Concentration-Dependent Effect of Nerve Growth Factor on Cell Fate Determination of Neural Progenitors

2011 ◽  
Vol 20 (10) ◽  
pp. 1723-1731 ◽  
Author(s):  
Lei Zhang ◽  
Hui Jiang ◽  
Zhengqing Hu
Stem Cells ◽  
2014 ◽  
Vol 32 (9) ◽  
pp. 2516-2528 ◽  
Author(s):  
Raffaella Scardigli ◽  
Paolo Capelli ◽  
Domenico Vignone ◽  
Rossella Brandi ◽  
Marcello Ceci ◽  
...  

2014 ◽  
Vol 19 (3) ◽  
pp. 239-253 ◽  
Author(s):  
Shohei Murakami ◽  
Ritsuko Shimizu ◽  
Paul-Henri Romeo ◽  
Masayuki Yamamoto ◽  
Hozumi Motohashi

2016 ◽  
Vol 104 (3) ◽  
pp. 324-329 ◽  
Author(s):  
Shin’ichiro Yasunaga ◽  
Yoshinori Ohno ◽  
Naoto Shirasu ◽  
Bo Zhang ◽  
Kyoko Suzuki-Takedachi ◽  
...  

10.1038/ni793 ◽  
2002 ◽  
Vol 3 (5) ◽  
pp. 443-450 ◽  
Author(s):  
Kenji Tanigaki ◽  
Hua Han ◽  
Norio Yamamoto ◽  
Kei Tashiro ◽  
Masaya Ikegawa ◽  
...  

RSC Advances ◽  
2019 ◽  
Vol 9 (64) ◽  
pp. 37300-37311 ◽  
Author(s):  
Zixiang Wu ◽  
Shujing Liang ◽  
Wenyu Kuai ◽  
Lifang Hu ◽  
Airong Qian

The recent advances of miRNAs and lncRNAs in determining the cell fate of MSCs.


2005 ◽  
Vol 25 (21) ◽  
pp. 9460-9468 ◽  
Author(s):  
Anita Borton Hjelmeland ◽  
Stephen H. Schilling ◽  
Xing Guo ◽  
Darryl Quarles ◽  
Xiao-Fan Wang

ABSTRACT Runx2 is required for osteoblast differentiation but is expressed in certain nonosteoblastic cells without activating the differentiation process, suggesting that its activity is suppressed through a lineage-specific mechanism. Here we report that primary mouse dermal fibroblasts lacking Smad3 can acquire an osteoblast-like phenotype, including activation of Runx2 activity, expression of osteoblast-specific genes, and calcium deposition. We further show that negative regulation of Runx2 activity by Smad3 in dermal fibroblasts is likely mediated by controlling the expression of Msx2, an antagonist of Runx2 in this cellular context. These data support the presence of a novel mechanism for controlling cell fate determination of mesenchymal lineages by preventing differentiation toward the osteoblastic lineage via negative regulation of Runx2 activity.


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