Faculty Opinions recommendation of Brat is a Miranda cargo protein that promotes neuronal differentiation and inhibits neuroblast self-renewal.

2006 ◽  
Author(s):  
Valeri Vasioukhin
Keyword(s):  
Neuronal Differentiation ◽  
Self Renewal ◽  
Cargo Protein

scholarly journals Brat Is a Miranda Cargo Protein that Promotes Neuronal Differentiation and Inhibits Neuroblast Self-Renewal

2006 ◽  
Vol 10 (4) ◽  
pp. 441-449 ◽  
Author(s):  
Cheng-Yu Lee ◽  
Brian D. Wilkinson ◽  
Sarah E. Siegrist ◽  
Robin P. Wharton ◽  
Chris Q. Doe
Keyword(s):  
Neuronal Differentiation ◽  
Self Renewal ◽  
Cargo Protein

scholarly journals Stabilized β-Catenin Functions through TCF/LEF Proteins and the Notch/RBP-Jκ Complex To Promote Proliferation and Suppress Differentiation of Neural Precursor Cells

2008 ◽  
Vol 28 (24) ◽  
pp. 7427-7441 ◽  
Author(s):  
Takeshi Shimizu ◽  
Tetsushi Kagawa ◽  
Toshihiro Inoue ◽  
Aya Nonaka ◽  
Shinji Takada ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Neuronal Differentiation ◽  
Glycogen Synthase ◽  
Precursor Cells ◽  
Precursor Cell ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Self Renewal ◽  
Fgf Receptor ◽  
Proliferation And Differentiation

ABSTRACT The proliferation and differentiation of neural precursor cells are mutually exclusive during brain development. Despite its importance for precursor cell self renewal, the molecular linkage between these two events has remained unclear. Fibroblast growth factor 2 (FGF2) promotes neural precursor cell proliferation and concurrently inhibits their differentiation, suggesting a cross talk between proliferation and differentiation signaling pathways downstream of the FGF receptor. We demonstrate that FGF2 signaling through phosphatidylinositol 3 kinase activation inactivates glycogen synthase kinase 3β (GSK3β) and leads to the accumulation of β-catenin in a manner different from that in the Wnt canonical pathway. The nuclear accumulated β-catenin leads to cell proliferation by activating LEF/TCF transcription factors and concurrently inhibits neuronal differentiation by potentiating the Notch1-RBP-Jκ signaling pathway. β-Catenin and the Notch1 intracellular domain form a molecular complex with the promoter region of the antineurogenic hes1 gene, allowing its expression. This signaling interplay is especially essential for neural stem cell maintenance, since the misexpression of dominant-active GSK3β completely inhibits the self renewal of neurosphere-forming stem cells and prompts their neuronal differentiation. Thus, the GSK3β/β-catenin signaling axis regulated by FGF and Wnt signals plays a pivotal role in the maintenance of neural stem/precursor cells by linking the cell proliferation to the inhibition of differentiation.

scholarly journals Anti-aging effects exerted by Tetramethylpyrazine enhances self-renewal and neuronal differentiation of rat bMSCs by suppressing NF-kB signaling

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Xiaoqing Song ◽  
Jin Dai ◽  
Huaguang Li ◽  
Yuemeng Li ◽  
Weixiao Hao ◽  
...  
Keyword(s):  
Neuronal Differentiation ◽  
Neuron Specific Enolase ◽  
Neuronal Morphology ◽  
Biologically Active ◽  
Therapeutic Effects ◽  
Aging Effects ◽  
Neuroprotective Effects ◽  
Self Renewal ◽  
Neuronal Markers ◽  
Wide Range

AbstractIn order to improve the therapeutic effects of mesenchymal stem cell (MSC)-based therapies for a number of intractable neurological disorders, a more favorable strategy to regulate the outcome of bone marrow MSCs (bMSCs) was examined in the present study. In view of the wide range of neurotrophic and neuroprotective effects, Tetramethylpyrazine (TMP), a biologically active alkaloid isolated from the herbal medicine Ligusticum wallichii, was used. It was revealed that treatment with 30–50 mg/l TMP for 4 days significantly increased cell viability, alleviated senescence by suppressing NF-κB signaling, and promoted bMSC proliferation by regulating the cell cycle. In addition, 40–50 mg/l TMP treatment may facilitate the neuronal differentiation of bMSCs, verified in the present study by presentation of neuronal morphology and expression of neuronal markers: microtubule-associated protein 2 (MAP-2) and neuron-specific enolase (NSE). The quantitative real-time polymerase chain reaction (qRT-PCR) revealed that TMP treatment may promote the expression of neurogenin 1 (Ngn1), neuronal differentiation 1 (NeuroD) and mammalian achaete–scute homolog 1 (Mash1). In conclusion, 4 days of 40–50 mg/l TMP treatment may significantly delay bMSC senescence by suppressing NF-κB signaling, and enhancing the self-renewal ability of bMSCs, and their potential for neuronal differentiation.

