Retinoic Acid- and Bone Morphogenetic Protein 4-Induced Apoptosis in P19 Embryonal Carcinoma Cells Requires p27

2001 ◽  
Vol 268 (2) ◽  
pp. 128-138 ◽  
Author(s):  
Michele A. Glozak ◽  
Melissa B. Rogers
Keyword(s):  
Retinoic Acid ◽  
Bone Morphogenetic Protein ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Bone Morphogenetic Protein 4 ◽  
Embryonal Carcinoma Cells ◽  
Morphogenetic Protein ◽  
P19 Embryonal Carcinoma Cells ◽  
Induced Apoptosis

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 Sequence and expression pattern of the Stra7 (Gbx-2) homeobox-containing gene induced by retinoic acid in P19 embryonal carcinoma cells

1995 ◽  
Vol 204 (4) ◽  
pp. 372-382 ◽  
Author(s):  
Philippe Bouillet ◽  
Claire Chazaud ◽  
Mustapha Oulad-Abdelghani ◽  
Pascal Dollé ◽  
Pierre Chambon
Keyword(s):  
Retinoic Acid ◽  
Expression Pattern ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
P19 Embryonal Carcinoma Cells

Modulation of the Retinoic Acid and Retinoid X Receptor Signaling Pathways in P19 Embryonal Carcinoma Cells by Calreticulin

1997 ◽  
Vol 230 (1) ◽  
pp. 50-60 ◽  
Author(s):  
Mary Shago ◽  
Grace Flock ◽  
Chung-Yee Leung Hagesteijn ◽  
Michael Woodside ◽  
Sergio Grinstein ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Signaling Pathways ◽  
Embryonal Carcinoma ◽  
Retinoid X Receptor ◽  
Carcinoma Cells ◽  
Receptor Signaling ◽  
Embryonal Carcinoma Cells ◽  
P19 Embryonal Carcinoma Cells

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.

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