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PMID |
Sentence |
1 |
11553328
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An essential aspect of progression through mitosis is the sequential degradation of key mitotic regulators in a process that is mediated by the anaphase promoting complex/cyclosome (APC/C) ubiquitin ligase [1].
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2 |
11553328
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In mitotic cells, two forms of the APC/C exist, APC/C(Cdc20) and APC/C(Cdh1), which differ in their associated WD-repeat proteins (Cdc20 and Cdh1, respectively), time of activation, and substrate specificity [2, 3].
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3 |
11553328
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One such APC/C substrate, the budding yeast anaphase inhibitor Pds1 (securin), is degraded prior to anaphase initiation in a destruction box and APC/C(Cdc20)-dependent manner [3, 7].
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4 |
15178645
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Here we report expressions of PTTG and its interacting protein, PTTG-binding factor in human astrocytic cells.
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5 |
15178645
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PTTG expression was higher in malignant cells than in primary astrocytes, whereas PTTG-binding factor was not.
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6 |
15178645
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Furthermore, in U87 cells PTTG expression was up-regulated by promalignant ligands epithelial growth factor (EGF) and TGFalpha, both at the protein and mRNA levels.
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7 |
15178645
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PTTG induction by EGF receptor (EGFR) ligands could be blocked by the specific EGFR inhibitor, AG1478.
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8 |
15178645
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Hepatocyte growth factor (HGF) also induced PTTG but to a lesser extent than EGF.
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9 |
15178645
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Although EGF stimulates HGF secretion in U87 cells, the effect of EGF on PTTG mRNA expression is independent of HGF as neutralizing antibody against HGF failed to abolish EGF-induced up-regulation of PTTG mRNA.
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10 |
15178645
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PTTG mRNA was unchanged by incubating U87 cells with the promalignant growth factor TGFbeta, apoptosis inducing TNFalpha and ligands for nuclear receptors, such as retinoic acid and retinoid X receptors and peroxisome proliferator-activated receptor-gamma, known for their growth-inhibitory and apoptosis-inducing effects on gliomas.
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11 |
15178645
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Finally, regulation of its expression has glioma-specific features and is selectively regulated by promalignant cytokines including EGFR ligands and HGF.
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12 |
15178645
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Here we report expressions of PTTG and its interacting protein, PTTG-binding factor in human astrocytic cells.
|
13 |
15178645
|
PTTG expression was higher in malignant cells than in primary astrocytes, whereas PTTG-binding factor was not.
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14 |
15178645
|
Furthermore, in U87 cells PTTG expression was up-regulated by promalignant ligands epithelial growth factor (EGF) and TGFalpha, both at the protein and mRNA levels.
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15 |
15178645
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PTTG induction by EGF receptor (EGFR) ligands could be blocked by the specific EGFR inhibitor, AG1478.
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16 |
15178645
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Hepatocyte growth factor (HGF) also induced PTTG but to a lesser extent than EGF.
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17 |
15178645
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Although EGF stimulates HGF secretion in U87 cells, the effect of EGF on PTTG mRNA expression is independent of HGF as neutralizing antibody against HGF failed to abolish EGF-induced up-regulation of PTTG mRNA.
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18 |
15178645
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PTTG mRNA was unchanged by incubating U87 cells with the promalignant growth factor TGFbeta, apoptosis inducing TNFalpha and ligands for nuclear receptors, such as retinoic acid and retinoid X receptors and peroxisome proliferator-activated receptor-gamma, known for their growth-inhibitory and apoptosis-inducing effects on gliomas.
