ライフサイエンスコーパス: untransformed cell

1 rence by vFosAP-1 compared with AP-1 from an untransformed cell.

2 h inhibitor selectively in cancer but not in untransformed cells.

3 eta interacted weakly with the apoptosome in untransformed cells.

4 itive to many signals that inhibit growth of untransformed cells.

5 eported NT ES cells derived from transfer of untransformed cells.

6 group of approximately 25 mRNAs compared to untransformed cells.

7 romotes and sustains cell-matrix adhesion of untransformed cells.

8 xygen species (ROS) compared with quiescent, untransformed cells.

9 protease phenotypes in both transformed and untransformed cells.

10 of inducing apoptosis of transformed but not untransformed cells.

11 was approximately 10-fold below the level of untransformed cells.

12 tivates caspases when added to extracts from untransformed cells.

13 are normally observed only during S-phase in untransformed cells.

14 t transcription while reducing toxicities to untransformed cells.

15 and 8-fold less, respectively, than those in untransformed cells.

16 urfaces to function when FANCD2 is absent in untransformed cells.

17 ifferent cancer cell lines and compare it to untransformed cells.

18 window between KRAS mutant cells and normal, untransformed cells.

19 screen based on competition between isogenic untransformed cells and BCR-Abl-transformed cells and id

20 is dispensable for FA pathway activation in untransformed cells and the Rad18 and FA pathways are se

21 totoxic effects on tumor cells while sparing untransformed cells, and Bcl-x(L) is reported to efficie

22 erent tissue origins have a lower pHlys than untransformed cells, and stably expressing oncogenic Ras

23 In addition, untransformed cells appear to possess one or more active

24 y in all three transformed lines compared to untransformed cells by VP16 treatment, while slight acti

25 rform a proteogenomic analysis of tumors and untransformed cells containing somatic copy number alter

26 atmospheric oxygen levels, proliferation of untransformed cells continues for extended periods of ti

27 We therefore tested primary untransformed cell cultures that lack CCR5 and CXCR4, in

28 tinuously exposed to microtubule inhibitors, untransformed cells eventually slip out of mitosis after

29 the apoptotic response that is triggered in untransformed cells following inappropriate cell-cycling

30 Notably, cytosolic replication in untransformed cells from both species was less pronounce

31 ht of beta-Ala betaine and Gly betaine) than untransformed cells grown in liquid medium containing 10

32 cultures, but genetic manipulation of these untransformed cells has been technically challenging.

33 We find that in untransformed cells, HER3 is not phosphorylated by MET i

34 ession imparted malignant characteristics to untransformed cells if p53 was compromised, promoting an

35 and the utility of studying transformed and untransformed cells in parallel.

36 lular matrix substrate arrests the growth of untransformed cells in the G1 phase.

37 transcriptionally upregulated these miRNA in untransformed cells, indicating that this Myc-induced mi

38 Hence, FANCD2-driven MiDAS in untransformed cells is built to protect CFS stability, w

39 er, suppression of this apoptotic pathway in untransformed cells is not mediated only by adhesion to

40 s, and stably expressing oncogenic RasV12 in untransformed cells is sufficient to decrease pHlys.

41 Ectopic CK2 expression in untransformed cells led to increased IKK-i/IKKepsilon mR

42 Inhibition of RNAP II in untransformed cells like Rat-1 or human AG1522 fibroblas

43 absent or substantially reduced compared to untransformed cell lines or leukemia cells lacking BCR/A

44 Untransformed cell lines were resistant to both ERBB4 an

45 Transfection of both E1A-transformed and untransformed cell lines with a series of mutant promote

46 er cells but not in the membranes of several untransformed cell lines.

47 high activities of src kinases as well as in untransformed cell lines.

48 tates from BCR/ABL-transformed, but not from untransformed, cell lines contained PI3K lipid kinase ac

49 Unlike untransformed cells, most cancer cells demonstrate reduc

50 Untransformed cells or those containing the parent const

51 BRG1 could not initiate tumor development in untransformed cells, our results indicate that transform

52 eta was phosphorylated at Ser 226/Ser 255 in untransformed cells, phosphorylation was absent in leuke

53 ur previous work has shown that, in cultured untransformed cells, preventing elimination of oxidized

54 RNA-Seq analysis in untransformed cells showed that they can regulate both d

55 Importantly, upon Ras expression, untransformed cells started responding to knockdown of H

56 n nine immortal human cell lines than in six untransformed cell strains.

57 ow rate of expression and activity levels in untransformed cells such as MCF10A.

58 transformed breast epithelial cells than in untransformed cells, suggesting a degree of tumor select

59 The assembly does not kill untransformed cells that the aptamer does not bind.

60 This interaction enables an untransformed cell to respond to stress-induced, p53-dep

61 ch hydrogen peroxide (H(2)O(2)) was added to untransformed cells to mimic the increase in ROS induced

62 w that induction of KRAS(G12V) expression in untransformed cells triggers H3K27me3 and HP1-associated

63 Whereas untransformed cells were sensitive to apoptotic death in

64 Also, while untransformed cells were sessile for long periods, BCR/A

65 Further, stimulation of untransformed cells with H(2)O(2) or pervanadate increas

66 Pretreatment of untransformed cells with low doses of arsenic induced co

67 In untransformed cells with normal p53, the preferred mode

68 regulation of ODC in RIE-1 cells, comparing untransformed cells with those transformed by an activat