ライフサイエンスコーパス: in control cells

1 In control cells, 3AT-inducible genes exhibit a series of dis

2 In control cells, complex I inhibition resulted in caspase-me

3 In control cells, pretreatment with 100 microM NaHS shifted t

4 lysis showed that of 114 genes regulated by 1,25(OH)(2)D(3) in control cells, almost all (113) were rendered insensitive

5 , 6 kV/cm) decreased cell survival to 34% compared with 51% in control cells (*, p < 0.01).

6 ith Cygb accounting for approximately 40% of the activation in control cells and approximately 60% in cells subjected to

7 to EGF stimulation, compared to a more transient activation in control cells expressing wild-type KSR1.

8 nd gemfibrozil, previously reported to induce TPP1 activity in control cells, failed to increase TPP1 activity in patient

9 bitor, lactacystin, resulted in a 3-fold increase in alpha4 in control cells and a similar level in mutant cells.

10 ized intracellularly, rather than at the plasma membrane as in control cells, along with proteins typically restricted to

11 n the cell and failed to respond to TGFbeta1 stimulation as in control cells.

12 targeted the cycling Golgi protein GPP130, which STx bound in control cells during sorting into Golgi-directed endosomal

13 causing mutant PS to the same level of activity as channels in control cells stimulated by significantly higher IP3 conce

14 Intracellular Cu in control cells was similar for all three species (2.5-3.2 x

15 esterol homeostasis cause mitochondrial DNA disorganization in control cells, while mitochondrial DNA aggregation in the

16 es actin dynamics), but the same general features are found in control cells.

17 ant virus with deletion of NS1 induced high levels of IFN-I in control cells, as expected; in contrast, shRNA-mediated kn

18 lls, whereas only the C(ko) mutant was an efficient inducer in control cells.

19 D motility and FN deposition defects were phenocopied by KD in control cells of the lysosomal fusion regulator synaptotag

20 gulated in cocultured HT-29 cells at 4 h compared to levels in control cells.

21 in CHI-D beta-cells compared with cytoplasmic localization in control cells.

22 ates in the cytosol only of TRPV1-expressing cells, and not in control cells.

23 of several cell cycle effectors in 231-GATA3 cells but not in control cells.

24 M1, was arranged in puncta in resting shTRPC2 cells but not in control cells.

25 curate genomic maps of nucleosome positions and occupancies in control cells and cells treated with 3-aminotriazole (3AT)

26 ulated barrier disruption, a response that rapidly occurred in control cells.

27 MMP13 promoter activity; conversely, Ankrd1 overexpression in control cells decreased PMA-induced MMP13 promoter activit

28 /AKT pathway manipulation recapitulated cellular phenotypes in control cells and attenuated them in CFC cells.

29 nt cells, whereas adding galectins impaired these processes in control cells.

30 uox2 suppression by siRNA led to an increase in ATP release in control cells and restoration of ATP release in cells trea

31 inase or Akt affected both k(ex) and release from retention in control cells but only k(ex) in AS160 knockdown cells.

32 tion of primary cells from patients with XLA with that seen in control cells.

33 and secreted cytokine levels were compared with those seen in control cells.

34 melanocytes subjected to TPC2 knockdown is less acidic than in control cells.

35 expression was significantly higher in knockdown cells than in control cells and Gata2 knockdown rescued some of the matu

36 HT(R) cells and miR-221/222-overexpressing MCF-7 cells than in control cells, which suggests modulation of mitogenic sign

37 lated to higher levels in TTP gene knockout (KO) cells than in control cells.

38 rbachol activated ERK1/2 better in T1R3-depleted cells than in control cells.

39 Intracellular Ca(2+) was higher in PC1-knock-out cells than in control cells.

40 tion in cells lacking IQGAP1 was significantly greater than in control cells.

41 nucleosome still slides and remains downstream longer than in control cells, suggesting that the product of the gene may

42 FE3(-/-) peritoneal mast cells was significantly lower than in control cells.

43 ent cells are approximately 2 x larger and more stable than in control cells, and vinculin displays an increased time for

44 f IFT injection in dynein mutant cells was higher than that in control cells.

45 ATP content in the mitochondrial matrix was lower than that in control cells.

46 ignificantly altered in tumour-induced DCs compared to that in control cells.

47 affected individuals were decreased in comparison to those in control cells.

48 actin microfilaments, which rendered them similar to those in control cells.

49 (CAG)(n) TNRs in control cells and in DM1 cells.

50 However, a synaptic priming protocol, which in control cells has no effect on synaptic plasticity, leads