Retinoic acid-induced neural differentiation of embryonal carcinoma cells.

Jones-Villeneuve, Elizabeth; Rudnicki, Michael A.; Harris, J F; McBurney, M W

doi:10.1128/mcb.3.12.2271

Cited by 280 publications

(204 citation statements)

References 21 publications

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“…The P19 cells differentiate to neuroectoderm-like phenotypes (29,30) when allowed to aggregate in the presence of 100 nM retinoic acid. In the absence of aggregation, P19 cells are induced to differentiate by RA but only to the endoderm-like phenotype (29, Fig.…”

Section: Resultsmentioning

confidence: 99%

“…P19 embryonal carcinoma cells are an attractive model for the study of differentiation, displaying a capacity to differentiate to endoderm, neuroectoderm, and beating cardiac myocytes under the appropriate culture conditions (29,30). The P19 cell line was adopted for the study of the role of heterotrimeric G-protein subunits G␣ 12 and G␣ 13 as well as MAP kinases in the differentiation of these embryonal cells to endoderm in response to RA.…”

Section: Resultsmentioning

confidence: 99%

“…P19 embryonal carcinoma (P19) cells have been used as a model system for murine pre-implantation development (27,28). These pluripotent cells have the ability to differentiate into derivatives of three germ layers, endoderm, mesoderm, and ectoderm, upon different inducer stimulation (29,30). Monolayer cultures of P19 cells challenged with 50 nM retinoic acid (RA) differentiate to endodermal-like cells (31).…”

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c-Jun Amino-terminal Kinase Is Regulated by Gα12/Gα13 and Obligate for Differentiation of P19 Embryonal Carcinoma Cells by Retinoic Acid

Jho¹,

Davis²,

Malbon³

1997

Journal of Biological Chemistry

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Retinoic acid induces P19 mouse embryonal carcinoma cells to differentiate to endoderm and increases expression of the heterotrimeric G-protein subunits G␣ 12 and G␣ 13 . Retinoic acid was found to induce differentiation and sustained activation of c-Jun amino-terminal kinase, but not of ERK1,2 or of p38 mitogen-activated protein kinases. Much like retinoic acid, expression of constitutively active forms of G␣ 12 and G␣ 13 induced differentiation and constitutive activation of c-Jun amino-terminal kinase. Expression of the dominant negative form of c-Jun amino-terminal kinase 1 blocked both the activation of c-Jun amino-terminal kinase and the induction of endodermal differentiation in the presence of retinoic acid. These data implicate c-Jun amino-terminal kinase as a downstream element of activation of G␣ 12 or G␣ 13 obligate for retinoic acid-induced differentiation.The role of heterotrimeric guanine nucleotide binding proteins (G-proteins) 1 in cell differentiation and development has been shown in several systems (1-4). Adipogenesis of NIH 3T3-L1 cells in response to inducers such as insulin or dexamethasone plus methylisobutylxanthine is accompanied by a sharp decline in G␣ s subunit (5). Both suppression of G␣ s by antisense oligodeoxynucleotides and overexpression of the constitutively active mutant form of G␣ i2 promote adipogenesis in the absence of classical inducers (5). Differentiation of F9 embryonic stem cells to endodermal cells provokes a sharp reduction of G␣ i2 (2), a de-repression of phospholipase C, and activation of protein kinase C and mitogen-activated protein (MAP) kinase, especially via ERK1,2 (6). The expression of constitutively active forms of G␣ q or G␣ 16 can induce neuronal differentiation of PC 12 cells (7), via activation of c-Jun aminoterminal kinase but not via ERK1,2.The extracellular signal-regulated kinase (ERK), stress-activated protein kinase (SAPK/JNK), and mammalian homolog of the yeast-osmosensing ERK HOG1 (p38 MAPK) are conserved members of a MAP kinase cascade for regulation of targets such as transcription factors in response to growth factors or environmental stresses, such as ultraviolet light, and protein synthesis inhibitors (8 -16). ERK appears to play a major role in provoking cell proliferation and differentiation (17-19), whereas JNK mediates stress responses and some forms of apoptosis (20 -23). JNK has been implicated also in the induction of differentiation (7, 24) and oncogenesis (25). The ability of overexpression of c-Jun, which is a target for JNK, to stimulate differentiation of P19 embryonal carcinoma cells to a mixed endoderm/mesoderm population supports a role of JNK in differentiation (26). P19 embryonal carcinoma (P19) cells have been used as a model system for murine pre-implantation development (27,28). These pluripotent cells have the ability to differentiate into derivatives of three germ layers, endoderm, mesoderm, and ectoderm, upon different inducer stimulation (29,30). Monolayer cultures of P19 cells challenged with 50 nM retinoic acid (...

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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c-Jun Amino-terminal Kinase Is Regulated by Gα12/Gα13 and Obligate for Differentiation of P19 Embryonal Carcinoma Cells by Retinoic Acid

Jho¹,

Davis²,

Malbon³

1997

Journal of Biological Chemistry

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“…P19, which carries a normal RARa, is growth-inhibited and can differentiate into neurons in response to RA (Jones-Villeneuve et al, 1982;Edwards and McBurney, 1983). In contrast, its mutant counterpart, the RAC65 cell line, is RA-resistant and cannot differentiate when grown as aggregates (Jones-Villeneuve et al, 1983). RAC65 harbors a mutant RARa protein, originally designated RARa 0 (Pratt et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

RAR-mediated epigenetic control of the cytochrome P450 Cyp26a1 in embryocarcinoma cells

et al. 2005

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“…When compared with murine EC cells such as P19, which are cultured as aggregates and are capable of differentiating into CNS neurons (3,12), NT2 cells require a relatively high concentration of RA (10 µ M) to induce differentiation. Furthermore, the purification of NT2-N neurons involves a time-consuming process (ca.…”

Section: Introductionmentioning

confidence: 99%

Production of Human CNS Neurons from Embryonal Carcinoma Cells Using a Cell Aggregation Method

Cheung

Hui

et al. 1999

BioTechniques

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Retinoic acid-induced neural differentiation of embryonal carcinoma cells.

Cited by 280 publications

References 21 publications

c-Jun Amino-terminal Kinase Is Regulated by Gα12/Gα13 and Obligate for Differentiation of P19 Embryonal Carcinoma Cells by Retinoic Acid

c-Jun Amino-terminal Kinase Is Regulated by Gα12/Gα13 and Obligate for Differentiation of P19 Embryonal Carcinoma Cells by Retinoic Acid

RAR-mediated epigenetic control of the cytochrome P450 Cyp26a1 in embryocarcinoma cells

Production of Human CNS Neurons from Embryonal Carcinoma Cells Using a Cell Aggregation Method

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