scholarly journals A novel RING finger protein, Znf179, modulates cell cycle exit and neuronal differentiation of P19 embryonal carcinoma cells

2011 ◽  
Vol 18 (11) ◽  
pp. 1791-1804 ◽  
Author(s):  
P-C Pao ◽  
N-K Huang ◽  
Y-W Liu ◽  
S-H Yeh ◽  
S-T Lin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Neuronal Differentiation ◽  
Embryonal Carcinoma ◽  
Ring Finger ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Cell Cycle Exit ◽  
Ring Finger Protein ◽  
Finger Protein ◽  
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 Neuronal Differentiation of P19 Embryonal Carcinoma Cells Modulates Kinin B2 Receptor Gene Expression and Function

2005 ◽  
Vol 280 (20) ◽  
pp. 19576-19586 ◽  
Author(s):  
Antonio Henrique B. Martins ◽  
Rodrigo R. Resende ◽  
Paromita Majumder ◽  
Marcella Faria ◽  
Dulce E. Casarini ◽  
...  
Keyword(s):  
Gene Expression ◽  
Neuronal Differentiation ◽  
Embryonal Carcinoma ◽  
Receptor Gene ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
P19 Embryonal Carcinoma Cells ◽  
And Function ◽  
Receptor Gene Expression

Mechanism of acetylcholine-induced calcium signaling during neuronal differentiation of P19 embryonal carcinoma cells in vitro

Cell Calcium ◽  
2008 ◽  
Vol 43 (2) ◽  
pp. 107-121 ◽  
Author(s):  
Rodrigo R. Resende ◽  
Katia N. Gomes ◽  
Avishek Adhikari ◽  
Luiz R.G. Britto ◽  
Henning Ulrich
Keyword(s):  
Calcium Signaling ◽  
Neuronal Differentiation ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
P19 Embryonal Carcinoma Cells

Mammalian Scratch participates in neuronal differentiation in P19 embryonal carcinoma cells

2001 ◽  
Vol 95 (1-2) ◽  
pp. 162-166 ◽  
Author(s):  
Eric K Nakakura ◽  
D.Neil Watkins ◽  
Virote Sriuranpong ◽  
Michael W Borges ◽  
Barry D Nelkin ◽  
...  
Keyword(s):  
Neuronal Differentiation ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
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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