ライフサイエンスコーパス: c-Myc protein

1 res with proteasome-dependent degradation of c-Myc protein.

2 n tumor cells overexpressing either N-MYC or c-MYC protein.

3 ocalized to amino acids 48 to 135 within the c-Myc protein.

4 ell lines, which are known to have increased c-Myc protein.

5 ll cycle progression by interacting with the C-MYC protein.

6 dependent decrease in steady-state levels of c-MYC protein.

7 of HIV-1 DNA but also inhibits expression of c-Myc protein.

8 translational upregulation in the levels of c-myc protein.

9 boxy terminus with an epitope from the human c-myc protein.

10 d Blimp-1 and caused a subsequent decline in c-Myc protein.

11 nduced no consistent change in expression of c-Myc protein.

12 eads to post-transcriptional deregulation of c-Myc protein.

13 ing c-Myc mRNA, leading to downregulation of c-Myc protein.

14 ed to be related to the stabilization of the c-Myc protein.

15 report that PEL cells have abnormally stable c-Myc protein.

16 e importance of maintaining normal levels of c-Myc protein.

17 ckground levels of endogenous c-myc mRNA and c-Myc protein.

18 significantly enhances the half-life of the c-Myc protein.

19 ponsible for stress-induced stability of the c-Myc protein.

20 cell extracts, that MLH1 interacts with the c-MYC protein.

21 in an efficient increase in the half-life of c-myc protein.

22 nin/Tcf-Lef complex, and decreased levels of c-Myc protein.

23 dependent protein synthesis of cyclin D1 and c-Myc proteins.

24 y affect the ubiquitylation and half-life of c-Myc protein, a key T-ALL oncogene.

25 ma is stabilized by overexpression of SLP-1, c-Myc protein abundance decreases, suggesting that the S

26 rotein was indicative of HSC quiescence, and c-Myc protein abundance was controlled by the ubiquitin

27 s thought to stabilize the mRNA and increase c-Myc protein abundance.

28 d with increased phosphorylation of Akt1 and c-Myc protein accumulation during EMT.

29 Dominant negative c-Myc protein also effectively suppressed induction of t

30 activity and the corresponding synthesis of c-myc protein although it is not fully understood how th

31 l reporter activity, as well as reduced both c-myc protein and basal cell proliferation.

32 In cells without p53, ARF directly binds to c-Myc protein and inhibits c-Myc-induced hyperproliferat

33 ctopic SALL4 overexpression causes increased c-Myc protein and mRNA expression, indicating that c-Myc

34 odomain inhibitor JQ1 affecting the level of c-Myc protein and protein kinase inhibitors targeting th

35 y dephosphorylated c-Myc Ser62, destabilized c-Myc protein and suppressed c-Myc transcriptional activ

36 OCK is necessary for both down-regulation of c-Myc protein and up-regulation of p21waf1 protein, dire

37 d that SPOP(WT) can physically interact with c-MYC protein and, upon exogenous expression in vitro, c

38 accumulation of two NH2-terminally truncated c-Myc proteins and abolished HIV-1 genome entry into hos

39 -myc gene activation and the function of the c-Myc protein are reviewed.

40 man, murine, and avian cells express smaller c-Myc proteins arising from translational initiation at

41 We propose SPOP(MT)-induced stabilization of c-MYC protein as a novel mechanism that can increase tot

42 that was shown to regulate the stability of c-Myc protein as well as c-Myc-dependent transcription.

43 tes the ubiquitin-proteasomal degradation of c-Myc protein, as knockdown of eEF-2K expression led to

44 d a dose-dependent decrease in the levels of c-MYC protein but not c-MYC mRNA in cell lines.

45 sing RT-PCR and Western blotting showed that c-Myc protein but not its mRNA levels were decreased in

46 hat they continued to express high levels of c-Myc protein, but did not maintain high levels of expre

47 a (MM) which exhibit increased expression of c- myc protein by an aberrant translational mechanism.

48 uce gene expression and the stabilization of c-MYC protein by decreased phosphorylation of Thr58 were

49 mma (CAMKIIgamma) was shown to stabilize the c-Myc protein by directly phosphorylating it at serine 6

50 Moreover, vIRF-3 can stabilize the c-Myc protein by increasing its half-life.

51 Anti-mu and anti-delta driven c-Myc protein changes precisely follow their effects on

52 ostaining of human placenta showed PEG10 and c-MYC proteins coexpressed in proliferating cytotrophobl

53 helial cell proliferation, and expression of c-MYC protein compared to littermate controls, and event

54 r of DNA binding/differentiation-2 (Id2) and c-Myc protein contents between the denervated and contro

55 tantly with this, the steady state levels of c-myc protein decline.