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19 |
15178645
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Finally, regulation of its expression has glioma-specific features and is selectively regulated by promalignant cytokines including EGFR ligands and HGF.
|
20 |
15178645
|
Here we report expressions of PTTG and its interacting protein, PTTG-binding factor in human astrocytic cells.
|
21 |
15178645
|
PTTG expression was higher in malignant cells than in primary astrocytes, whereas PTTG-binding factor was not.
|
22 |
15178645
|
Furthermore, in U87 cells PTTG expression was up-regulated by promalignant ligands epithelial growth factor (EGF) and TGFalpha, both at the protein and mRNA levels.
|
23 |
15178645
|
PTTG induction by EGF receptor (EGFR) ligands could be blocked by the specific EGFR inhibitor, AG1478.
|
24 |
15178645
|
Hepatocyte growth factor (HGF) also induced PTTG but to a lesser extent than EGF.
|
25 |
15178645
|
Although EGF stimulates HGF secretion in U87 cells, the effect of EGF on PTTG mRNA expression is independent of HGF as neutralizing antibody against HGF failed to abolish EGF-induced up-regulation of PTTG mRNA.
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26 |
15178645
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PTTG mRNA was unchanged by incubating U87 cells with the promalignant growth factor TGFbeta, apoptosis inducing TNFalpha and ligands for nuclear receptors, such as retinoic acid and retinoid X receptors and peroxisome proliferator-activated receptor-gamma, known for their growth-inhibitory and apoptosis-inducing effects on gliomas.
|
27 |
15178645
|
Finally, regulation of its expression has glioma-specific features and is selectively regulated by promalignant cytokines including EGFR ligands and HGF.
|
28 |
15178645
|
Here we report expressions of PTTG and its interacting protein, PTTG-binding factor in human astrocytic cells.
|
29 |
15178645
|
PTTG expression was higher in malignant cells than in primary astrocytes, whereas PTTG-binding factor was not.
|
30 |
15178645
|
Furthermore, in U87 cells PTTG expression was up-regulated by promalignant ligands epithelial growth factor (EGF) and TGFalpha, both at the protein and mRNA levels.
|
31 |
15178645
|
PTTG induction by EGF receptor (EGFR) ligands could be blocked by the specific EGFR inhibitor, AG1478.
|
32 |
15178645
|
Hepatocyte growth factor (HGF) also induced PTTG but to a lesser extent than EGF.
|
33 |
15178645
|
Although EGF stimulates HGF secretion in U87 cells, the effect of EGF on PTTG mRNA expression is independent of HGF as neutralizing antibody against HGF failed to abolish EGF-induced up-regulation of PTTG mRNA.
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34 |
15178645
|
PTTG mRNA was unchanged by incubating U87 cells with the promalignant growth factor TGFbeta, apoptosis inducing TNFalpha and ligands for nuclear receptors, such as retinoic acid and retinoid X receptors and peroxisome proliferator-activated receptor-gamma, known for their growth-inhibitory and apoptosis-inducing effects on gliomas.
|
35 |
15178645
|
Finally, regulation of its expression has glioma-specific features and is selectively regulated by promalignant cytokines including EGFR ligands and HGF.
|
36 |
15178645
|
Here we report expressions of PTTG and its interacting protein, PTTG-binding factor in human astrocytic cells.
|
37 |
15178645
|
PTTG expression was higher in malignant cells than in primary astrocytes, whereas PTTG-binding factor was not.
|
38 |
15178645
|
Furthermore, in U87 cells PTTG expression was up-regulated by promalignant ligands epithelial growth factor (EGF) and TGFalpha, both at the protein and mRNA levels.
|
39 |
15178645
|
PTTG induction by EGF receptor (EGFR) ligands could be blocked by the specific EGFR inhibitor, AG1478.
|
40 |
15178645
|
Hepatocyte growth factor (HGF) also induced PTTG but to a lesser extent than EGF.
|
41 |
15178645
|
Although EGF stimulates HGF secretion in U87 cells, the effect of EGF on PTTG mRNA expression is independent of HGF as neutralizing antibody against HGF failed to abolish EGF-induced up-regulation of PTTG mRNA.
