ライフサイエンスコーパス: Id-1

1 Id-1 expression also correlates with the invasive and ag

2 Id-1 expression levels positively correlate with glioma

3 Id-1 is restricted to the cytoplasm; levels do not decre

4 Id-1 knockdown dramatically reduces glioblastoma cell in

5 Id-1 stimulated proliferation in sparse cultures but ind

6 Id-1 was widely expressed in proliferating bi- and unipo

7 Id-1, the most well-studied member of this family, has s

8 ional regulator, inhibitor of DNA binding-1 (Id-1), previously shown to function as an oncogene in se

9 ination of inhibitor of differentiation 1/2 (Id-1/2) by catalyzing phosphorylation of Id proteins and

10 The interrelationship between COX-2, PGE(2), Id-1, and cell invasiveness was also compared in nontumo

11 However, little is known about Id-1 target genes that are important for regulating norm

12 many of the cancer cells exhibited abundant Id-1, Id-2, and Id-3 immunoreactivity.

13 The ability of PGE(2) to activate Id-1 transcription was mediated by enhanced binding of E

14 X-2-derived prostaglandin (PGE(2)) activated Id-1 transcription, leading in turn to increased invasiv

15 In addition, Id-1 is aberrantly over-expressed in aggressive and meta

16 helix-loop-helix transcription factor, as an Id-1-interacting protein.

17 ghts into the relationship between COX-2 and Id-1 and their potential role in metastasis.

18 Cyclooxygenase-2 (COX-2) and Id-1 are overexpressed in a variety of human malignancie

19 tumors expressed less activated Smad-1/5 and Id-1 than that of controls.

20 o found to express an activated Smad-1/5 and Id-1.

21 d significantly less Smad-1/5 activation and Id-1 expression, and produced significant growth inhibit

22 8 phosphorylation, nuclear translocation and Id-1 expression, cell spreading, and tubulogenesis of en

23 ulated by stable transduction with antisense Id-1.

24 as measured by growth and invasiveness; (b) Id-1 was an important mediator of the effects of sex ste

25 To investigate the relationship between Id-1, telomerase activity, telomere length, p16, Rb cell

26 We demonstrate significant reduction of both Id-1 and MT1-MMP expressions as well as the metastatic s

27 extended the lifespan of keratinocytes, but Id-1 did not prevent the onset of replicative senescence

28 Under these experimental conditions, Id-1 expression did not trigger induction of telomerase

29 s prior to differentiation, and constitutive Id-1 expression blocks differentiation.

30 ate cell proliferation, whereas constitutive Id-1 expression rendered cells refractory to growth inhi

31 stem cells, transfected with DNA containing Id-1 under the control of transcriptional regulatory ele

32 splastic and atypical papillary ducts in CP, Id-1 and Id-2 immunoreactivity was as significantly elev

33 human tissue sections identified cytoplasmic Id-1 expression and nuclear Id-2 and Id-3 expression in

34 led to reduced PGE(2) production, decreased Id-1 expression, and reduced migration of cells through

35 -regulation of inhibitor of differentiation (Id-1).

36 deficient for inhibitor of differentiation (Id-1).

37 nd, cannabidiol, significantly downregulates Id-1 gene expression and associated glioma cell invasive

38 In these unselected cultures, enhanced Id-1 levels clearly extended the lifespan of keratinocyt

39 pyranoside-inducible expression of exogenous Id-1 in Con8 cells was shown to strongly facilitate the

40 that SCp2 cells that constitutively express Id-1 slowly invade the basement membrane but remain anch

41 to have an activated Smad-1/5 and expressed Id-1.

42 cancer cells: (a) a constitutively expressed Id-1 cDNA, when introduced into a nonaggressive breast c

43 n and apoptosis, we constitutively expressed Id-1 in mammary epithelial cell cultures.

44 Cells expressing Id-1 secreted a approximately 120-kDa gelatinase.

45 y epithelial cells constitutively expressing Id-1 protein are unable to differentiate, acquire the ab

46 ntibodies demonstrated the presence of faint Id-1 and Id-2 immunostaining in pancreatic ductal cells

47 e primers to specifically amplify cDNAs from Id-1-transfected SCp2 cells.

48 To understand how Id-1 acts, we screened a yeast two-hybrid library from d

49 is mediated by a 2.2-kb region of the human Id-1 promoter.

50 is mediated by a 2.2-kb region of the human Id-1 promoter.

