ライフサイエンスコーパス: c-Myc protein

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

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

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

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

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

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

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

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

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

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

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

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

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

14 ing of the hit compounds with the disordered c-Myc protein.

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

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

17 olyubiquitination and increased stability of c-Myc protein.

18 negatively regulated translation of oncogene c-Myc protein.

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

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

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

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

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

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

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

26 cycle progression and levels of p53, p21 and c-Myc proteins.

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

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

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

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

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

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

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

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

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

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

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

38 f survival and self-renewal via depletion of c-Myc protein and p53 activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 An abbreviated form of the c-Myc protein, called Omomyc, consists of the Myc DNA-bi

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

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

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

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

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

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

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

64 confirmed significant inhibition of GLI1 and c-MYC protein expression in DAOY and HD-MB03 cells, resp

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

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

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

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

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

70 Hes family BHLH transcription factor 1), and c-MYC protein expression levels are elevated in two enza

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

72 Similarly, c-Myc protein expression was reduced in Fraxini treated

73 In contrast, ABHD5 knockout increased c-MYC protein expression, enhanced cell proliferation, a

74 rgets AR and AR-V7 and indirectly influences c-Myc protein expression, reveals new molecular mechanis

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

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

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

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

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

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

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

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

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

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

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

86 w here that Gfi1 augmented the expression of c-Myc protein in cells transfected with c-Myc expression

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

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

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

90 PRDM1/Blimp1 and increased the abundance of c-Myc protein in reactivated Akata BL with pRb knockdown

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 ive arm of TTFL, causes up-regulation of the c-MYC protein level in mouse spleen.

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

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

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

114 ence with HDAC1/-2 elicited a suppression of c-Myc protein levels and a concomitant increase in 2 tra

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

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

117 ncy also led to a Pim2-dependent increase in c-Myc protein levels and was associated with reduced c-M

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

119 vated NOTCH1 intracellular domain (NICD) and c-MYC protein levels as well as elevated hypoxia-inducib

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

121 mpounds that can rapidly decrease endogenous c-MYC protein levels in a MYC-amplified cell line led to

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

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

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

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

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

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

128 The reduction of c-Myc protein levels in vitro Hep3B cells appears to be

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

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

131 c-Myc protein levels were positively correlated with tho

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

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

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

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

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

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

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

139 n downregulates MYC target genes and reduces c-MYC protein levels.

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

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

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

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

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

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

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

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

148 ly, expression of a proteasome-nondegradable c-Myc protein mutant was sufficient to avoid glutathione

149 To meet this demand, c-Myc protein (Myc henceforth) drives the expression of

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

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

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

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

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

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

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

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

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

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

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

161 c-Myc protein stability in mammalian cells is controlled

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

163 CB-839 treatment resulted in a reduction in c-Myc protein stability via a ubiquitin-specific peptida

164 d that FOXR2 interacts with N-MYC, increases C-MYC protein stability, and activates FAK/SRC signaling

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 3K-Akt-mTOR signaling pathway that increases c-myc protein to activate ZEB1 gene expression leading t

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

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

183 c levels: namely, deubiquitination of AR and c-Myc proteins to increase their stability and deubiquit

184 The c-Myc protein transactivates cellular promoters by recru

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

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

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

188 d effective drug targeting of the disordered c-Myc protein via the determination of hot spot residues

189 Furthermore, c-MYC protein was also decreased by GSK-J4.

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

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

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

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

194 MYC target genes and c-MYC protein were upregulated in the chemoresistant CDX

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

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

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

198 depletion acutely reduces the expression of c-MYC protein without changing its mRNA expression.