ライフサイエンスコーパス: oncogenicity

1 with the requirement of dcSAM production for oncogenicity.

2 hat inactivate lipid kinase activity abolish oncogenicity.

3 t of MEK did not significantly perturb R-Ras oncogenicity.

4 AKT modulates HH/GLI signal strength and its oncogenicity.

5 erefore an essential mediator of p3k-induced oncogenicity.

6 ic activities, but have dramatically reduced oncogenicity.

7 stoma pathogenicity that contributes to MYCN oncogenicity.

8 ics, a metabolic route that is essential for oncogenicity.

9 d E2288K) domains of mTOR, and studied their oncogenicity.

10 ytes, which was necessary for ETV1-dependent oncogenicity.

11 rongly than c-Rel contributes to its greater oncogenicity.

12 ively activate kinase activity and increased oncogenicity.

13 2 months to identify genetic determinants of oncogenicity.

14 ts expression correlates with papillomavirus oncogenicity.

15 reveals surprising diversity in Kras variant oncogenicity.

16 rexpression of p110alpha are correlated with oncogenicity.

17 , a mouse pathogen that is capable of potent oncogenicity.

18 ) that is thought to contribute to the viral oncogenicity.

19 (BCR-ABL) mutants in regulating adhesion and oncogenicity.

20 gulation of the ErbB2-mediated signaling and oncogenicity.

21 figure out their mechanisms and differential oncogenicity.

22 itro; its cellular counterpart, c-P3k, lacks oncogenicity.

23 t palmitates make important contributions to oncogenicity.

24 ssociated with viral attenuation and loss of oncogenicity.

25 -terminus of v-Rel are required for its full oncogenicity.

26 EF) revealed the following prerequisites for oncogenicity: (1) removal of the N terminal phosphorylat

27 This mutation markedly enhances v-Jun oncogenicity [4] [5]; however, its transcriptional conse

28 RB1BvIL-8DeltasmGFP retained oncogenicity, albeit at a greatly reduced level.

29 en synthase kinase 3 activity for MLL fusion oncogenicity and identifies novel therapeutic targets fo

30 These effects may explain the oncogenicity and immunological perturbation of HCV infec

31 However, the molecular mechanism of ACTR oncogenicity and its function independent of nuclear rec

32 Our results suggest the oncogenicity and potential targeting of HER2 missense mu

33 ng a role for Bin1 as a negative modifier of oncogenicity and progression in breast cancer.

34 DeltaEGFR makes a unique contribution to its oncogenicity and propose that this venue provides new ta

35 et, and Met contributes to EGFRvIII-mediated oncogenicity and resistance to treatment.

36 in c-Rel's cTAD1 and cTAD2 contribute to its oncogenicity and that of v-Rel.

37 On the basis of this model, both oncogenicity and tissue tropism appear to have evolved o

38 lly active mutants, to further examine their oncogenicity and tumorigenicity.

39 ide a biochemical explanation for vav family oncogenicity, and establish a new signaling model in whi

40 V1 genes with functions involving virulence, oncogenicity, and immune evasion.

41 These mutant MDVs retained oncogenicity, and LBCLs have been established from the m

42 oreover, the immortalized cells exhibited no oncogenicity, and no up-regulation of c-Myc was detected

43 ferative capacity, hepatocellular functions, oncogenicity, and their in vivo maturation potential.

44 istinct mechanisms by which pluripotency and oncogenicity are established and regulated.

45 B-231 breast cancer cell line suppressed the oncogenicity as revealed by inhibition of the anchorage-

46 for normal regulation of kinase activity and oncogenicity as well as substrate selection.

47 Most importantly, chick oncogenicity assays demonstrated that bic can cooperate

48 espite concerns for fetal teratogenicity and oncogenicity associated with diagnostic testing, and pot

49 gues of MDV1 oncoprotein MEQ, CxC chemokine, oncogenicity-associated phosphoprotein pp24, and conserv

50 e gene products include the oncoprotein MEQ, oncogenicity-associated phosphoproteins pp38 and pp24, a

51 he differences in host range, virulence, and oncogenicity between nonpathogenic HVT and highly pathog

52 n the 1990s, is critically involved in viral oncogenicity, but only a few of its host target genes ha

53 e identity of the gatekeeper residue impacts oncogenicity by altered P-loop phosphorylation.

54 bitor, LY3009120, could suppress CRAF-fusion oncogenicity by inhibiting dimer-mediated signaling.

55 e further dissection of the requirements for oncogenicity by the E4orf6 protein.

56 localization signal in v-Rel did not affect oncogenicity by v-Rel.

57 essing pool cells exhibited greatly enhanced oncogenicity compared with control pool cells.

58 cated or mutant isoforms that show increased oncogenicity compared with the wild-type receptor are fo

59 those showing minimal DNA binding, retained oncogenicity for CEF.

60 rminal repeat, which may explain the loss of oncogenicity for this strain.

61 gical controls were comparable, the measured oncogenicity from exactly one alpha particle was signifi

62 ls resulted in accelerated EGFRvIII-mediated oncogenicity in an orthotopic mouse model.

63 tively blocked ErbB signaling and attenuated oncogenicity in breast cancer cells, yet had little effe

64 to the mechanisms that may contribute to 2HG oncogenicity in glioma and acute myeloid leukaemia progr

65 ate the cell cycle through E2F underlies its oncogenicity in human cancers.

