ライフサイエンスコーパス: cell growth arrest

1 factor alpha (TNF-alpha) that induced tumor cell growth arrest.

2 p21 and p27, the tumor suppressor, p53, and cell growth arrest.

3 ppression of cyclin D1 promoter activity and cell growth arrest.

4 to isolate minigenes whose expression causes cell growth arrest.

5 gized with IFN-gamma in the promotion of NB4 cell growth arrest.

6 ins is necessary to induce apoptosis but not cell growth arrest.

7 /Cdk4 protein complexes were associated with cell growth arrest.

8 a Schwann cell-specific protein that induces cell growth arrest.

9 d MCM7 DNA replication licensing and induced cell growth arrest.

10 hed 5 S and 45 S ribosomal RNA synthesis and cell growth arrest.

11 cyclin-dependent kinase inhibitor 1A-induced cell growth arrest.

12 to be necessary and sufficient for normal T-cell growth arrest.

13 that significantly exceed those required for cell growth arrest.

14 A sensitizes LNCaP-RF cells to apoptosis and cell growth arrest.

15 her binding to tubulin by ITCs could lead to cell growth arrest.

16 nces to inhibit protein synthesis leading to cell growth arrest.

17 results in p53- and p21-dependent mesodermal cell growth arrest.

18 activity, leading to vascular smooth muscle cell growth arrest.

19 CA nucleotide sequences, results in complete cell growth arrest.

20 for ceramide-induced vascular smooth muscle cell growth arrest.

21 sm of UV-dependent checkpoint activation and cell growth arrest.

22 ort interference RNA treatment results in MM cell growth arrest.

23 gnified in a manner consistent with enhanced cell growth arrest.

24 an important role in lytic cycle-associated cell growth arrest.

25 ssociated with decreased viability and tumor cell growth arrest.

26 ow levels of p202 are upregulated during the cell growth arrest.

27 ribute to senescence-associated irreversible cell growth arrest.

28 Irreversible cell growth arrest, a process termed cellular senescence

29 esveratrol (10 microM, 48 hr) induces both a cell growth arrest and a metabolic reprogramming in colo

30 ive oxygen species (ROS) are able to mediate cell growth arrest and activate proteins that inhibit th

31 Furthermore, immune dormancy promotes cancer cell growth arrest and angiogenic control.

32 Cell growth arrest and apoptosis are two best-known biol

33 The p53 tumor suppressor induces cell growth arrest and apoptosis in response to DNA dama

34 Curcumin induces cancer cell growth arrest and apoptosis in vitro, but its poor

35 ere, we show that Tip60 is required for both cell growth arrest and apoptosis mediated by p53 and als

36 n, and functions by inducing a p53-dependent cell growth arrest and apoptosis program.

37 ion of Akt by API-1 resulted in induction of cell growth arrest and apoptosis selectively in human ca

38 However, besides inducing cell growth arrest and apoptosis, p53 activation also mo

39 ion, and, notably, it modulates p53-mediated cell growth arrest and apoptosis.

40 econd messenger that has been shown to cause cell growth arrest and apoptosis.

41 icipants in orchestration of the cell cycle, cell growth arrest and apoptosis.

42 are more resistant to BET-inhibitor-induced cell growth arrest and apoptosis.

43 itized MDA-MB-468 cells to tamoxifen-induced cell growth arrest and apoptosis.

44 part to its ability to induce p53-dependent cell growth arrest and apoptosis.

45 tylation of nucleosomal histones and promote cell growth arrest and apoptosis.

46 Cell growth arrest and autophagy are required for autoph

47 them at specific sequences leading to rapid cell growth arrest and cell death.

48 and trigger signaling pathways essential to cell growth arrest and death by inducing an HSP90-active

49 n reduced susceptibility of TGF-beta-induced cell growth arrest and decreased phosphorylation of Smad

50 Loss of p44/wdr77 gene expression led to cell growth arrest and differentiation.

51 toxin module wherein MazF(Sa) leads to rapid cell growth arrest and loss in viable CFU upon overexpre

52 Doc expression resulted in rapid cell growth arrest and marked inhibition of translation

53 on its chromosome, which are responsible for cell growth arrest and possible cell death.