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42 |
15178645
|
PTTG mRNA was unchanged by incubating U87 cells with the promalignant growth factor TGFbeta, apoptosis inducing TNFalpha and ligands for nuclear receptors, such as retinoic acid and retinoid X receptors and peroxisome proliferator-activated receptor-gamma, known for their growth-inhibitory and apoptosis-inducing effects on gliomas.
|
43 |
15178645
|
Finally, regulation of its expression has glioma-specific features and is selectively regulated by promalignant cytokines including EGFR ligands and HGF.
|
44 |
15178645
|
Here we report expressions of PTTG and its interacting protein, PTTG-binding factor in human astrocytic cells.
|
45 |
15178645
|
PTTG expression was higher in malignant cells than in primary astrocytes, whereas PTTG-binding factor was not.
|
46 |
15178645
|
Furthermore, in U87 cells PTTG expression was up-regulated by promalignant ligands epithelial growth factor (EGF) and TGFalpha, both at the protein and mRNA levels.
|
47 |
15178645
|
PTTG induction by EGF receptor (EGFR) ligands could be blocked by the specific EGFR inhibitor, AG1478.
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48 |
15178645
|
Hepatocyte growth factor (HGF) also induced PTTG but to a lesser extent than EGF.
|
49 |
15178645
|
Although EGF stimulates HGF secretion in U87 cells, the effect of EGF on PTTG mRNA expression is independent of HGF as neutralizing antibody against HGF failed to abolish EGF-induced up-regulation of PTTG mRNA.
|
50 |
15178645
|
PTTG mRNA was unchanged by incubating U87 cells with the promalignant growth factor TGFbeta, apoptosis inducing TNFalpha and ligands for nuclear receptors, such as retinoic acid and retinoid X receptors and peroxisome proliferator-activated receptor-gamma, known for their growth-inhibitory and apoptosis-inducing effects on gliomas.
|
51 |
15178645
|
Finally, regulation of its expression has glioma-specific features and is selectively regulated by promalignant cytokines including EGFR ligands and HGF.
|
52 |
15178645
|
Here we report expressions of PTTG and its interacting protein, PTTG-binding factor in human astrocytic cells.
|
53 |
15178645
|
PTTG expression was higher in malignant cells than in primary astrocytes, whereas PTTG-binding factor was not.
|
54 |
15178645
|
Furthermore, in U87 cells PTTG expression was up-regulated by promalignant ligands epithelial growth factor (EGF) and TGFalpha, both at the protein and mRNA levels.
|
55 |
15178645
|
PTTG induction by EGF receptor (EGFR) ligands could be blocked by the specific EGFR inhibitor, AG1478.
|
56 |
15178645
|
Hepatocyte growth factor (HGF) also induced PTTG but to a lesser extent than EGF.
|
57 |
15178645
|
Although EGF stimulates HGF secretion in U87 cells, the effect of EGF on PTTG mRNA expression is independent of HGF as neutralizing antibody against HGF failed to abolish EGF-induced up-regulation of PTTG mRNA.
|
58 |
15178645
|
PTTG mRNA was unchanged by incubating U87 cells with the promalignant growth factor TGFbeta, apoptosis inducing TNFalpha and ligands for nuclear receptors, such as retinoic acid and retinoid X receptors and peroxisome proliferator-activated receptor-gamma, known for their growth-inhibitory and apoptosis-inducing effects on gliomas.
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59 |
15178645
|
Finally, regulation of its expression has glioma-specific features and is selectively regulated by promalignant cytokines including EGFR ligands and HGF.
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60 |
15281346
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Clinical studies reveal that PTTG-binding factor, fibroblast growth factor 2, and vascular endothelial growth factor are elevated in pituitary tumors, and mostly correlate with PTTG levels, also confirming the PTTG role in angiogenesis.
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61 |
15281346
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PTTG overexpression disrupts mitosis and causes aneuploidy in single live cells and PTTG modulates p53 activity and p53 also mediates DNA damage-induced inhibition of PTTG transcription.
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62 |
15281346
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Clinical studies reveal that PTTG-binding factor, fibroblast growth factor 2, and vascular endothelial growth factor are elevated in pituitary tumors, and mostly correlate with PTTG levels, also confirming the PTTG role in angiogenesis.