56 The c-Myc protein exhibits sequence-specific DNA binding whe

57 Here, we report inverse patterns of p27 and c-Myc protein expression follow BCR engagement.

58 sion and subsequent failure to down-regulate c-myc protein expression in SKBr3 and LNCaP cells was co

59 The c-myc protein expression in these lesions was evaluated

60 In contrast to Nur77-eGFP, c-Myc protein expression integrates mitogenic signals do

61 Although high c-Myc protein expression is observed alongside MYC ampli

62 ncy and magnitude of c-MYC amplification and c-MYC protein expression is significantly higher in brea

63 viously, in 32D-123 TGF-beta1 treated cells, c-Myc protein expression was decreased.

64 d mechanisms, both Igs transiently stimulate c-Myc protein expression.

65 ntracellular calcium or alteration in p53 or c-myc protein expression.

66 der hypoxia, siRNA knockdown of HuR elevated c-Myc protein expression.

67 pression via small interfering RNA increased c-Myc protein expression.

68 tein, suggesting p107 negative regulation of c-Myc protein function.

69 The c-Myc protein functions as a transcription factor to fac

70 A conditionally active chimeric form of the c-Myc protein fused to the ligand-binding domain of the

71 e have stably expressed MycER(TM), the human c-Myc protein fused to the modified ligand-binding domai

72 We demonstrate that c-Myc proteins harboring a naturally occurring mutation

73 increased target c-myc promoter activity and c-Myc protein, hnRNP K protein levels, and enhanced brea

74 Here we report that expression of c-Myc protein in CD4+ T cells is induced only after such

75 p-regulated miR17-92 expression and elevated c-Myc protein in ischemic neural progenitor cells, where

76 hetic molecule, induces rapid degradation of c-Myc protein in MM-1 multiple myeloma and other tumor c

77 Exogenous p21 expression down-regulated c-myc protein in PMA-sensitive cancer cells.

78 Interestingly, we found the reduction of the c-Myc protein in several clones of dominant-negative (DN

79 e a 10- to 25-fold increase in the amount of c-myc protein in several independent cell lines derived

80 by v-Src, consistent with a requirement for c-Myc protein in v-Src transformation.

81 Here we report that p202a also bound the c-Myc protein in vitro and in vivo; the C-terminal p202a

82 rphology, as well as the increased levels of c-myc protein induced by K-Ras V12 and B-Raf V600E.

83 urthermore, adenoviral overexpression of the c-Myc protein induced glucose-6-phosphatase mRNA in the

84 main, we tested whether Jak2 was involved in c-Myc protein induction by Bcr-Abl.

85 tyrosine kinase inhibitor STI-571, inhibited c-Myc protein induction by Bcr-Abl.

86 The c-Myc protein is a helix-loop-helix leucine zipper oncog

87 It is also known that c-Myc protein is a labile protein that is increased in a

88 The c-Myc protein is a site-specific DNA-binding transcripti

89 The c-Myc protein is a transcription factor that is a centra

90 MYC genomic locus is structurally intact and c-Myc protein is deregulated at the post-translational l

91 The c-Myc protein is involved in cell proliferation, differe

92 The c-Myc protein is normally degraded very rapidly with a h

93 The turnover of c-Myc protein is stringently regulated by post-transcrip

94 that while the overexpression of the smaller c-Myc protein is sufficient to induce morphological tran

95 The c-Myc protein is up-regulated in many different types of

96 Although HSCs express low levels of c-Myc protein, its expression increases steadily during

97 alysis showed a significant 65% reduction of c-myc protein level in ODN-G-4 treated cells compared wi

98 levels in all of these lines, as well as in c-Myc protein level in the two lines investigated, Daudi

99 This was correlated with a 93% reduction in c-myc protein level.

100 However, c-myc protein levels and myc translation was maintained.

101 lpha in normal human melanocytes upregulated C-MYC protein levels and suppressed BRAF(V600E)- and, le

102 Similarly, c-myc protein levels are synergistically increased by ep

103 t adenoviral vectors that interfere with (i) c-Myc protein levels by antisense expression or (ii) c-M

104 sense or anti-sense CK2 constructs modulates c-myc protein levels in concert with the alteration in C

105 an up to tenfold serum-dependent increase of c-myc protein levels in Epstein-Barr virus immortalized

106 Knockdown of SCP1 increased the c-Myc protein levels in liver cancer cells.

107 compound ON 01910.Na decreased cyclin D1 and c-Myc protein levels in MCL cells, whereas mRNA levels o

108 Moreover, antisense down-regulation of the c-Myc protein levels in these growth-arrested cells reve

109 a positive feedback loop that maintains high c-MYC protein levels in tumors.

110 A decrease of either c-Myc protein levels or attenuation of the p53 response

111 under control of the endogenous c-myc locus, c-Myc protein levels were assessed.

