix (bHLH) family of transcription factors. We show here that murine P19 embryonal carcinoma cells can be used as a model system to study the regulation and function of these genes. MASH1 and MASH2 display complementary patterns of expression during the retinoic-acid-induced neuronal differentiation of P19 cells. MASH1 mRNA is undetectable in undifferentiated P19 cells but is induced to high levels by retinoic acid coincident with neuronal differentiation. In contrast, MASH2 mRNA is expressed in undifferentiated P19 cells and is repressed by retinoic acid treatment. These complementary expression patterns suggest distinct functions for MASH1 and MASH2 in development, despite their sequence homology. In retinoic-acid-treated P19 cells, MASH1 protein expression precedes and then overlaps expression of neuronal markers. However, MASH1 is expressed by a smaller proportion of cells than expresses such markers. MASH1 immunoreactivity is not detected in differentiated cells displaying a neuronal morphology, suggesting that its expression is transient. These features of MASH1 expression are similar to those observed in vivo, and suggest that P19 cells represent a good model system in which to study the regulation of this gene. Forced expression of MASH1 was achieved in undifferentiated P19 cells by transfection of a cDNA expression construct. The transfected cells expressing exogenous MASH1 protein contained E-box-binding activity that could be super-shifted by an anti-MASH1 antibody, but exhibited no detectable phenotypic changes. Thus, unlike myogenic bHLH genes, such as MyoD, which are sufficient to induce muscle differentiation, expression of MASH1 appears insufficient to promote neurogenesis.

scholarly journals Specific and Redundant Functions of Retinoid X Receptor/Retinoic Acid Receptor Heterodimers in Differentiation, Proliferation, and Apoptosis of F9 Embryonal Carcinoma Cells

1997 ◽  
Vol 139 (3) ◽  
pp. 735-747 ◽  
Author(s):  
Hideki Chiba ◽  
John Clifford ◽  
Daniel Metzger ◽  
Pierre Chambon
Keyword(s):  
Retinoic Acid ◽  
Embryonal Carcinoma ◽  
Retinoic Acid Receptor ◽  
Retinoid X Receptor ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Acid Receptor ◽  
Proliferation And Apoptosis ◽  
Redundant Functions

We have generated F9 murine embryonal carcinoma cells in which either the retinoid X receptor (RXR)α and retinoic acid receptor (RAR)α genes or the RXRα and RARγ genes are knocked out, and compared their phenotypes with those of wild-type (WT), RXRα−/−, RARα−/−, and RARγ−/− cells. RXRα−/−/ RARα−/− cells were resistant to retinoic acid treatment for the induction of primitive and parietal endodermal differentiation, as well as for antiproliferative and apoptotic responses, whereas they could differentiate into visceral endodermlike cells, as previously observed for RXRα−/− cells. In contrast, RXRα−/−/RARγ−/− cells were defective for all three types of differentiation, as well as antiproliferative and apoptotic responses, indicating that RXRα and RARγ represent an essential receptor pair for these responses. Taken together with results obtained by treatment of WT and mutant F9 cells with RAR isotype– and panRXR-selective retinoids, our observations support the conclusion that RXR/ RAR heterodimers are the functional units mediating the retinoid signal in vivo. Our results also indicate that the various heterodimers can exert both specific and redundant functions in differentiation, proliferation, and apoptosis. We also show that the functional redundancy exhibited between RXR isotypes and between RAR isotypes in cellular processes can be artifactually generated by gene knockouts. The present approach for multiple gene targeting should allow inactivation of any set of genes in a given cell.

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