51 In conclusion, our studies have identified Id-1 as a critical regulator of breast cancer progressio

52 Our results implicate Id-1 as acting as a critical regulator of mammary epithe

53 s decreased in proportion to the decrease in Id-1 protein levels, representing a potential mechanism

54 ed proliferation and produced an increase in Id-1 expression.

55 Expression of LANA in ECs resulted in Id-1 induction that was almost identical to the inductio

56 K1/2 --> Egr-1 pathway, leading to increased Id-1 transcription and cell invasion.

57 -MB-231 cells, treatment with PGE(2) induced Id-1, an effect that was mimicked by an EP(4) agonist.

58 A-MB-231 cells, COX-2-derived PGE(2) induced Id-1, leading in turn to increased cell invasiveness.

59 strogen stimulated proliferation and induced Id-1 expression, whereas progesterone inhibited prolifer

60 hanced expression, as KSHV infection induced Id-1 27-fold in ECs under our experimental conditions.

61 We show that BMP-2 induces Id-1 expression in lung cancer cell lines through its ac

62 Moreover, Id-1 has the potential to serve as a marker for aggressi

63 Moreover, Id-1 was highly expressed in aggressive breast cancer ce

64 We observed Id-1, Id-2, and Id-3 mRNA expression in proliferating hu

65 Thus, while no immortalization was observed, Id-1 could delay the onset of replicative senescence in

66 The ability of Id-1 to postpone, but not prevent, senescence may be rel

67 cell signaling regulating the expression of Id-1 and ATF-3, thus contributing to melanoma metastasis

68 These results demonstrate the expression of Id-1 in KS tumor cells and indicate the KSHV LANA protei

69 sponsible for the constitutive expression of Id-1 in metastatic human breast cancer cells.

70 We have shown that ectopic expression of Id-1 in murine mammary epithelial cells resulted in loss

71 ry has shown that constitutive expression of Id-1 in SCp2 mouse mammary epithelial cells inhibits the

72 Forced expression of Id-1 in the 129/Sv epithelium results in a decline in Id

73 examined the effects of forced expression of Id-1 in the small intestinal epithelium of adult chimeri

74 We have shown that ectopic expression of Id-1 inhibits differentiation and stimulates the prolife

75 We demonstrate that ectopic expression of Id-1 leads to activation of telomerase activity and immo

76 -MB231 cells, Pg inhibited the expression of Id-1 mRNA drastically.

77 In these cells, expression of Id-1, an inhibitor of basic helix-loop-helix transcripti

78 We demonstrated that the expression of Id-1, Id-2, and Id-3 genes was significantly induced at

79 In this study we compared the expression of Id-1, Id-2, and Id-3 in the normal pancreas, in pancreat

80 disrupted by the immortalizing functions of Id-1 through activation of telomerase activity and inact

81 The steroid induction of Id-1 was robust by 4 h of treatment and maintained over

82 Importantly, genetic knockdown of Id-1 leads to a significant increase in survival in an o

83 on proliferation and on expression level of Id-1, which generally stimulates cell proliferation and

84 cer cells lack PR and express high levels of Id-1 constitutively, and Pg showed no effect on Id expre

85 Moreover, high levels of Id-1 expression and the activity of a approximately 120-

86 c breast cancer cells express high levels of Id-1 mRNA because of a loss of serum-dependent regulatio

87 there is a correlation between the levels of Id-1 protein and the aggressiveness of several human bre

88 invasion through Id-1, as overexpression of Id-1 in MUC18-silenced cells resulted in increased MMP-2

89 Ectopic overexpression of Id-1 in the SCp2 nontumorigenic mammary epithelial cells

90 ith a retrovirus to induce overexpression of Id-1.

91 8, which reversed the expression patterns of Id-1 and ATF-3.

92 itro and repressed the invasive phenotype of Id-1-expressing cells in culture.

93 fect which correlated well with reduction of Id-1 mRNA.

94 Moreover, antisense reduction of Id-1 protein in SCp2 cells prevented the apical junction

95 se a mechanism for the loss of regulation of Id-1 promoter in invasive and metastatic human breast ca

96 cient for this hypoxia-induced repression of Id-1.

97 t only follows a pattern opposite to that of Id-1 during mammary gland development and breast cancer

98 Id-2 expression ran counter to that of Id-1 not only during maturation, but during periods of c

99 During mid-pregnancy, Id-1 expression declined to undetectable levels as the e

100 and which appear to be necessary for proper Id-1 repression.

