scholarly journals Sodium butyrate induces histone hyperacetylation and differentiation of murine embryonal carcinoma cells.

1984 ◽  
Vol 98 (2) ◽  
pp. 602-608 ◽  
Author(s):  
P A McCue ◽  
M L Gubler ◽  
M I Sherman ◽  
B N Cohen
Keyword(s):  
Sodium Butyrate ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
The Other ◽  
Response To Treatment ◽  
Embryonal Carcinoma Cells ◽  
Histone Hyperacetylation ◽  
Butyrate Treatment ◽  
Ec Cells ◽  
Modest Level

Cells from embryonal carcinoma (EC) lines 6050AJ and PCC4.aza 1R differentiate in response to treatment with sodium butyrate as well as retinoic acid (RA) or hexamethylenebisacetamide (HMBA). Murine 6050AJ EC cells exposed to sodium butyrate possess hyperacetylated forms of histones H4 and altered forms of histones H2a and H2b, whereas histones from cells treated with other inducers appear to be unaffected. These results might indicate that the mechanism by which sodium butyrate promotes differentiation of EC cells is different from the ways in which RA and HMBA act. Differentiation-defective PCC4(RA)-1 EC cells fail to respond to RA, presumably because they possess minimal amounts of active binding protein for RA (cRABP). Sodium butyrate treatment of these cells results in only a modest level of differentiation. On the other hand, exposure to sodium butyrate plus RA leads to extensive differentiation. As is the case with 6050AJ cells, PCC4(RA)-1 cells treated with sodium butyrate also contain hyperacetylated histones. Furthermore, these cells now possess high levels of cRABP. The latter observations suggest that sodium butyrate has the ability to reactivate a silent cRABP gene in PCC4(RA)-1 cells and thereby lead to extensive differentiation via the retinoid pathway when RA is added.

Accumulation of microtubule-associated protein 1A (MAP1A) in differentiating P19 embryonal carcinoma cells

1995 ◽  
Vol 73 (9-10) ◽  
pp. 695-702 ◽  
Author(s):  
A. R. Vaillant ◽  
D. L. Brown
Keyword(s):  
Neurite Outgrowth ◽  
Mitotic Spindle ◽  
Embryonal Carcinoma ◽  
Growth Cones ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Protein Levels ◽  
Undifferentiated Cells ◽  
P19 Embryonal Carcinoma Cells ◽  
Ec Cells

We have examined the accumulation of MAP1A in retinoic acid induced P19 embryonal carcinoma (EC) neurons. By immunofluorescent confocal microscopy, MAP1A was detected in the mitotic spindle of undifferentiated cells but was not evident in association with the interphase microtubules in most cells. By day 4 of differentiation, when neurite outgrowth was underway, MAP1A was co-localized with microtubules in all neurites but was absent from growth cones. By day 8, substantial neurite outgrowth had occurred and MAP1A was seen in all processes. At day 12, no further neurite outgrowth was evident and existing neurites were organized into fascicles. Western blotting and ELISA showed that MAP1A protein levels increased during differentiation. Peak accumulation occurred no later than day 8, coinciding with the period of neurite outgrowth, and then decreased after day 8. The results suggest that in differentiating P19 EC cells MAP1A modulates microtubule dynamics during neurite outgrowth.Key words: MAP1A, neuronal cytoskeleton, neurite outgrowth.

scholarly journals SNF2beta-BRG1 is essential for the viability of F9 murine embryonal carcinoma cells.

1997 ◽  
Vol 17 (10) ◽  
pp. 5976-5986 ◽  
Author(s):  
C Sumi-Ichinose ◽  
H Ichinose ◽  
D Metzger ◽  
P Chambon
Keyword(s):  
Transcriptional Activation ◽  
Embryonal Carcinoma ◽  
Regulatory Elements ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Nucleosome Remodeling ◽  
Transfected Cells ◽  
Activation Of Transcription ◽  
Ec Cells ◽  
Mutant Cells

