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1 eration, we find no evidence to suggest that dedifferentiated cells acquire a ductal fate during this
2                                 We find that dedifferentiated cells adopt a progenitor-like fate due
3 , the proliferation and the migration of the dedifferentiated cells are dependent on Hh signaling.
4                          Factors secreted by dedifferentiated cells, but not by melanocytic cells, st
5  transcription factors and that diseased and dedifferentiated cells can be returned to normal functio
6 transition, and exogenous PHD2 expression in dedifferentiated cells can restore an epithelial phenoty
7 lular matrix, and proliferation of partially dedifferentiated cells, evidence strongly supports the l
8  and three IR-resistant clones isolated from dedifferentiated cells have acquired the ability to prol
9           RNAi-mediated knockdown of Oct4 in dedifferentiated cells led to diminished CSC phenotypes.
10 could be detected in similar assays with the dedifferentiated cell line HepG2.1 or the nonhepatic cel
11                 Upon various challenges, the dedifferentiated cells proliferate and redifferentiate i
12                    Melanomas can switch to a dedifferentiated cell state upon exposure to cytotoxic T
13 n organized structure of lineage restricted, dedifferentiated cells that cooperate to regenerate the
14 erogeneous population of lineage-restricted, dedifferentiated cells that ultimately orchestrates rege
15 g of IPF-ABC towards a KRT17(high) PTEN(low) dedifferentiated cell type.
16                     Finally, IL1 produced by dedifferentiated cells was involved in the inhibition of
17                                              Dedifferentiated cells were morphologically indistinguis
18  order to perform genetic lineage tracing of dedifferentiated cells while measuring the cellular tran
19 val may be manifested by the production of a dedifferentiated cell with broader potential and that th