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63 |
15281346
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PTTG overexpression disrupts mitosis and causes aneuploidy in single live cells and PTTG modulates p53 activity and p53 also mediates DNA damage-induced inhibition of PTTG transcription.
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64 |
15579722
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Budding yeast securin/Pds1p, an inhibitor of the anaphase activator separase/Esp1p, is involved in several checkpoint pathways and in promoting Esp1p's nuclear localization.
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65 |
17065388
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Murine pituitary tumor-transforming gene functions as a securin protein in insulin-secreting cells.
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66 |
17065388
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We tested whether mPTTG exhibits securin properties in mouse insulin-secreting insulinoma MIN6 cells, using a live-cell system to monitor mitosis in cells transfected with an enhanced green fluorescent protein (EGFP)-tagged mPTTG conjugate (mPTTG-EGFP).
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67 |
17065388
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These results show that mPTTG exhibits properties consistent with a murine securin in insulin-secreting mouse cells and mPTTG overexpression inhibits cell proliferation, suggesting that defective beta-cell proliferation observed in PTTG-/- mice is likely due to abnormal cell-cycle progression.
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68 |
17065388
|
Murine pituitary tumor-transforming gene functions as a securin protein in insulin-secreting cells.
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69 |
17065388
|
We tested whether mPTTG exhibits securin properties in mouse insulin-secreting insulinoma MIN6 cells, using a live-cell system to monitor mitosis in cells transfected with an enhanced green fluorescent protein (EGFP)-tagged mPTTG conjugate (mPTTG-EGFP).
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70 |
17065388
|
These results show that mPTTG exhibits properties consistent with a murine securin in insulin-secreting mouse cells and mPTTG overexpression inhibits cell proliferation, suggesting that defective beta-cell proliferation observed in PTTG-/- mice is likely due to abnormal cell-cycle progression.
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71 |
17065388
|
Murine pituitary tumor-transforming gene functions as a securin protein in insulin-secreting cells.
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72 |
17065388
|
We tested whether mPTTG exhibits securin properties in mouse insulin-secreting insulinoma MIN6 cells, using a live-cell system to monitor mitosis in cells transfected with an enhanced green fluorescent protein (EGFP)-tagged mPTTG conjugate (mPTTG-EGFP).
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73 |
17065388
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These results show that mPTTG exhibits properties consistent with a murine securin in insulin-secreting mouse cells and mPTTG overexpression inhibits cell proliferation, suggesting that defective beta-cell proliferation observed in PTTG-/- mice is likely due to abnormal cell-cycle progression.
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74 |
17287403
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Invasive prolactinomas may be associated with a high Ki-67/MIB-1 labelling index indicating increased cell proliferation, although this is not a universal finding.
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75 |
17287403
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Increased expression of the polysialylated neural cell adhesion molecule (NCAM) and reduced expression of the E-cadherin/catenin complex implies a contribution of altered cell-to-cell adhesion and cellular migration.
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76 |
17287403
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The induction of fibroblast growth factor and vascular endothelial growth factor via oestrogen-induced overexpression of novel genes (PTTG, hst and Edpm5) enhance cell growth, proliferation and angiogenesis contributing to invasiveness in prolactinomas.
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77 |
18566344
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Neurotrophin p75 receptor (p75NTR) promotes endothelial cell apoptosis and inhibits angiogenesis: implications for diabetes-induced impaired neovascularization in ischemic limb muscles.
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78 |
18566344
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The p75 receptor of neurotrophins (p75(NTR)), which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice.
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79 |
18566344
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Here, we show that gene transfer-induced p75(NTR) expression impairs the survival, proliferation, migration, and adhesion capacities of cultured ECs and endothelial progenitor cells (EPCs) and inhibits angiogenesis in vitro.
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80 |
18566344
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Moreover, intramuscular p75(NTR) gene delivery impairs neovascularization and blood flow recovery in a mouse model of limb ischemia.
