Malignant neoplasm of ovary
|
0.010 |
PosttranslationalModification
|
disease |
BEFREE |
These results suggest that, at least partly, epigenetic silencing by hypermethylation of the ANGPTL2 promoter leads to a loss of ANGPTL2 function, which may be a factor in the carcinogenesis of OC in a stage-dependent manner.
|
18593905 |
2008 |
Carcinoma, Ovarian Epithelial
|
0.010 |
PosttranslationalModification
|
disease |
BEFREE |
These results suggest that, at least partly, epigenetic silencing by hypermethylation of the ANGPTL2 promoter leads to a loss of ANGPTL2 function, which may be a factor in the carcinogenesis of OC in a stage-dependent manner.
|
18593905 |
2008 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Characterization of the 7q21-q22 amplicon identifies ARPC1A, a subunit of the Arp2/3 complex, as a regulator of cell migration and invasion in pancreatic cancer.
|
19145645 |
2009 |
Obesity
|
0.060 |
Biomarker
|
disease |
BEFREE |
Thus, Angptl2 is a key adipocyte-derived inflammatory mediator that links obesity to systemic insulin resistance.
|
19723494 |
2009 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
ERK1/2 phosphorylation of cortactin has emerged as an important positive regulatory modification, enabling cortactin to bind and activate the Arp2/3 regulator neuronal Wiskott-Aldrich syndrome protein (N-WASp), promoting actin polymerization and enhancing tumor cell movement.
|
21079800 |
2010 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
These cells grew slowly and were expanded over a period of 3 years and have maintained characteristics consistent with those of both the original ASPS tumor from the patient and the xenograft tumor including (1) presence of the alveolar soft part locus-transcription factor E3 type 1 fusion transcript and nuclear expression of the alveolar soft part locus-transcription factor E3 type 1 fusion protein; (2) maintenance of the t(X;17)(p11;q25) translocation characteristic of ASPS; and (3) expression of upregulated ASPS transcripts involved in angiogenesis (ANGPTL2, HIF-1-α, MDK, c-MET, VEGF, and TIMP-2), cell proliferation (PRL, PCSK1), metastasis (ADAM9), as well as the transcription factor BHLHB3 and the muscle-specific transcripts TRIM63 and ITGβ1BP3.
|
21552147 |
2011 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In vivo, the combination of Ad-HARPΔ111-136 and radiation therapy resulted in a striking inhibition (92%) of the growth of U87MG xenografts, resulting from the potent effect on tumor angiogenesis and tumor cell apoptosis as determined by TUNEL analysis.
|
21109939 |
2011 |
Tumor Angiogenesis
|
0.020 |
GeneticVariation
|
phenotype |
BEFREE |
In vivo, the combination of Ad-HARPΔ111-136 and radiation therapy resulted in a striking inhibition (92%) of the growth of U87MG xenografts, resulting from the potent effect on tumor angiogenesis and tumor cell apoptosis as determined by TUNEL analysis.
|
21109939 |
2011 |
Glioblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
HARPΔ111-136 enhances radiation-induced apoptosis of U87MG glioblastoma by induction of the proapoptotic protein CHOP.
|
21109939 |
2011 |
Alveolar Soft Part Sarcoma
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
These cells grew slowly and were expanded over a period of 3 years and have maintained characteristics consistent with those of both the original ASPS tumor from the patient and the xenograft tumor including (1) presence of the alveolar soft part locus-transcription factor E3 type 1 fusion transcript and nuclear expression of the alveolar soft part locus-transcription factor E3 type 1 fusion protein; (2) maintenance of the t(X;17)(p11;q25) translocation characteristic of ASPS; and (3) expression of upregulated ASPS transcripts involved in angiogenesis (ANGPTL2, HIF-1-α, MDK, c-MET, VEGF, and TIMP-2), cell proliferation (PRL, PCSK1), metastasis (ADAM9), as well as the transcription factor BHLHB3 and the muscle-specific transcripts TRIM63 and ITGβ1BP3.
|
21552147 |
2011 |
Adult Glioblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
HARPΔ111-136 enhances radiation-induced apoptosis of U87MG glioblastoma by induction of the proapoptotic protein CHOP.
|
21109939 |
2011 |
Childhood Glioblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
HARPΔ111-136 enhances radiation-induced apoptosis of U87MG glioblastoma by induction of the proapoptotic protein CHOP.
|
21109939 |
2011 |
Glioblastoma Multiforme
|
0.010 |
Biomarker
|
disease |
BEFREE |
HARPΔ111-136 enhances radiation-induced apoptosis of U87MG glioblastoma by induction of the proapoptotic protein CHOP.
|
21109939 |
2011 |
Dermatomyositis
|
0.210 |
Biomarker
|
disease |
BEFREE |
We propose that keratinocyte-derived Angptl2 functions in DM pathogenesis by inducing chronic inflammation in skin tissue.
|
22281496 |
2012 |
Schimke immunoosseous dysplasia
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
For example, mutations in SMARCAL1 (also named HARP) cause Schimke immuno-osseous dysplasia (SIOD); a multi-system disorder characterized by growth defects, immune deficiencies, renal failure and other complex phenotypes.
|
21327070 |
2012 |
Aortic Aneurysm
|
0.010 |
Biomarker
|
disease |
BEFREE |
AAA development was also significantly suppressed in wild-type mice that underwent Angptl2-deficient bone marrow transplantation.
|
22556334 |
2012 |
Aortic Aneurysm, Abdominal
|
0.010 |
Biomarker
|
disease |
BEFREE |
Macrophage-derived Angptl2 contributes to AAA development by inducing inflammation and degradation of extracellular matrix in the vessel wall, suggesting that targeting the Angptl2-induced inflammatory axis in macrophages could represent a new strategy for AAA therapy.
|
22556334 |
2012 |
Adult type dermatomyositis
|
0.010 |
Biomarker
|
disease |
BEFREE |
We propose that keratinocyte-derived Angptl2 functions in DM pathogenesis by inducing chronic inflammation in skin tissue.
|
22281496 |
2012 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Immunofluorescence and western blotting showed a positive correlation between the expression of Arp2/3 and the malignancy of glioma specimens (r=0.686, P=0.02) and confocal microscopy demonstrated localization of the Arp2/3 complex in lamellipodia of glioma cells.
|
23969835 |
2013 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
At the molecular level, the mesenchymal-but not the epithelial-isoform of Exo70 interacts with the Arp2/3 complex and stimulates actin polymerization for tumor invasion.
|
24331928 |
2013 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The Arp2/3 complex contributes to Salmonella invasion but is not essential, indicating other actin regulatory factors are involved.
|
23869992 |
2013 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Expression of the Arp2/3 complex in human gliomas and its role in the migration and invasion of glioma cells.
|
23969835 |
2013 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Immunofluorescence and western blotting showed a positive correlation between the expression of Arp2/3 and the malignancy of glioma specimens (r=0.686, P=0.02) and confocal microscopy demonstrated localization of the Arp2/3 complex in lamellipodia of glioma cells.
|
23969835 |
2013 |
Cardiovascular Diseases
|
0.060 |
Biomarker
|
group |
BEFREE |
Overall, our studies demonstrate that perivascular adipose tissue-secreted Angptl2 accelerates vascular inflammation and the subsequent CVD development.
|
23333801 |
2013 |
Obesity
|
0.060 |
AlteredExpression
|
disease |
BEFREE |
These findings may provide insight into the molecular mechanisms of the increased expression of Angptl2 and TGF-β1 in obesity.
|
23261458 |
2013 |