54 messengers with opposing roles in mammalian cell growth arrest and survival; their relative cellular

55 tant component of p53-mediated apoptosis and cell growth arrest and that inactivation of the apoptoti

56 r methylated leukemic cell lines resulted in cell growth arrest and the induction of apoptosis.

57 RG1 and pRB is not required for induction of cell growth arrest and transcriptional repression of E2F

58 ylase (HDAC) inhibitors (HDACi) cause cancer cell growth arrest and/or apoptosis in vivo and in vitro

59 on of this protein, which is associated with cell growth arrest and/or apoptosis under various stress

60 down-regulating survivin expression induced cell-growth arrest and subsequent cell death regardless

61 ne M1 myeloblastic leukemia cells, where the cells growth arrest and ultimately undergo programmed ce

62 y peptidic inhibitors, GrB induced in Jurkat cells growth arrest and, over a delayed time period, cel

63 mRNA-specific endoribonuclease causing host cell growth arrest, and culture condensation) to facilit

64 f MCM8 in PC3, DU145 and LNCaP cells induced cell growth arrest, and decreased tumour volumes and mor

65 d by extension, CTLA-4 surface expression, T cell growth arrest, and self-tolerance.

66 nses including induction of target genes and cell growth arrest, and this inhibition is dependent on

67 RG1 is necessary to induce formation of flat cells, growth arrest, and finally, cell senescence.

68 inase inhibitor p21(Waf1/Cip1/Sdi1) triggers cell growth arrest associated with senescence and damage

69 or p21Waf1/ Cip1/Sdi1 is an integral part of cell growth arrest associated with senescence and damage

70 attenuated Stat3 signaling, thereby inducing cell growth arrest at G0/G1 phase and apoptosis.

71 and CWR22rv1 cells causes cell apoptosis and cell growth arrest at the G(1) phase.

72 le progression, as evidenced by induction of cell growth arrest at the G0/G1 phase, inhibition of DNA

73 ed activation of CCN5 in TNBC cells promotes cell growth arrest at the G0/G1 phase, reduces cell prol

74 In each case cell growth arrested at 24-h post-induction and at all s

75 nhibited VEGF-induced EC proliferation, with cell growth arrested at the G(0)/G(1) phase and a concom

76 Normal BJ cells growth arrest at senescence before developing sign

77 n of supplementation) are maintained through cell growth arrest by serum depletion and when prolifera

78 promoter and induces proliferation of SAOS2 cells growth arrested by p53.

79 4 complexes were found to increase in CA-OV3 cells growth arrested by RA.

80 adation and that wts mutants have defects in cell growth arrest, caspase activity, and autophagy.

81 The PTEN-induced localization defect and the cell growth arrest could be rescued by the expression of

82 -UCA and SSR were associated with apoptosis, cell growth arrest, cytokines, and oxidative stress.

83 ts play in histone deacetylase inducement of cell growth arrest, differentiation, or apoptotic cell d

84 vival, but that its overexpression may cause cell growth arrest due to an accumulation of sphingosine

85 B or NIR causes p53-dependent apoptosis and cell growth arrest, due to the up-regulation of p21 and

86 The mechanism of hyperoxia-induced cell growth arrest has not been well elucidated, especia

87 rotestosterone (DHT) treatment by undergoing cell growth arrest in association with cytoskeletal reor

88 de that telomerase inhibition by PPA induces cell growth arrest in BEAC cells and demonstrate the pot

89 n of telomerase activity was paralleled by a cell growth arrest in G2-M.

90 caused increased apoptosis, cell cycle, and cell growth arrest in HCT-116 cells.

91 to overcome completely the beta1D-triggered cell growth arrest in NIH 3T3 fibroblasts.

92 es p53 response genes and affects UV-induced cell growth arrest in normal cells.

93 These studies show that LY290181 induces cell growth arrest in prometaphase/metaphase, and tubuli

94 tumors may be crucial to induce p21-mediated cell growth arrest in RXR ligand therapy.

