ライフサイエンスコーパス: non-dividing cell

1 levels of DRAP1 expression in differentiated non dividing cells.

2 , possibly resulting in neurodegeneration in non-dividing cells.

3 of those prevailing either in cycling or in non-dividing cells.

4 g as replacement histone genes in long-lived non-dividing cells.

5 evelopment of gene-targeting applications in non-dividing cells.

6 tinuous accumulation of repeat expansions in non-dividing cells.

7 s of dGTP or GTP found in either dividing or non-dividing cells.

8 viability, homeostasis and DNA synthesis in non-dividing cells.

9 fficient long-term infection of dividing and non-dividing cells.

10 limitations, with good ability to transfect non-dividing cells.

11 (HIV-1), like other lentiviruses, can infect non-dividing cells.

12 tissues, the H2A-1 gene is expressed in many non-dividing cells.

13 is the ability of the virus to replicate in non-dividing cells.

14 eneration of mutant proteins in dividing and non-dividing cells.

15 nd the nuclear import of the viral genome in non-dividing cells.

16 or contains no viral genes and can transduce non-dividing cells.

17 upply the NLS(s) that enable HIV-1 to infect non-dividing cells.

18 rent disease conditions and the existence of non-dividing cells.

19 to genome stability especially in slowly or non-dividing cells.

20 ich highlights the utility of cRNAs in these non-dividing cells.

21 CF remains essential for TAD organization in non-dividing cells.

22 ently extended silencing duration, unlike in non-dividing cells.

23 istone turnover, discriminating dividing and non-dividing cells.

24 ved site-specific integration frequencies in non-dividing cells.

25 creating a therapeutic window compared with non-dividing cells.

26 le sensitivity to study somatic mutations in non-dividing cells across several tissues, comparing ste

27 Hypotonic stress to flattened, non-dividing cells activated no additional current.

28 end joining-based methods, with activity in non-dividing cells and in vivo with fewer detectable off

29 been shown to improve knock-in efficiency in non-dividing cells and to harness HDR after direct injec

30 ar macrophages as terminally differentiated, non-dividing cells and underscores biological difference

31 other lentiviruses are capable of infecting non-dividing cells and, therefore, need to be imported i

32 3, (2) animals can recover from silencing in non-dividing cells, and (3) cleavage and tailing of mRNA

33 ion of DNA damage and apoptosis, activity in non-dividing cells, and bystander activity.

34 BRCA2 is not expressed in the non-dividing cells, and expression is cell cycle stage-d

35 tion of most mammalian cell types, including non-dividing cells, and features are included that give

36 ions reveal a role of heterochronic genes in non-dividing cells, and provide an example of cell-auton

37 In general, non-dividing cells are likely to have low cellular dNTP

38 HIV can infect non-dividing cells because the viral capsid can overcome

39 thrin-coated vesicles occurs continuously in non-dividing cells, but is shut down during mitosis, whe

40 llow dividing cells to be distinguished from non-dividing cells by a greater than two-fold increase i

41 Lentiviruses, such as HIV-1, infect non-dividing cells by traversing the nuclear pore comple

42 herefore, SAMHD1 expression, particularly in non-dividing cells, can restrict retroviral infections s

43 man immunodeficiency virus type 1 (HIV-1) in non-dividing cells critically depends on import of the v

44 man immunodeficiency virus type 1 (HIV-1) in non-dividing cells depends critically on import of the v

45 upport long-term expression of transgenes in non-dividing cells, exhibiting a decreased risk of inser

46 ral preintegration complex to the nucleus of non-dividing cells following virus entry.

47 hough H3.3-YFP deposition stably remained in non-dividing cells for days after IFN stimulation, it wa

48 The efficacy of in vivo transduction of non-dividing cells has been demonstrated in a wide varie

49 We transcriptionally profiled dividing and non-dividing cells in regenerating stump tissues, as wel

50 Cilia are found on most non-dividing cells in the human body and, when faulty, c

51 iviral (HIV)-based vector that can transduce non-dividing cells in vitro and deliver genes in vivo.

52 for robust DNA knock-in in both dividing and non-dividing cells in vitro and, more importantly, in vi

53 irectional DNA knock-in in both dividing and non-dividing cells in vivo.

54 in activity in the double mutant converted a non-dividing cell into a novel highly proliferating cell

55 The data indicate that YycG activity in non-dividing cells is suppressed by its interaction with

56 ocytes of Xenopus laevis, as an example of a non-dividing cell, is exclusive to the nuclear pore comp

57 s that could produce revertant phenotypes in non-dividing cells of both pro- and eukaryotes, we note

58 efined nucleotide edits in both dividing and non-dividing cells, offering potential for correcting pa

59 her somatic expansion of the repeat tract in non-dividing cells, particularly striatal neurons, haste

60 ve cells in the late embryonic brainstem are non-dividing cells, presumably immature oligodendrocytes

61 (HIV-1) contributes to viral replication in non-dividing cells, specifically those of the myeloid li

62 cargoes up to 12 kb for stable expression in non-dividing cells, stem cells and primary human T cells

63 iently deliver siRNAs into both dividing and non-dividing cells, stem cells, zygotes, and their diffe

64 ortant mechanism for repairing DNA damage in non-dividing cells such as neurons.

65 iency virus type-1 (HIV-1) is able to infect non-dividing cells such as tissue macrophages productive

66 y type 1 (HIV-1) have the capacity to infect non-dividing cells such as tissue macrophages.

67 with fewer byproducts in slowly dividing or non-dividing cells, such as those that make up most of t

68 that this metabolic adaptation can occur in non-dividing cells, suggesting a role for the Warburg ef

69 s, are capable of efficiently replicating in non-dividing cells (terminally differentiated macrophage

70 nctional proteins after cell division and in non-dividing cells that elongated.

71 While RNAi therapies are highly effective in non-dividing cells, their efficacy in rapidly dividing c

72 other lentiviruses mediate the infection of non-dividing cells through the ability of the capsid pro

73 oliferation it is also strongly expressed in non-dividing cells undergoing DNA synthesis and repair.

74 Although expansions can accrue in non-dividing cells, we also show that cell cycle arrest

75 Importantly, the rates of expansion in non-dividing cells were at least as high as those of pro

76 includes access of the pDNA to the nuclei of non-dividing cells where the presence of an intact nucle

77 ting module for selective gene expression in non-dividing cells, which allows us to radically alter p

78 urrent tools are inefficient, especially for non-dividing cells, which compose most adult tissues.

79 ersistent HIV reservoir in both dividing and non-dividing cells while avoiding immunogenicity.

80 In non-dividing cells with lengths increased to 10 times no

81 ess programmable integration in dividing and non-dividing cells, with both research and therapeutic a