scholarly journals Sox1 Maintains the Undifferentiated State of Cortical Neural Progenitor Cells via the Suppression of Prox1-Mediated Cell Cycle Exit and Neurogenesis

Stem Cells ◽  
2011 ◽  
Vol 29 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Maximilianos Elkouris ◽  
Nikos Balaskas ◽  
Maria Poulou ◽  
Panagiotis K. Politis ◽  
Elena Panayiotou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Cell Cycle Exit ◽  
Undifferentiated State

scholarly journals Loss of YAP/TAZ impaired the proliferation and differentiation ability of neural progenitor cells

2018 ◽  
Author(s):  
Shanshan Kong
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Hippo Pathway ◽  
Neural Progenitor ◽  
Cell Junctions ◽  
Binding Motif ◽  
Cell Cycle Exit ◽  
Conditional Deletion ◽  
Proliferation And Differentiation

AbstractYAP (Yes-associated protein) and TAZ (transcriptional coactivator with PDZ-binding motif) are downstream effectors of the Hippo pathway, they activate the expression of transcriptional targets that promote cell growth, cell proliferation, and prevent apoptosis. Here I examined the function of YAP/TAZ in mouse neocortex development through conditional deletion of Yap and Taz by Emx1-Cre. Loss of YAP/TAZ cause the hydrocephalus after birth, leads to aberrant development and dilated ventricle in adult stage, this phenotype can be detected as early as P0. YAP/TAZ are expressed in Sox2+ neural progenitor cells, when YAP/TAZ are deleted, the neuroepithelial cell junctions are disrupted; the numbers of Sox2+ cell and Tbr2+ cell are reduced and the ratio of tbr2/Sox2 is also reduced at E15.5. Results of cell cycle analyzing experiments display YAP/TAZ deletion increased the cell cycle exit. The improperly increased expression of Tuj1+ in progenitor cells in the YAP/TAZ deleted cortex indicates the premature of Sox2+ progenitor cells. Together, our results reveal that YAP/TAZ deletion changed the polarity of neuroepithelial cells, and increased the cell cycle exit, reduced the differentiation of Sox2+ cells into Tbr2+ cells through promoting the premature of Tuj1+ cells. These results define the functions of YAP/TAZ in keeping the cell polarity neural progenitors and ensuring their proliferation and differentiation, and also reveal the roles of YAP/TAZ in developing cortex.

Chemokine receptor CXCR4 signaling modulates the growth factor-induced cell cycle of self-renewing and multipotent neural progenitor cells

Glia ◽  
2010 ◽  
Vol 59 (1) ◽  
pp. 108-118 ◽  
Author(s):  
Meizhang Li ◽  
Cathleen J. Chang ◽  
Justin D. Lathia ◽  
Li Wang ◽  
Holly L. Pacenta ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Progenitor Cells ◽  
Chemokine Receptor ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Cxcr4 Signaling ◽  
Chemokine Receptor Cxcr4

scholarly journals Targeted Deletion of the S-Phase-Specific Myc Antagonist Mad3 Sensitizes Neuronal and Lymphoid Cells to Radiation-Induced Apoptosis

2001 ◽  
Vol 21 (3) ◽  
pp. 703-712 ◽  
Author(s):  
Christophe Quéva ◽  
Grant A. McArthur ◽  
Brian M. Iritani ◽  
Robert N. Eisenman
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Cellular Response ◽  
Leucine Zipper ◽  
Neural Progenitor Cells ◽  
Expression Patterns ◽  
S Phase ◽  
Lymphoid Cells ◽  
Cell Cycle Exit ◽  
Proliferating Cells

ABSTRACT The Mad family comprises four basic-helix-loop-helix/leucine zipper proteins, Mad1, Mxi1, Mad3, and Mad4, which heterodimerize with Max and function as transcriptional repressors. The balance between Myc-Max and Mad-Max complexes has been postulated to influence cell proliferation and differentiation. The expression patterns of Mad family genes are complex, but in general, the induction of most family members is linked to cell cycle exit and differentiation. The expression pattern ofmad3 is unusual in that mad3 mRNA and protein were found to be restricted to proliferating cells prior to differentiation. We show here that during murine developmentmad3 is specifically expressed in the S phase of the cell cycle in neuronal progenitor cells that are committed to differentiation. To investigate mad3 function, we disrupted the mad3 gene by homologous recombination in mice. No defect in cell cycle exit and differentiation could be detected inmad3 homozygous mutant mice. However, upon gamma irradiation, increased cell death of thymocytes and neural progenitor cells was observed, implicating mad3 in the regulation of the cellular response to DNA damage.

Cell cycle progression is required for nuclear migration of neural progenitor cells

2006 ◽  
Vol 1088 (1) ◽  
pp. 57-67 ◽  
Author(s):  
Masaki Ueno ◽  
Kei-ichi Katayama ◽  
Hirofumi Yamauchi ◽  
Hiroyuki Nakayama ◽  
Kunio Doi
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Neural Progenitor Cells ◽  
Nuclear Migration ◽  
Neural Progenitor ◽  
Cycle Progression
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