ライフサイエンスコーパス: redifferentiation

1 lving cellular dedifferentiation followed by redifferentiation).

2 eral donors, into iPSCs and their subsequent redifferentiation.

3 y of their initial lineage choice and resist redifferentiation.

4 eprogramming of somatic cells and subsequent redifferentiation.

5 Loss of STAT1 prevents redifferentiation.

6 plast development or early stages of eoplast redifferentiation.

7 ential for dedifferentiation, expansion, and redifferentiation.

8 e matrix remodeling and induces PC glandular redifferentiation.

9 ury-induced neointima formation, induced SMC redifferentiation.

10 ement binding protein and, consequently, SMC redifferentiation.

11 tion factors are devoted to promoting acinar redifferentiation after injury.

12 ession accompanied proximal tubule epithelia redifferentiation, again coincident with decreased BMP s

13 activating digitalislike compounds (DLCs) on redifferentiation and concomitant restoration of iodide

14 Syncytium formation involves the redifferentiation and fusion of hundreds of root cells.

15 cabazitaxel treatment induced MET, glandular redifferentiation, and AR nuclear localization that was

16 inhibition is sufficient to induce BCD cell redifferentiation, as manifested by a significant increa

17 dogenous regeneration response that involves redifferentiation by direct ossification (evolved regene

18 drogenic and osteogenic markers we show that redifferentiation does not occur by endochondral ossific

19 ient phases of inflammation, metaplasia, and redifferentiation, driven by cell-cell interactions betw

20 used to analyze chloroplast development and redifferentiation during petal development.

21 hat HES1 inhibition may also affect BCD cell redifferentiation following expansion.

22 st stage; however, problems may occur during redifferentiation for tissue genesis and organogenesis,

23 ctivate matrilin-1 expression rather than by redifferentiation from the flattened cells of the interz

24 mechanisms of nuclear dedifferentiation and redifferentiation in oocyte cytoplasm.

25 that inhibition of this pathway may promote redifferentiation in poorly differentiated thyroid carci

26 he MAPK pathway controls both MDCK p-EMT and redifferentiation, in part by activating MMP13 and TIMP1

27 ate-like aberrant bodies with no evidence of redifferentiation into elementary bodies.

28 rogenitor cells, suggesting an inhibition of redifferentiation into mature exocrine cells.

29 differentiation followed by stimulus-induced redifferentiation into multiple lineage cell types.

30 cell-specific toxin suggested that prespore redifferentiation may not in fact occur.

31 tic Ppargamma ligand supplementation induces redifferentiation of Ad/N1ICD adipocytes and tumor cells

32 ntiated cells, proliferation, and subsequent redifferentiation of adult tissues.

33 e an effective protocol for the promotion of redifferentiation of autologous chondrocytes obtained fr

34 re of soluble factors further stimulated the redifferentiation of BCD cells.

35 Redifferentiation of beta-cells after expansion is still

36 fferentiation, migration, proliferation, and redifferentiation of cells proximal to the amputation pl

37 nical stimuli have been harnessed to enhance redifferentiation of chondrocytes and chondroinduction o

38 By using the redifferentiation of four patient-derived induced plurip

39 The redifferentiation of T reg cells into Th cells has been

40 ting that macrophages play a key role in the redifferentiation of the blastema.

41 nd endothelial cell migration and subsequent redifferentiation of the fibroblasts to a contractile st

42 Redifferentiation of the monolayer chondrocyte cultures

43 of how the pEMT phase is turned off and the redifferentiation phase is initiated is largely unknown.

44 , and its up-regulation is necessary for the redifferentiation phase.

45 ntial progression from the pEMT phase to the redifferentiation phase.

46 These findings demonstrate the redifferentiation potential of ex vivo expanded BCD cell

47 In differentiation and redifferentiation processes, tubulin expression may prov

48 ured tubular cells activates epithelial cell redifferentiation rather than dedifferentiation during o

49 De- and redifferentiation represent phenotypic transitions that

50 Dictyostelium discoideum amoebae to undergo redifferentiation so as to reestablish normal spore/stal

51 teinases (MMPs) are necessary for the second redifferentiation stage.

52 on of actin stress fibers using any of these redifferentiation stimuli also supported the superinduct

53 Constitutively active STAT1 allows redifferentiation to occur even when cells are otherwise

54 mmon regulatory mechanisms governing de- and redifferentiation transitions in cartilage and tendon ce

55 efractory thyroid cancer and who underwent a redifferentiation treatment with the mitogen-activated e

56 In this study of chondrocyte redifferentiation we have provided further evidence of t