ライフサイエンスコーパス: growth suppressor

1 inson's disease, and was first reported as a growth suppressor.

2 ocation in acute promyelocytic leukemia is a growth suppressor.

3 thereby keeping pRb in its active form as a growth suppressor.

4 9, as an IFN/all-trans retinoic acid-induced growth suppressor.

5 GRIM-19 is an IFN/retinoic acid-regulated growth suppressor.

6 istent with a role for endogenous Grb10 as a growth suppressor.

7 of Protein 4.1B to function as a meningioma growth suppressor.

8 uces the expression of GADD45A, a known cell growth suppressor.

9 suggesting that it also has properties of a growth suppressor.

10 to oppose inflammatory pathways and act as a growth suppressor.

11 hat is dominant over its potential role as a growth suppressor.

12 in-oral-cancer-1 (DOC-1), a highly conserved growth suppressor.

13 d is a strong candidate, since it is a known growth suppressor.

14 onal regulation of the RPP5 gene, encoding a growth suppressor.

15 onsive genes, induce apoptosis, and act as a growth suppressor.

16 p16beta can act as a functional glioma cell growth suppressor.

17 s that limit Wnt signals and may function as growth suppressors.

18 ferons (IFNs) and retinoids are potent tumor growth suppressors.

19 from the maternally derived genome should be growth suppressors.

20 nd the RECQ4 helicases--the Arabidopsis slow growth suppressor 1 (Sgs1)/Bloom syndrome protein (BLM)

21 the chick homologue of mammalian leprecan or growth suppressor 1.

22 ith antibody to DLC-1 and the possible tumor growth suppressor activity of DLC-1 was investigated by

23 Thus, the growth suppressor activity of E-cadherin is adhesion ind

24 The loss of growth suppressor activity when the Cdk2-repressor domai

25 general repressor activity, and most of the growth suppressor activity.

26 1 alpha binds necdin, a nuclear protein with growth suppressor activity.

27 ding to HRS does not negatively regulate HRS growth suppressor activity.

28 -cycle regulator, originally identified as a growth suppressor and a prognostic marker for human oral

29 elocytic leukemia protein PML is a tumor and growth suppressor and plays an important role in a multi

30 Together, the results suggest that the growth suppressor and transcriptional activator function

31 observations suggest that LATS1 is a potent growth suppressor and, like other tumor suppressors, it

32 PML-homo and hetero interactions conferring growth suppressor, apoptotic and anti-viral activities.

33 sting that GAP43 functions as a novel glioma growth suppressor by modulating mitogenic signaling path

34 a transcription factor, functions as a cell growth suppressor by negatively regulating the expressio

35 hematopoietic progenitors and functions as a growth suppressor by repressing cyclin A2 and other targ

36 tent with the hypothesis that GPC3 acts as a growth suppressor by sequestering or downregulating an I

37 Growth suppressor c-Abl interacts with p53 in response t

38 ugh different mechanisms, and a constitutive growth suppressor can be generated through the combined

39 These data have demonstrated the growth-suppressor characteristics of PTPRO that are uniq

40 for deletion or substitution mutation in the growth suppressor domains of MDM2 in several breast canc

41 In addition, RGS2 functioned as a growth suppressor for androgen-independent LNCaP cells w

42 ecific missense mutations within the minimal growth suppressor fragment of Protein 4.1B (DAL-1, diffe

43 onstrate a new approach for the isolation of growth suppressors from cDNA libraries, and identify a p

44 lin A/E-CDK2 sites, negatively regulates the growth suppressor function associated with the N-termina

45 s a new target of miR-335 that regulates its growth suppressor function by complex crosstalk with oth

46 Our data suggest that the growth suppressor function of BRCA1 depends, at least in

47 ent kinase inhibitors, and activation of the growth suppressor function of pocket proteins.

48 main activates, rather than inactivates, the growth suppressor function of pRb.

49 t binding to 14-3-3 is not essential for the growth suppressor function of Protein 4.1B in meningioma

50 of the full-length DAL-1 molecule eliminated growth suppressor function, as measured by thymidine inc

51 tional activity, which may contribute to its growth suppressor function.

52 lity to form colonies in vitro, suggesting a growth suppressor function.

53 sed a similar functional assay to localize a growth suppressor gene for the RD cell line centromeric

54 a prove that wild-type IGFIIR functions as a growth suppressor gene in colorectal cancer cells and pr

55 hese data suggest that SLC5A8 functions as a growth suppressor gene in vitro and that it is silenced

56 These data therefore implicate a new growth suppressor gene involved in breast cancer that is

57 H19, an untranslated RNA that is a putative growth suppressor gene regulating IGF-II; (c) p57KIP2, a

58 We have further localized this growth suppressor gene to 17q24-q25 by transfer of chrom

59 Though BRCA1 is thought to be a growth suppressor gene, no change in BRCA1 protein level

60 rt for the hypothesis that IGFIIR is a human growth suppressor gene.

