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1 lving cellular dedifferentiation followed by redifferentiation).
2 n secretion in many individuals, possibly by redifferentiation.
3 ury-induced neointima formation, induced SMC redifferentiation.
4 ement binding protein and, consequently, SMC redifferentiation.
5 eral donors, into iPSCs and their subsequent redifferentiation.
6 y of their initial lineage choice and resist redifferentiation.
7 eprogramming of somatic cells and subsequent redifferentiation.
8                       Loss of STAT1 prevents redifferentiation.
9 plast development or early stages of eoplast redifferentiation.
10 ential for dedifferentiation, expansion, and redifferentiation.
11 e matrix remodeling and induces PC glandular redifferentiation.
12 y of stromal and immune phenotypes and tumor redifferentiation.
13 tion factors are devoted to promoting acinar redifferentiation after injury.
14 el of HB, demonstrating tumor regression and redifferentiation after YAP1 withdrawal through genome-w
15 ession accompanied proximal tubule epithelia redifferentiation, again coincident with decreased BMP s
16 activating digitalislike compounds (DLCs) on redifferentiation and concomitant restoration of iodide
17             Syncytium formation involves the redifferentiation and fusion of hundreds of root cells.
18 cabazitaxel treatment induced MET, glandular redifferentiation, and AR nuclear localization that was
19  dysfunction, failed epithelial recovery and redifferentiation, and subsequent tubulointerstitial fib
20  inhibition is sufficient to induce BCD cell redifferentiation, as manifested by a significant increa
21 lmonary metastases, who underwent dabrafenib redifferentiation before RAI therapy.
22 nase inhibitors (TKIs) for 3-6 wk to achieve redifferentiation, but preclinical data suggest that max
23 dogenous regeneration response that involves redifferentiation by direct ossification (evolved regene
24 As a result, metabolic reprogramming or cell redifferentiation destabilized latent infection.
25 drogenic and osteogenic markers we show that redifferentiation does not occur by endochondral ossific
26 ient phases of inflammation, metaplasia, and redifferentiation, driven by cell-cell interactions betw
27  used to analyze chloroplast development and redifferentiation during petal development.
28                                              Redifferentiation efficiency was boosted by three-dimens
29 hat HES1 inhibition may also affect BCD cell redifferentiation following expansion.
30 st stage; however, problems may occur during redifferentiation for tissue genesis and organogenesis,
31 ctivate matrilin-1 expression rather than by redifferentiation from the flattened cells of the interz
32 us-mediated mini ATP7B gene transfection and redifferentiation, functional LPC-ATP7B-derived hepatocy
33  mechanisms of nuclear dedifferentiation and redifferentiation in oocyte cytoplasm.
34  that inhibition of this pathway may promote redifferentiation in poorly differentiated thyroid carci
35 he MAPK pathway controls both MDCK p-EMT and redifferentiation, in part by activating MMP13 and TIMP1
36 ate-like aberrant bodies with no evidence of redifferentiation into elementary bodies.
37 rogenitor cells, suggesting an inhibition of redifferentiation into mature exocrine cells.
38 differentiation followed by stimulus-induced redifferentiation into multiple lineage cell types.
39  cell-specific toxin suggested that prespore redifferentiation may not in fact occur.
40 tic Ppargamma ligand supplementation induces redifferentiation of Ad/N1ICD adipocytes and tumor cells
41 ntiated cells, proliferation, and subsequent redifferentiation of adult tissues.
42 e an effective protocol for the promotion of redifferentiation of autologous chondrocytes obtained fr
43 re of soluble factors further stimulated the redifferentiation of BCD cells.
44                                              Redifferentiation of beta-cells after expansion is still
45 fferentiation, migration, proliferation, and redifferentiation of cells proximal to the amputation pl
46 nical stimuli have been harnessed to enhance redifferentiation of chondrocytes and chondroinduction o
47                                 By using the redifferentiation of four patient-derived induced plurip
48 n, and their development involves sequential redifferentiation of many cell types to perform distinct
49 kdown of extracellular matrix components and redifferentiation of stromal adipocytes.
50                                          The redifferentiation of T reg cells into Th cells has been
51 ting that macrophages play a key role in the redifferentiation of the blastema.
52 nd endothelial cell migration and subsequent redifferentiation of the fibroblasts to a contractile st
53                                              Redifferentiation of the monolayer chondrocyte cultures
54                                              Redifferentiation of these stem-like cells into cells ve
55                        FR evoked melanocytic redifferentiation of UM tumor cells with low (class 1),
56  of how the pEMT phase is turned off and the redifferentiation phase is initiated is largely unknown.
57 , and its up-regulation is necessary for the redifferentiation phase.
58 ntial progression from the pEMT phase to the redifferentiation phase.
59               These findings demonstrate the redifferentiation potential of ex vivo expanded BCD cell
60 red chondrocyte dedifferentiation/osteoblast redifferentiation process.
61                       In differentiation and redifferentiation processes, tubulin expression may prov
62 ured tubular cells activates epithelial cell redifferentiation rather than dedifferentiation during o
63                                      De- and redifferentiation represent phenotypic transitions that
64  Dictyostelium discoideum amoebae to undergo redifferentiation so as to reestablish normal spore/stal
65 teinases (MMPs) are necessary for the second redifferentiation stage.
66 on of actin stress fibers using any of these redifferentiation stimuli also supported the superinduct
67 roaches to improve thyroid cancer prognosis, redifferentiation strategies and targeted therapies.
68           Constitutively active STAT1 allows redifferentiation to occur even when cells are otherwise
69 mmon regulatory mechanisms governing de- and redifferentiation transitions in cartilage and tendon ce
70 ne treatment, tyrosine kinase treatment, and redifferentiation treatment for metastasized DTC.
71 efractory thyroid cancer and who underwent a redifferentiation treatment with the mitogen-activated e
72 mal adipocytes undergo dedifferentiation and redifferentiation under physiological and pathophysiolog
73                 In this study of chondrocyte redifferentiation we have provided further evidence of t