101 The helix-loop-helix protein Id-1 inhibits the activity of basic helix-loop-helix tra

102 The helix-loop-helix protein Id-1 is a dominant negative regulator of basic helix-loo

103 erexpression of the helix-loop-helix protein Id-1 was capable of immortalizing keratinocytes, seconda

104 g domain (Inhibitor of DNA binding proteins (Id-1 to Id-4)).

105 verexpression of ITF-2 significantly reduced Id-1-stimulated proliferation and apoptosis.

106 y, an antisense oligonucleotide that reduced Id-1 protein levels reduced the ability of estrogen to s

107 Additionally, we found that MUC18 regulated Id-1 expression at the transcriptional level via ATF-3,

108 uced transcription factor HIF-1 up-regulates Id-1 in hypoxic neuroblastoma cells.

109 show here that the transcriptional regulator Id-1 plays a critical role in modulating the invasivenes

110 terone inhibited proliferation and repressed Id-1 expression.

111 Progesterone repressed Id-1 expression, at least in part by repressing transcri

112 F-3 in hypoxic neuroblastoma cells represses Id-1 and prevents the loss of these markers.

113 ies from infiltrating carcinomas, suggesting Id-1 might be an important regulator of breast cancer pr

114 Surprisingly, Id-1 increased during involution, when the epithelium un

115 ough cooperative interactions between 129/Sv(Id-1) and B6 ROSA26/+ cells.

116 oping novel therapeutic approaches to target Id-1 expression to reduce breast cancer metastasis in hu

117 approaches to tumor metastasis, we targeted Id-1 expression systemically in tumor-bearing mice by us

118 ays in glioblastoma and that drugs targeting Id-1 represent a novel and promising strategy for improv

119 ant phenotypes on treatment with Pg and that Id-1 plays an important role as a mediator of the effect

120 In this report, we demonstrate that Id-1 is expressed at high levels in KS tumor cells both

121 We found that Id-1, an inhibitor of basic helix-loop-helix transcripti

122 d intensity of immunostaining indicated that Id-1 and Id-2 were increased significantly in the cancer

123 We further show that Id-1 expression is negatively regulated by 2ME(2), which

124 Here we show that Id-1 is down-regulated in multiple primary, immortalized

125 Here, we show that Id-1 is expressed highly during mammary development in v

126 er of breast cancer biopsies, we showed that Id-1 was more frequently expressed in infiltrating carci

127 stigations in our laboratory have shown that Id-1 mRNA was constitutively expressed in highly aggress

128 Our results suggest that Id-1 can control the malignant progression of breast can

129 We suggest that Id-1 controls invasion by normal and neoplastic mammary

130 Our results suggest that Id-1 regulates multiple tumor-promoting pathways in glio

131 Our results suggest that Id-1, ITF-2, and Id-2 comprise a network of interacting

132 are coordinately expressed and suggests that Id-1 and Id-2 might be regulating very different events

133 partial inhibition of p16 expression, as the Id-1-overexpressing cultures displayed a decreased capac

134 rleukin-3 (IL-3)-dependent expression of the Id-1 gene, encoding a helix-loop-helix (HLH) transcripti

135 esults in IL-3-independent expression of the Id-1 gene.

136 dly and strongly stimulated the level of the Id-1 protein, which is a serum-inducible helix-loop-heli

137 is potentially an important mediator of the Id-1-induced proliferation pathway in mammary epithelial

138 sis showed increased binding of ATF-3 to the Id-1 promoter after MUC18 silencing.

139 mediated by enhanced binding of Egr-1 to the Id-1 promoter.

140 This Id-1-regulated invasive phenotype could contribute to in

141 hat MUC18 promotes melanoma invasion through Id-1, as overexpression of Id-1 in MUC18-silenced cells

142 We show further that, in contrast to Id-1, Id-2 was expressed highly in differentiated mammar

143 In contrast to Id-1, we found that, in vitro and in vivo, Id-2 mRNA and

144 Ubiquitinated Id-1/Id-2 can then bind to p62 and be transported to aut

145 e lines of evidence suggest that unregulated Id-1 expression may be an important regulator of the agg

146 ar decrease in cell migration was found when Id-1 was silenced.

147 mammary gland during involution, a time when Id-1 expression is high and there is extensive tissue re

148 ve in vitro and less metastatic in vivo when Id-1 is down-regulated by stable transduction with antis

149 To determine whether Id-1 could act as a key mediator of the effects of Pg, w

150 To determine whether Id-1 regulates both proliferation and apoptosis, we cons

151 p289 mRNA expression pattern correlates with Id-1 expression in SCp2 mammary epithelial cells under v

152 ts of Pg, we prepared cells transfected with Id-1 and PR.