The yeast and animal SNF-SWI and related multiprotein complexes are thought to play an important role in processes, such as transcription factor binding to regulatory elements, which require nucleosome remodeling in order to relieve the repressing effect of packaging DNA in chromatin. There are two mammalian homologs of the yeast SNF2-SWI2 subunit protein, SNF2alpha-brm and SNF2beta-BRG1, and overexpression of either one of them has been shown to enhance transcriptional activation by glucocorticoid, estrogen, and retinoic acid (RA) receptors in transiently transfected cells. We have investigated here the function of SNF2beta-BRG1 in the RA receptor-retinoid X receptor-mediated transduction of the retinoid signal in F9 embryonal carcinoma (EC) cells which differentiate into endodermal-like cells upon RA treatment. The two SNF2beta-BRG1 alleles have been targeted by homologous recombination and subsequently disrupted by using a conditional Cre recombinase. We show that F9 EC cells inactivated on both SNF2beta alleles are not viable and that heterozygous mutant cells are affected in proliferation but not in RA-induced differentiation. Thus, in F9 EC cells, SNF2beta-BRG1 appears to play an essential role in basal processes involved in cell proliferation, in addition to its putative role in the activation of transcription mediated by nuclear receptors.

scholarly journals Embryonal carcinoma cells transfected with ZP3 genes differentially glycosylate similar polypeptides and secrete active mouse sperm receptor.

1991 ◽  
Vol 115 (3) ◽  
pp. 655-664 ◽  
Author(s):  
R A Kinloch ◽  
S Mortillo ◽  
C L Stewart ◽  
P M Wassarman
Keyword(s):  
Acrosome Reaction ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Transfected Cells ◽  
Mouse Sperm ◽  
Large Numbers ◽  
Ec Cells ◽  
Sperm Receptor

Mouse and hamster sperm receptors, called mZP3 (approximately 83,000 Mr) and hZP3 (approximately 56,000 Mr), respectively, are glycoproteins located in the ovulated egg zona pellucida. Certain of the glycoprotein O-linked oligosaccharides are essential for sperm receptor activity. Here, we transfected mouse embryonal carcinoma (EC) cells with mZP3 and hZP3 genes placed under control of a constitutive promoter. Transfected cells synthesized and secreted large amounts of the glycoproteins, called EC-mZP3 and EC-hZP3. Although the primary structures of mZP3 and hZP3 polypeptides (44,000 Mr) are very similar to one another, EC-mZP3 (approximately 83,000 Mr) and EC-hZP3 (approximately 49,000 Mr) were glycosylated to very different extents, such that they resembled their egg counterparts. Like egg mZP3, EC-mZP3 inhibited binding of sperm to ovulated eggs and induced sperm to acrosome-react in vitro. In addition, large numbers of sperm bound to aggregates of mZP3-transfected EC cells in vitro. On the other hand, unlike egg hZP3, EC-hZP3 did not exhibit either sperm receptor or acrosome reaction-inducing activity, and sperm failed to bind to aggregates of hZP3-transfected EC cells. Thus, transfected EC cells not only express sperm receptor genes, but also discriminate between very similar polypeptides with respect to glycosylation and, in the case of mZP3, add specific oligosaccharides essential for biological activity. In addition, the results demonstrate that EC cells can serve as a source for large amounts of functional mouse sperm receptor.

Reversible effects of sodium butyrate on the differentiation of F9 embryonal carcinoma cells

1991 ◽  
Vol 192 (1) ◽  
pp. 46-51 ◽  
Author(s):  
Mitsuko Kosaka ◽  
Yukio Nishina ◽  
Masashi Takeda ◽  
Keishi Matsumoto ◽  
Yoshitake Nishimune
Keyword(s):  
Sodium Butyrate ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
F9 Embryonal Carcinoma Cells

Neutral amino acid transport in embryonal carcinoma cells

1985 ◽  
Vol 122 (3) ◽  
pp. 379-386 ◽  
Author(s):  
John S. Zuzack ◽  
Richard J. Tasca ◽  
Stephen M. DiZio
Keyword(s):  
Amino Acid ◽  
Amino Acid Transport ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Neutral Amino Acid ◽  
Embryonal Carcinoma Cells ◽  
Acid Transport

Dickkopf-3 alters the morphological response to retinoic acid during neuronal differentiation of human embryonal carcinoma cells

2014 ◽  
Vol 74 (12) ◽  
pp. 1243-1254 ◽  
Author(s):  
Rocío Jiménez Alfonso ◽  
Irantzu Gorroño-Etxebarria ◽  
Miriam Rabano ◽  
Maria dM. Vivanco ◽  
Robert Kypta
Keyword(s):  
Retinoic Acid ◽  
Neuronal Differentiation ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Morphological Response
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