112 c-Myc protein levels were positively correlated with tho

113 c-Myc protein levels were reduced in the presence of bot

114 lation at regulatory sites, sustained higher c-Myc protein levels, and maintained a balance of cyclin

115 d K-562 cells correlates with a reduction in c-Myc protein levels, suggesting that Bcr may in fact be

116 UV-irradiation elicited an increase in c-myc protein levels, which could be attenuated by inhib

117 agonists blocked the synergistic increase in c-Myc protein levels.

118 ctivity with concomitant decreased hTERT and c-Myc protein levels.

119 paB elements, and in induction of endogenous c-Myc protein levels.

120 subsequent degradation of c-Myc, increasing c-Myc protein levels.

121 anscription factor E2F, leading to decreased c-Myc protein levels.

122 Myc transcripts is correlated with increased c-Myc protein levels.

123 target of rapamycin signaling and decreased c-myc protein levels.

124 TCR signaling resulted in rapid elevation of c-Myc protein levels.

125 ng that SPOP inactivation directly increases c-MYC protein levels.

126 cells, the addition of serum rapidly induced c-MYC (protein) levels.

127 ion of Nmi and overexpression of hnRNP-K and c-myc proteins may explain why the prostate cancer cells

128 MG132 and AG490 blocked the reduction of the c-Myc protein observed by AG490 alone.

129 ar grade and immunohistochemical evidence of c-myc protein overexpression.

130 It has been found that c-Myc protein plays a critical role in controlling self-

131 pe II (PKA-II), on the steady-state level of c-Myc protein, providing a likely mechanism by which cAM

132 Fine changes in the stability of c-Myc protein regulated the HSC gene-expression signatur

133 A morpholino-mediated "knockdown" of c-Myc protein results in the absence of neural crest pre

134 Here we study the regulation of c-myc protein stability and identify domains of c-myc th

135 Thus, CK2 is a critical regulator of c-myc protein stability and of the proliferation of thes

136 an B cell lines, we found that PAX5 controls c-MYC protein stability and steady-state levels.

137 rved Myc homology box I region that controls c-Myc protein stability by oncogenic Ras.

138 erine 62 (Ser62) phosphorylation affects the c-Myc protein stability in cancer cells.

139 c-Myc protein stability in mammalian cells is controlled

140 the contribution of JNK to the regulation of c-Myc protein stability under normal growth conditions.

141 phosphorylation sites that help to regulate c-Myc protein stability, and altered ratios of T58 and S

142 anscriptional activity of c-Myc by promoting c-Myc protein stability, and ROCK inhibition reduced c-M

143 eonine58 (T58) and serine62 (S62), regulates c-Myc protein stability.

144 type in the N-terminal region that regulates c-Myc protein stability.

145 of Thr-58 is also associated with increased c-Myc protein stability.

146 e stress conditions are required to increase c-myc protein stability.

147 This effect results from both c-myc protein stabilization and activation of the c-myc

148 tion activity and was also found to bind the c-Myc protein, suggesting p107 negative regulation of c-

149 and inhibited transactivation by full-length c-Myc proteins, suggesting a dominant-negative inhibitor

150 trate that both mechanisms can contribute to c- myc protein synthesis.

151 ernal ribosome entry segment (IRES) and thus c-myc protein synthesis can be initiated by a cap-indepe

152 pression may contribute to the high level of c-Myc protein that is observed in Bcr-Abl transformed ce

153 When fused to a full-length c-Myc protein, the Mad1 SID specifically represses both

154 As with full-length c-Myc proteins, the c-Myc S proteins appear to be locali

155 EP led to immediate suppression of targeted c-myc protein; this was associated with rapid cell death

156 3K-Akt-mTOR signaling pathway that increases c-myc protein to activate ZEB1 gene expression leading t

157 hat NPM is necessary for the localization of c-Myc protein to nucleoli, whereas c-Myc nucleolar local

158 geted expression of a switchable form of the c-Myc protein to the skin epidermis, a well characterize

159 The c-Myc protein transactivates cellular promoters by recru

160 n factor 4E-binding protein 1, and increased c-Myc protein translation.

161 This is caused by accelerated c-myc protein turnover, which occurs in a proteasome-dep

162 In parallel, GLIPR1 also promoted c-Myc protein ubiquitination and degradation by glycogen

163 The stability of c-Myc protein was indicative of HSC quiescence, and c-My

164 Furthermore, accumulation of SKP2 and c-Myc proteins was significantly higher in metastatic me

165 re rejected; lymphomas expressing only human c-MYC protein were not rejected.

166 The effects of ceramide on the c-Myc protein were shown to be due to a reduction in hal

167 ed that p38a, STAT1, STAT3, CREB1, CCNE1 and c-MYC proteins were decreased after LINC00152 siRNA trea

168 analysis was used to identify regions of the c-Myc protein which are required for rapid proteolysis.

169 z-423 is the rapid and specific depletion of c-myc protein, which is coupled to growth-suppressing ef