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81 |
18566344
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In fact, p75(NTR) depresses the VEGF-A/Akt/eNOS/NO pathway and additionally reduces the mRNA levels of ITGB1 [beta (1) integrin], BIRC5 (survivin), PTTG1 (securin) and VEZF1.
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82 |
18566344
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Diabetic mice, which typically show impaired postischemic muscular neovascularization and blood perfusion recovery, have these defects corrected by intramuscular gene transfer of a dominant negative mutant form of p75(NTR).
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83 |
18566344
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Collectively, our data newly demonstrate the antiangiogenic action of p75(NTR) and open new avenues for the therapeutic use of p75(NTR) inhibition to combat diabetes-induced microvascular liabilities.
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84 |
19213844
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Cyclin-dependent kinase inhibitor p21 was progressively up-regulated in PTTG(-/-) islets, and p21 deletion partially rescued PTTG(-/-) mice from development of diabetes. mRNA array showed that DNA damage-associated genes were activated in PTTG(-/-) islets.
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85 |
19472104
|
Transcripts of PTTG and growth factors bFGF and IGF-1 are correlated in pituitary adenomas.
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86 |
19472104
|
The reasons for the increase of pituitary tumor-transforming gene (PTTG) transcripts in about 90% of pituitary adenomas are still not fully understood, although upregulation by basic fibroblast growth factor (bFGF) has been discussed as a potential cause.
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87 |
19472104
|
Moreover, the principal regulation of the PTTG gene by IGF-1 and Insulin has been demonstrated in astrocytoma and breast cancer cells.
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88 |
19472104
|
From total RNA of frozen tumor samples (all subtypes) cDNA ( COMPLEMENTARY DNA) was synthesized and transcripts of PTTG, bFGF, IGF-1 were measured by Real-Time-PCR.
|
89 |
19472104
|
Not only mRNA ( MESSENGER RNA) levels of bFGF, but also of IGF-1, correlated strongly with PTTG transcripts.
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90 |
19472104
|
Our study suggests a connection between PTTG and IGF-1 in pituitary adenomas.
|
91 |
19472104
|
Transcripts of PTTG and growth factors bFGF and IGF-1 are correlated in pituitary adenomas.
|
92 |
19472104
|
The reasons for the increase of pituitary tumor-transforming gene (PTTG) transcripts in about 90% of pituitary adenomas are still not fully understood, although upregulation by basic fibroblast growth factor (bFGF) has been discussed as a potential cause.
|
93 |
19472104
|
Moreover, the principal regulation of the PTTG gene by IGF-1 and Insulin has been demonstrated in astrocytoma and breast cancer cells.
|
94 |
19472104
|
From total RNA of frozen tumor samples (all subtypes) cDNA ( COMPLEMENTARY DNA) was synthesized and transcripts of PTTG, bFGF, IGF-1 were measured by Real-Time-PCR.
|
95 |
19472104
|
Not only mRNA ( MESSENGER RNA) levels of bFGF, but also of IGF-1, correlated strongly with PTTG transcripts.
|
96 |
19472104
|
Our study suggests a connection between PTTG and IGF-1 in pituitary adenomas.
|
97 |
19472104
|
Transcripts of PTTG and growth factors bFGF and IGF-1 are correlated in pituitary adenomas.
|
98 |
19472104
|
The reasons for the increase of pituitary tumor-transforming gene (PTTG) transcripts in about 90% of pituitary adenomas are still not fully understood, although upregulation by basic fibroblast growth factor (bFGF) has been discussed as a potential cause.
|
99 |
19472104
|
Moreover, the principal regulation of the PTTG gene by IGF-1 and Insulin has been demonstrated in astrocytoma and breast cancer cells.
|
100 |
19472104
|
From total RNA of frozen tumor samples (all subtypes) cDNA ( COMPLEMENTARY DNA) was synthesized and transcripts of PTTG, bFGF, IGF-1 were measured by Real-Time-PCR.
|
101 |
19472104
|
Not only mRNA ( MESSENGER RNA) levels of bFGF, but also of IGF-1, correlated strongly with PTTG transcripts.
