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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 Untransformed cell lines were resistant to both ERBB4 an

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

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

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

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

37 Unlike untransformed cells, most cancer cells demonstrate reduc

38 Untransformed cells or those containing the parent const

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

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

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

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

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

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

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

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

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

48 Whereas untransformed cells were sensitive to apoptotic death in

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

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

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

52 In untransformed cells with normal p53, the preferred mode

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