scholarly journals p73 deficiency results in impaired self renewal and premature neuronal differentiation of mouse neural progenitors independently of p53

2010 ◽  
Vol 1 (12) ◽  
pp. e109-e109 ◽  
Author(s):  
L Gonzalez-Cano ◽  
M Herreros-Villanueva ◽  
R Fernandez-Alonso ◽  
A Ayuso-Sacido ◽  
G Meyer ◽  
...  
Keyword(s):  
Neuronal Differentiation ◽  
Neural Progenitors ◽  
Self Renewal

scholarly journals Dual Function of Wnt Signaling during Neuronal Differentiation of Mouse Embryonic Stem Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Hanjun Kim ◽  
Sewoon Kim ◽  
Yonghee Song ◽  
Wantae Kim ◽  
Qi-Long Ying ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Neuronal Differentiation ◽  
Expression Profiles ◽  
Es Cells ◽  
Embryonic Stem ◽  
Dual Function ◽  
Self Renewal ◽  
Neural Stem Progenitor Cells ◽  
Ectopic Activation ◽  
Endogenous Activity

Activation of Wnt signaling enhances self-renewal of mouse embryonic and neural stem/progenitor cells. In contrast, undifferentiated ES cells show a very low level of endogenous Wnt signaling, and ectopic activation of Wnt signaling has been shown to block neuronal differentiation. Therefore, it remains unclear whether or not endogenous Wnt/β-catenin signaling is necessary for self-renewal or neuronal differentiation of ES cells. To investigate this, we examined the expression profiles of Wnt signaling components. Expression levels of Wnts known to induceβ-catenin were very low in undifferentiated ES cells. Stable ES cell lines which can monitor endogenous activity of Wnt/β-catenin signaling suggest that Wnt signaling was very low in undifferentiated ES cells, whereas it increased during embryonic body formation or neuronal differentiation. Interestingly, application of small molecules which can positively (BIO, GSK3βinhibitor) or negatively (IWR-1-endo, Axin stabilizer) control Wnt/β-catenin signaling suggests that activation of that signaling at different time periods had differential effects on neuronal differentiation of 46C ES cells. Further, ChIP analysis suggested thatβ-catenin/TCF1 complex directly regulated the expression ofSox1during neuronal differentiation. Overall, our data suggest that Wnt/β-catenin signaling plays differential roles at different time points of neuronal differentiation.

RGCC balances self‐renewal and neuronal differentiation of neural stem cells in the developing mammalian neocortex

EMBO Reports ◽  
2021 ◽  
Author(s):  
Zhenming Guo ◽  
Mengxia Chen ◽  
Yiming Chao ◽  
Chunhai Cai ◽  
Liangjie Liu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Neuronal Differentiation ◽  
Self Renewal

scholarly journals Cyclin-Dependent Kinase-Dependent Phosphorylation of Sox2 at Serine 39 Regulates Neurogenesis

2017 ◽  
Vol 37 (16) ◽  
Author(s):  
Shuhui Lim ◽  
Akshay Bhinge ◽  
Sara Bragado Alonso ◽  
Irene Aksoy ◽  
Julieta Aprea ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Neuronal Differentiation ◽  
Kinase Activity ◽  
Phosphorylation Site ◽  
Cyclin Dependent Kinase ◽  
Truncated Form ◽  
Self Renewal ◽  
Cdk Phosphorylation

ABSTRACT Sox2 is known to be important for neuron formation, but the precise mechanism through which it activates a neurogenic program and how this differs from its well-established function in self-renewal of stem cells remain elusive. In this study, we identified a highly conserved cyclin-dependent kinase (Cdk) phosphorylation site on serine 39 (S39) in Sox2. In neural stem cells (NSCs), phosphorylation of S39 enhances the ability of Sox2 to negatively regulate neuronal differentiation, while loss of phosphorylation is necessary for chromatin retention of a truncated form of Sox2 generated during neurogenesis. We further demonstrated that nonphosphorylated cleaved Sox2 specifically induces the expression of proneural genes and promotes neurogenic commitment in vivo. Our present study sheds light on how the level of Cdk kinase activity directly regulates Sox2 to tip the balance between self-renewal and differentiation in NSCs.

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