66 dition to amplifications, could activate its oncogenicity in human lymphomas.

67 s that cofactors could be required for viral oncogenicity in some cases.

68 To determine whether the AIB1 oncogenicity in this model depended on its function as a

69 usion proteins and tested their activity and oncogenicity in vitro and in vivo in transgenic mice (TM

70 efractory to nuclear export display heighten oncogenicity in vitro compared with WT D1, we generated

71 et no experimental model demonstrating their oncogenicity in vivo.

72 alized rodent fibroblasts in vitro and their oncogenicity in vivo.

73 factor that may contribute to the dissimilar oncogenicities of Ad and HPV.

74 blasts, suggesting a correlation between the oncogenicity of Akt and phosphorylation of S6K and 4E-BP

75 ults in suppression of kinase activation and oncogenicity of associated p185neu-activated receptors.

76 l protein with p40 did not increase the weak oncogenicity of c-Rel.

77 ession of Atoh1 in primary GNPs enhances the oncogenicity of cells overexpressing Gli1 by almost thre

78 We evaluated the oncogenicity of eight kinase inhibitor-resistant BCR-ABL

79 tively, these data provide evidence that the oncogenicity of ERG is mediated, in part, by competition

80 lts underscore the qualitative difference in oncogenicity of GLI1 and Gli2 when overexpressed in skin

81 on of this domain substantially enhanced the oncogenicity of HOXB4, inducing acute leukemia in mice.

82 In light of recent studies on the oncogenicity of JCV and the transforming ability of the

83 The oncogenicity of Jun probably results from transcriptiona

84 relevance of noncanonical functions for the oncogenicity of KV10.1, which need to be considered when

85 ting that this pathway may contribute to the oncogenicity of LMP1 through its ability to promote cell

86 tem cell biology and for the analysis of the oncogenicity of LRP receptors that are often overexpress

87 -encoded protein (Meq), is essential for the oncogenicity of MDV.

88 that this signaling connection sustains the oncogenicity of Merlin-deficient tumor cells.

89 s (CR2 and CR3) of AFX are required for full oncogenicity of MLL-AFX and also endow it with the poten

90 missive cellular environment is required for oncogenicity of Mll-associated translocations and Mll fu

91 llular environment is therefore required for oncogenicity of Mll-associated translocations since the

92 as protein and PI 3-kinase are causal in the oncogenicity of mutant Ras proteins.

93 nd functional analysis provides insight into oncogenicity of mutations in RbN and identifies a unique

94 The oncogenicity of Myc stems from its ability to regulate e

95 hese results support the conclusion that the oncogenicity of P3k depends on constitutive lipid kinase

96 The in vivo oncogenicity of PIK3CA mutants in an avian species stron

97 Our results demonstrate the direct oncogenicity of Rac1 and ROS and their contribution to a

98 Our findings suggest that the oncogenicity of RARalpha-fusion proteins results from th

99 educed level of transactivation enhances the oncogenicity of REL; (3) that REL shuttles from the cyto

100 The oncogenicity of Sox3 is correlated with nuclear localiza

101 ptibility to AAP1 regulation correlates with oncogenicity of the activated forms of c-ABL.

102 Finally, our simulations suggest that the oncogenicity of the R335L mutation may be due to a reduc

103 d in recent years, consistent with the acute oncogenicity of the viral oncoprotein v-Rel in animal mo

104 Therefore, the oncogenicity of therapeutically valuable patient-specifi

105 1 into exosomes is associated with increased oncogenicity of these secreted vesicles.

106 ts that this pathway contributes both to the oncogenicity of this molecule and its role in the establ

107 The oncogenicity of this virus is reflected in vitro by its

108 These experiments document the oncogenicity of transactivating LEF-1 and show that the

109 en selected for their ability to enhance the oncogenicity of v-Rel by increasing its ability to activ

110 The potent oncogenicity of v-Rel is the consequence of a number of

111 amino acids into v-Rel markedly reduced the oncogenicity of v-Rel.

112 Brk also conferred in vivo oncogenicity on the BaF3 cells.

113 intact gD homolog gene is not essential for oncogenicity or horizontal transmission of MDV.

114 RBP2 oncogenicity relied on its demethylase and DNA-binding a

115 However, mechanisms underlying HBx-mediated oncogenicity remain unclear.

116 critical determinants of their differential oncogenicity reside in their divergent transactivation d

117 active PTEN mutant (G129R) to suppress MSP58 oncogenicity, support the view that the C-terminal regio

118 udy provides some insight into the potential oncogenicity that may arise via cellular reprogramming,

119 mmunogenicity of mesenchymal stem cells, and oncogenicity) that have been addressed and will be follo

120 e therefore conclude that AIB1 can exert its oncogenicity through tissue-specific estrogen-dependent

121 specifically at three positions that confer oncogenicity to Ras (12, 59, and 61).

122 ly, autophosphorylation at this site confers oncogenicity to this receptor.

123 s regulatory connection contributes to Myb's oncogenicity, we expressed a dominant negative Myb in th

124 Similar to CtBP's role in attenuating E1A's oncogenicity, we propose that dCtBP can interfere with c

125 l-xL and Bcl-2 significantly increased their oncogenicity, whereas other NF-kappaB-regulated death in