61 ossible mechanisms including reexpression of growth suppressor genes and formation of covalent adduct

62 modify the expression of proto-oncogenes and growth suppressor genes during embryogenesis.

63 ones selected for by loss of dominant-acting growth suppressor genes.

64 p12(DOC-1) is a growth suppressor identified and isolated from normal ke

65 d Mortality-19) was originally isolated as a growth suppressor in a genome-wide knockdown screen with

66 t in vivo evidence that LRIG1 functions as a growth suppressor in breast cancer.

67 vide functional validation for its role as a growth suppressor in EGFR-mutant lung adenocarcinoma.

68 vations suggest that C-CAM1 may be a general growth suppressor in epithelial cells.

69 vide a functional test of its candidacy as a growth suppressor in glioma cells.

70 activation of this gene and that it can be a growth suppressor in human gliomas.

71 r the first time that nSMase2 functions as a growth suppressor in MCF7 cells, linking confluence to t

72 mation, suggesting that it may function as a growth suppressor in normal brain cells.

73 her, these data indicate that PML is a tumor growth suppressor in prostate cancer and that Ad-PML may

74 he first time that N-cadherin functions as a growth suppressor in the context of oncogenic K-ras.

75 ngs demonstrate that Mzf1 can act as a tumor/growth suppressor in the hemopoietic compartment.

76 t these miRs function as metastasis (but not growth) suppressors in prostate cancer.

77 p12(CDK2-AP1) (p12) is a growth suppressor isolated from normal keratinocytes.

78 p12(DOC-1) is a growth suppressor isolated from normal keratinocytes.

79 eveal the post-translational regulation of a growth suppressor like CHK2 within the microenvironment

80 The growth suppressor MST1 kinase modulates androgen-depende

81 and were severely impaired for growth; recB growth suppressor mutants arose at high frequencies.

82 Here we characterize a growth suppressor mutation in eIF2beta that prevents eIF

83 All-trans retinoic acid (RA) is an effective growth suppressor of CA-OV3 cells but not SK-OV3 cells.

84 inoic acid (RA) combination is a more potent growth suppressor of human tumor xenografts in vivo than

85 RCA1a and BRCA1b splice variants function as growth suppressors of human breast cancer cells.

86 within 8 weeks, suggesting the presence of a growth suppressor on chromosome 17.

87 ation might be specifically repressed by the growth suppressor p107 through direct interaction with B

88 ogenes and indirectly by down-regulating the growth suppressor p21(WAF1/CIP1).

89 We have investigated the role of the growth suppressor p27(Kip1) (p27) on endothelial cell fu

90 restoring normal activation of the Hippo-YAP growth-suppressor pathway.

91 Although deregulation of the putative growth suppressor PML and delocalization of other nuclea

92 The growth suppressor promyelocytic leukemia protein (PML) i

93 onsistent with a role for the retinoblastoma growth suppressor protein in protein kinase C-induced ap

94 ent kinase inhibitors and the retinoblastoma growth suppressor protein.

95 phosphorylation status of the pRB family of growth suppressor proteins is regulated in a cell cycle

96 med acquisition of the endogenously produced growth suppressor PTEN.

97 We show that both PML and Tif1alpha are growth suppressors required for the growth-inhibitory ac

98 s sustained proliferation, refractoriness to growth suppressors, resistance to cell death or aberrant

99 afficking events; and (f) down-regulation of growth suppressors, such as the Prader-Willi gene NECDIN

100 ation of PRDX2 as an epigenetically silenced growth suppressor, suggesting a possible role of ROS in

101 protein (RB110), is a more potent tumor and growth suppressor than RB110.

102 e, we found that knock-down of KLF9, an axon growth suppressor that is normally upregulated 250-fold

103 but frequently gave rise to spontaneous slow growth suppressors that segregated as single-gene mutati

104 entified, including inactivation of cellular growth suppressors through direct interaction with SV40

105 To conclude, JunD changed from growth suppressor to growth promoter when its binding to

106 er we reported the isolation of GRIM-19 as a growth suppressor using a genome-wide expression knockdo

107 We have previously isolated GRIM-19, a novel growth suppressor, using a genetic method.

108 te the basis for these defects, a screen for growth suppressors was performed.

109 on as a potent transcriptional repressor and growth suppressor, while the Mxi1-WR protein lacks these