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The proteins involved in self renewal in embryonic and adult stem cells appear to be subverted in tumorigenesis to allow the tumor-initiating cells to maintain self renewal capacity.
However, small subsets of SCs are LRCs and retain self-renewal potential in pathogenic muscle, implicating a cell-autonomous property of LRCs to maintain self-renewal potential.
Similar to female GSCs, BALL is required to maintain self-renewal of male GSCs, suggesting a tissue independent requirement of BALL for self-renewal of germline stem cells.
SOX2 is required to maintain self-renewal of undifferentiated embryonic and neural stem cells.
It is, therefore, imperative to develop methods to acquire enough hMSCs that maintain self-renewal and differentiation potential.
Furthermore, TAZ is required for and sufficient to maintain self-renewal and tumor initiation capability of breast cancer stem cells (Cordenonsi et al., 2011).
Firstly, what are the regulatory mechanisms that maintain self-renewal and pluripotency?
We tested four independent human skin fibroblasts for the potential to maintain self-renewal of iPS cells.
In our previous study, we have used hFLSCs expressing hypoxia inducible factor 1α (HIF-1α) to maintain self-renewal and pluripotency of hES cells [46].
These findings lead us to the following question, what is the underlying mechanism by which soft-substrates can maintain self-renewal and pluripotency of mESCs?
Embryonic stem (ES) cell pluripotency is regulated in part by transcription factor (TF) pathways that maintain self-renewal and inhibit differentiation.
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