95 Expression of Bop1Delta leads to cell growth arrest in the G(1) phase and results in a sp

96 tively inhibits protein synthesis leading to cell growth arrest in the quasidormant state.

97 tion of p33(QIK)-specific kinase activity of cells growth-arrested in the quiescent phase and deactiv

98 ation of the gene, A20 induced apoptosis and cell growth arrest, indicating a tumour suppressor role.

99 t MetAP-2 is responsible for the endothelial cell growth arrest induced by Fg and its derivatives.

100 Stra13 expression is closely associated with cell growth arrest induced by several triggers such as r

101 This led to liver cell growth arrest involving cyclin-dependent kinase inh

102 Human melanoma cells growth arrest irreversibly, lose tumorigenic poten

103 Human melanoma cells growth-arrest irreversibly and terminally differen

104 These results suggest that cell growth arrest is not sufficient for HCV replicon in

105 Thus, hypoxia-induced cell growth arrest is tightly linked to an ATR-signaling

106 ial role for Zta's basic domain in eliciting cell growth arrest, its amino terminus is required for e

107 s associated with a dose- and time-dependent cell growth arrest, mitochondrial damage, and apoptosis

108 DNA nanoparticles can transfect nondividing cells, growth-arrested neuroblastoma and hepatoma cells

109 uently, MDM2 suppressed p21waf1/cip1-induced cell growth arrest of human p53(-/-) and p53(-/-)/Rb(-/-

110 Hyposmosis caused reversible cell growth arrest of the five cell lines in a cell cycl

111 een MDM2 and p53, activates p53 resulting in cell growth arrest or apoptosis in various cancer cells.

112 Ro5-4864 and PK11195, failed to induce tumor cell growth arrest or apoptosis.

113 enotoxic stress and, once activated, induces cell growth arrest or apoptosis.

114 inhibit tumorigenesis by promoting permanent cell growth arrest or death.

115 kinase inhibitor p21WAF1/CIP1 and subsequent cell growth arrest or senescence is one mechanism by whi

116 However, a role for p202 in cell growth arrest remains to be defined.

117 In all GIST lines, cell growth arrest resulted from PI3-K inhibition, and -

118 tion of YjhX (85 amino acid residues) causes cell-growth arrest resulting in cell death, while YjhQ (

119 are often induced into pathways that lead to cell growth arrest, senescence, and/or apoptosis in resp

120 In three of these systems, G0 or G1 cell growth arrest signaling is observed prior to detect

121 Cellular senescence is a stable cell growth arrest that is characterized by the silencin

122 duced M-MITF expression, leading to melanoma cell growth arrest that was rescued by ectopic expressio

123 mote osteoblastic differentiation and induce cell growth arrest, the highly related ZEB-2/SIP1 protei

124 ghtforward mechanism for C/EBPalpha-mediated cell growth arrest through repression of E2F-DP-mediated

125 This constitutes the first demonstration of cell growth arrest through telomerase inhibition, upon t

126 r rescue because native hepatocytes overcame cell growth-arrest to regenerate the liver.

127 These D1/CDK4 inhibitors inhibited tumor cell growth, arrested tumor cells at the G1 phase, and i

128 stress response characterized by persistent cell growth arrest under various stress conditions, incl

129 K-mediated Bax activation and that increased cell growth arrest was associated with elevated expressi

130 ha down-regulation using shRNA, which caused cell growth arrest, was accompanied by increased H3K27me

131 elevant aspects of HIF-1 function in primary cell growth arrest, we examined two different primary di

132 hich (MazF-mt1, -mt3, -mt4, and -mt6) caused cell growth arrest when induced in E. coli.

133 Cell growth arrests when the concentrations of anionic p

134 Induction of mqsR caused cell growth arrest, whereas ygiT co-induction recovered

135 ggest that overexpression of HO-1 results in cell growth arrest, which may facilitate cellular protec

136 atment of cultured human PA-SMCs resulted in cell growth arrest with the induction of senescence but