|
102 |
19472104
|
Our study suggests a connection between PTTG and IGF-1 in pituitary adenomas.
|
103 |
19472104
|
Transcripts of PTTG and growth factors bFGF and IGF-1 are correlated in pituitary adenomas.
|
104 |
19472104
|
The reasons for the increase of pituitary tumor-transforming gene (PTTG) transcripts in about 90% of pituitary adenomas are still not fully understood, although upregulation by basic fibroblast growth factor (bFGF) has been discussed as a potential cause.
|
105 |
19472104
|
Moreover, the principal regulation of the PTTG gene by IGF-1 and Insulin has been demonstrated in astrocytoma and breast cancer cells.
|
106 |
19472104
|
From total RNA of frozen tumor samples (all subtypes) cDNA ( COMPLEMENTARY DNA) was synthesized and transcripts of PTTG, bFGF, IGF-1 were measured by Real-Time-PCR.
|
107 |
19472104
|
Not only mRNA ( MESSENGER RNA) levels of bFGF, but also of IGF-1, correlated strongly with PTTG transcripts.
|
108 |
19472104
|
Our study suggests a connection between PTTG and IGF-1 in pituitary adenomas.
|
109 |
19472104
|
Transcripts of PTTG and growth factors bFGF and IGF-1 are correlated in pituitary adenomas.
|
110 |
19472104
|
The reasons for the increase of pituitary tumor-transforming gene (PTTG) transcripts in about 90% of pituitary adenomas are still not fully understood, although upregulation by basic fibroblast growth factor (bFGF) has been discussed as a potential cause.
|
111 |
19472104
|
Moreover, the principal regulation of the PTTG gene by IGF-1 and Insulin has been demonstrated in astrocytoma and breast cancer cells.
|
112 |
19472104
|
From total RNA of frozen tumor samples (all subtypes) cDNA ( COMPLEMENTARY DNA) was synthesized and transcripts of PTTG, bFGF, IGF-1 were measured by Real-Time-PCR.
|
113 |
19472104
|
Not only mRNA ( MESSENGER RNA) levels of bFGF, but also of IGF-1, correlated strongly with PTTG transcripts.
|
114 |
19472104
|
Our study suggests a connection between PTTG and IGF-1 in pituitary adenomas.
|
115 |
19472104
|
Transcripts of PTTG and growth factors bFGF and IGF-1 are correlated in pituitary adenomas.
|
116 |
19472104
|
The reasons for the increase of pituitary tumor-transforming gene (PTTG) transcripts in about 90% of pituitary adenomas are still not fully understood, although upregulation by basic fibroblast growth factor (bFGF) has been discussed as a potential cause.
|
117 |
19472104
|
Moreover, the principal regulation of the PTTG gene by IGF-1 and Insulin has been demonstrated in astrocytoma and breast cancer cells.
|
118 |
19472104
|
From total RNA of frozen tumor samples (all subtypes) cDNA ( COMPLEMENTARY DNA) was synthesized and transcripts of PTTG, bFGF, IGF-1 were measured by Real-Time-PCR.
|
119 |
19472104
|
Not only mRNA ( MESSENGER RNA) levels of bFGF, but also of IGF-1, correlated strongly with PTTG transcripts.
|
120 |
19472104
|
Our study suggests a connection between PTTG and IGF-1 in pituitary adenomas.
|
121 |
21536883
|
Here, we generated germline transgenic zebrafish with overexpression of pituitary tumor transforming gene (PTTG/securin) targeted to the adenohypophyseal proopiomelanocortin (POMC) lineage, which recapitulated early features pathognomonic of corticotroph adenomas, including corticotroph expansion and partial glucocorticoid resistance.
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122 |
21536883
|
Molecular analyses in vitro and in vivo showed that R-roscovitine suppresses ACTH expression, induces corticotroph tumor cell senescence and cell cycle exit by up-regulating p27, p21 and p57, and downregulates cyclin E expression.
|