A Role of N-Cadherin in Neuronal Differentiation of Embryonic Carcinoma P19 Cells

2001 ◽  
Vol 284 (5) ◽  
pp. 1098-1103 ◽  
Author(s):  
X. Gao ◽  
W. Bian ◽  
J. Yang ◽  
K. Tang ◽  
H. Kitani ◽  
...  
Keyword(s):  
Neuronal Differentiation ◽  
P19 Cells ◽  
Embryonic Carcinoma

NSSR1 promotes neuronal differentiation of mouse embryonic carcinoma P19 cells

Neuroreport ◽  
2004 ◽  
Vol 15 (5) ◽  
pp. 823-828 ◽  
Author(s):  
Lei Liu ◽  
Xian-hua Chen ◽  
Jia Huang ◽  
Jun-ji Lin ◽  
Wan-min Lin ◽  
...  
Keyword(s):  
Neuronal Differentiation ◽  
P19 Cells ◽  
Embryonic Carcinoma

scholarly journals Deletion of the Prdm3 Gene Causes a Neuronal Differentiation Deficiency in P19 Cells

2020 ◽  
Vol 21 (19) ◽  
pp. 7192
Author(s):  
Paweł Leszczyński ◽  
Magdalena Śmiech ◽  
Aamir Salam Teeli ◽  
Effi Haque ◽  
Robert Viger ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Mrna Expression ◽  
Neuronal Differentiation ◽  
Regulatory Mechanism ◽  
Gene Knockout ◽  
Luciferase Reporter ◽  
P19 Cells ◽  
Binding Factor ◽  
Domain I

PRDM (PRDI-BF1 (positive regulatory domain I-binding factor 1) and RIZ1 (retinoblastoma protein-interacting zinc finger gene 1) homologous domain-containing) transcription factors are a group of proteins that have a significant impact on organ development. In our study, we assessed the role of Prdm3 in neurogenesis and the mechanisms regulating its expression. We found that Prdm3 mRNA expression was induced during neurogenesis and that Prdm3 gene knockout caused premature neuronal differentiation of the P19 cells and enhanced the growth of non-neuronal cells. Interestingly, we found that Gata6 expression was also significantly upregulated during neurogenesis. We further studied the regulatory mechanism of Prdm3 expression. To determine the role of GATA6 in the regulation of Prdm3 mRNA expression, we used a luciferase-based reporter assay and found that Gata6 overexpression significantly increased the activity of the Prdm3 promoter. Finally, the combination of retinoic acid receptors α and β, along with Gata6 overexpression, further increased the activity of the luciferase reporter. Taken together, our results suggest that in the P19 cells, PRDM3 contributed to neurogenesis and its expression was stimulated by the synergism between GATA6 and the retinoic acid signaling pathway.

scholarly journals Ectopic Expression of Axin Blocks Neuronal Differentiation of Embryonic Carcinoma P19 Cells

2003 ◽  
Vol 278 (15) ◽  
pp. 13487-13495 ◽  
Author(s):  
Jungmook Lyu ◽  
Frank Costantini ◽  
Eek-hoon Jho ◽  
Choun-ki Joo
Keyword(s):  
Neuronal Differentiation ◽  
Ectopic Expression ◽  
P19 Cells ◽  
Embryonic Carcinoma

scholarly journals Tcf4 Is Involved in Subset Specification of Mesodiencephalic Dopaminergic Neurons

Biomedicines ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 317
Author(s):  
Simone Mesman ◽  
Iris Wever ◽  
Marten P. Smidt
Keyword(s):  
Neuronal Differentiation ◽  
Dopaminergic Neurons ◽  
Neuronal Development ◽  
Neuronal Population ◽  
Minor Role ◽  
Initial Increase ◽  
E Box ◽  
A Minor ◽  
Bhlh Factor

During development, mesodiencephalic dopaminergic (mdDA) neurons form into different molecular subsets. Knowledge of which factors contribute to the specification of these subsets is currently insufficient. In this study, we examined the role of Tcf4, a member of the E-box protein family, in mdDA neuronal development and subset specification. We show that Tcf4 is expressed throughout development, but is no longer detected in adult midbrain. Deletion of Tcf4 results in an initial increase in TH-expressing neurons at E11.5, but this normalizes at later embryonic stages. However, the caudal subset marker Nxph3 and rostral subset marker Ahd2 are affected at E14.5, indicating that Tcf4 is involved in correct differentiation of mdDA neuronal subsets. At P0, expression of these markers partially recovers, whereas expression of Th transcript and TH protein appears to be affected in lateral parts of the mdDA neuronal population. The initial increase in TH-expressing cells and delay in subset specification could be due to the increase in expression of the bHLH factor Ascl1, known for its role in mdDA neuronal differentiation, upon loss of Tcf4. Taken together, our data identified a minor role for Tcf4 in mdDA neuronal development and subset specification.

Myt/NZF family transcription factors regulate neuronal differentiation of P19 cells

2011 ◽  
Vol 497 (2) ◽  
pp. 74-79 ◽  
Author(s):  
Toshiki Kameyama ◽  
Fumio Matsushita ◽  
Yuzo Kadokawa ◽  
Tohru Marunouchi
Keyword(s):  
Transcription Factors ◽  
Neuronal Differentiation ◽  
P19 Cells

The Role of GM1 and Other Gangliosides in Neuronal Differentiation Overview and New Findingsa

1998 ◽  
Vol 845 (1 SPHINGOLIPIDS) ◽  
pp. 161-175 ◽  
Author(s):  
Robert W. Ledeen ◽  
Gusheng Wu ◽  
Zi-Hua Lu ◽  
Diane Kozireski-Chuback ◽  
Yu Fang
Keyword(s):  
Neuronal Differentiation

scholarly journals The Potential Role of Human NME1 in Neuronal Differentiation of Porcine Mesenchymal Stem Cells: Application of NB-hNME1 as a Human NME1 Suppressor

2021 ◽  
Vol 22 (22) ◽  
pp. 12194
Author(s):  
Jin Hyoung Cho ◽  
Won Seok Ju ◽  
Sang Young Seo ◽  
Bo Hyun Kim ◽  
Ji-Su Kim ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Neuronal Differentiation ◽  
Nucleoside Diphosphate Kinase ◽  
Inhibitory Effect ◽  
Human Macrophage ◽  
Potential Candidate ◽  
Xenograft Rejection ◽  
Ganglioside Gd3

This study aimed to investigate the effects of the human macrophage (MP) secretome in cellular xenograft rejection. The role of human nucleoside diphosphate kinase A (hNME1), from the secretome of MPs involved in the neuronal differentiation of miniature pig adipose tissue-derived mesenchymal stem cells (mp AD-MSCs), was evaluated by proteomic analysis. Herein, we first demonstrate that hNME1 strongly binds to porcine ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1 (pST8SIA1), which is a ganglioside GD3 synthase. When hNME1 binds with pST8SIA1, it induces degradation of pST8SIA1 in mp AD-MSCs, thereby inhibiting the expression of ganglioside GD3 followed by decreased neuronal differentiation of mp AD-MSCs. Therefore, we produced nanobodies (NBs) named NB-hNME1 that bind to hNME1 specifically, and the inhibitory effect of NB-hNME1 was evaluated for blocking the binding between hNME1 and pST8SIA1. Consequently, NB-hNME1 effectively blocked the binding of hNME1 to pST8SIA1, thereby recovering the expression of ganglioside GD3 and neuronal differentiation of mp AD-MSCs. Our findings suggest that mp AD-MSCs could be a potential candidate for use as an additive, such as an immunosuppressant, in stem cell transplantation.

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