ライフサイエンスコーパス: pillar cell

1 ate transformation of a Deiters' cell into a pillar cell.

2 division with an increase in cell number of pillar cells.

3 it did not transfer between inner and outer pillar cells.

4 but is restricted to developing Deiters' and pillar cells.

5 ole in the commitment and differentiation of pillar cells.

6 in the fate of supporting cells (Deiters'-to-pillar cells) along the entire length of the cochlear du

7 emonstrated that, similar to Deiters' cells, pillar cells also possess Ca(2+)-dependent contractile m

8 anges in the shape and distribution of outer pillar cell and Deiters' cell phalangeal processes that

9 Cs; these phase-led vibrations beneath outer pillar cells and adjacent to the spiral ligament by appr

10 ar proliferation, suggesting that additional pillar cells and inner hair cells were a result of incre

11 In addition, AAV2.7m8 infects inner pillar cells and inner phalangeal cells with high effici

12 ween neuronal loss and abnormalities of both pillar cells and Reissner's membrane, however.

13 d to a significant increase in the number of pillar cells and to a small increase in the number of in

14 to-basal progression of pathology of limbus, pillar cells, and Reissner's membrane run counter to mos

15 companied by abnormalities of spiral limbus, pillar cells, and Reissner's membrane.

16 cells (IHCs) and its supporting cells, inner pillar cells, and synaptic region of the outer hair cell

17 packing density, but not identity, of inner pillar cells; and (iii) embryonic formation and (iv) cyt

18 Moreover, the position of the pillar cells appears to be determined by the activation

19 on and maintenance of pillar cell fate, that pillar cells are distinguished by Hey2 expression, and t

20 ated decreasing GJIC between inner and outer pillar cells around the onset of hearing.

21 ich abort cell division, postmitotic Rb(-/-) pillar cells can proliferate, maintain their SC fate and

22 In the dissociated Deiters cells and pillar cells, Cx30 showed dense labeling at the cell bod

23 The factors that regulate pillar cell development have not been determined; howeve

24 To examine the specific effects of FGFR3 on pillar cell development, we inhibited receptor activatio

25 Inner ear defects include failure of pillar cell differentiation and tunnel of Corti formatio

26 ation of FGFR3 resulted in the resumption of pillar cell differentiation.

27 ient inhibition of FGFR3 did not inhibit the pillar cell fate permanently, because reactivation of FG

28 y for the differentiation and maintenance of pillar cell fate, that pillar cells are distinguished by

29 render Hey2 Notch independent also liberated pillar cells from the need for direct contact with surro

30 Pillar cell head enlargement continued until 20 days pos

31 n the middle turn, before enlargement of the pillar cell heads at 8 days postnatally.

32 not move as a stiff plate hinging around the pillar-cell heads near the first row as has been assumed

33 ing was found in supporting cells, including pillar cells, Hensen cells, Claudius cells, and Boettche

34 alian cochlea is the presence of two rows of pillar cells in the region between the single row of inn

35 ner phalangeal cells, Hensen's, Deiters' and pillar cells, in a subset of spiral ganglion neurons, an

36 he proliferation of SCs, including the inner pillar cells (IPCs), inner border cells (IBCs), and late

37 In neonatal mice, Sox2-null inner pillar cells (IPCs, a subtype of SCs) proliferated and g

38 Results indicated that differentiation of pillar cells is dependent on continuous activation of FG

39 by aberrant expression of cadherins and the pillar cell markers P75 and Lgr6.

40 ctorial membrane, reticular lamina (RL), and pillar cell motion; the inner rows of OHCs moved antipha

41 scaffold, including Deiters' (DC) and outer pillar cells (OPC), to enable the sensitivity and exquis

42 cells (e.g., Deiters' cells [DCs] and outer pillar cells [OPCs]), but this has never been establishe

43 ieved in vivo conversion of two SC subtypes, pillar cells (PCs) and Deiters' cells (DCs), into HCs by

44 e/loxP system in mice to specifically ablate pillar cells (PCs) and Deiters' cells (DCs).

45 Two of these cell types, inner and outer pillar cells (PCs), are arranged in adjacent rows that f

46 ed cells, including Deiters' cells (DCs) and pillar cells (PCs), coupled by gap-junctions composed of

47 s were present in the medial compartment and pillar cell region of Jag1Ndr/Ndr cochleae, yet they exh

48 erentiation, whereas mutation of Hey2 leaves pillar cells sensitive to the loss of Notch signaling an

49 her spontaneous rate fibers terminate on the pillar-cell side of the IHC and lower rate fibers termin

50 gion than in the 1 mm region and also on the pillar-cell side of the IHC compared with the modiolar s

51 8 and FGFR3, both of which are essential for pillar cell specification, the radial patterning of orga

52 was more pronounced in the Deiters cells and pillar cells than in the Hensen cells.

53 an of Corti cytoarchitecture: instead of two pillar cells, there are three, resulting in the formatio

54 on of connexin 26 in Deiters cells and outer pillar cells, which constrain outer hair cells standing

55 ells but not to stereociliary ankle links or pillar cells, which nonspecifically react with two antis