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Under conditions in which differentiation would be induced in NSCs, GSCs showed an intrinsic potential to maintain their undifferentiated state or to resist differentiation and even tended to retro-differentiate under certain circumstances.
Supporting the importance of Nanog downregulation at implantation, ES cells overexpressing Nanog resist differentiation into EpiSCs, and retain, albeit at reduced levels, expression of ES cell markers after repeated passaging in Activin/FGF [ 4].
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In the presence of Tam, however, many cells resisted differentiation.
It has been known for some time that a subpopulation of ES cells tends to resist neural differentiation, but the reasons for this are not clear.
Overexpression of the TUs, in transient or stable transfectants, could be attempted as an additional functional test in order to determine whether higher levels of the TU RNAs enable ES cells to resist chemical differentiation drivers.
Stimulating the MUC1* receptor with either the cognate antibody or its ligand NM23 enabled hESC growth in a feeder cell-free system and produced pluripotent colonies that resisted spontaneous differentiation.
In fact, stem cell growth supported by the addition of MUC1* ligands to minimal media resisted spontaneous differentiation and produced more pluripotent cells than any other growth condition that we tested.
With the exception of those comparisons made between high latitude populations of F. p. tundrius (see below), we remain cautious and resist equating reported population differentiation estimates with actual relative degree of differentiation between populations [e.g., 55,94 96].
Germline progenitors resist signals that promote differentiation into somatic cells.
Germline progenitor cells resist signals that promote differentiation into somatic cells during development, thus maintaining their cell fate.
In healthy articular cartilage, chondrocytes resist proliferation and terminal differentiation.
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