|
Obesity
|
0.240 |
AlteredExpression
|
disease |
BEFREE |
Since upregulation of ANGPTL6 is induced on metabolic stress, we investigated the hepatic expression of ANGPTL6 by leptin, a representative adipokine of obesity.
|
29852166 |
2018 |
|
Obesity
|
0.240 |
AlteredExpression
|
disease |
BEFREE |
Baseline ANGPTL6 levels in patients with obesity and T2DM did not differ from the control group.
|
27135654 |
2017 |
|
Obesity
|
0.240 |
GeneticVariation
|
disease |
BEFREE |
Further validation in cohorts with severe obesity and engineering the variants in model organisms will be needed to explore whether human variants in ANGPTL6 and other genes that lead to obesity when deleted in mice, do contribute to obesity.
|
28663568 |
2017 |
|
Obesity
|
0.240 |
Biomarker
|
disease |
BEFREE |
Specially, bANGPTL6β gene probably contributes to a new target for treatment of obesity and obesity-related diseases.
|
31102716 |
2019 |
|
Hypertensive disease
|
0.110 |
Biomarker
|
group |
BEFREE |
We observed a higher rate of individuals with a history of high blood pressure among affected versus healthy individuals carrying ANGPTL6 variants, suggesting that ANGPTL6 could trigger cerebrovascular lesions when combined with other risk factors such as hypertension.
|
29304371 |
2018 |
|
Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
AGF support tumor growth and progression.
|
27419371 |
2017 |
|
Neoplasms
|
0.030 |
AlteredExpression
|
group |
BEFREE |
Three bioinformatics-verified miRNA-128 targets, angiopoietin-related growth factor protein 5 (ARP5; ANGPTL6), a transcription suppressor that promotes stem cell renewal and inhibits the expression of known tumor suppressor genes involved in senescence and differentiation, Bmi-1, and a transcription factor critical for the control of cell-cycle progression, E2F-3a, were found to be up-regulated.
|
19941032 |
2010 |
|
Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
ANGPTL6 loss results in tumor growth in vivo.
|
31146977 |
2019 |
|
Diabetes Mellitus
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Poor glycemic control in diabetes mellitus as reflected by higher serum HbA<sub>1c</sub> levels is associated with raised serum ANGPTL6 levels.
|
29033485 |
2018 |
|
Diabetes Mellitus
|
0.020 |
Biomarker
|
group |
BEFREE |
Although the physiologic functions of human AGF have not yet been identified, serum levels of AGF displayed up-regulation in groups with diseases including preeclampsia and diabetes; and there was little association between genetic variability of AGF and metabolic syndrome-related phenotypes.
|
20673930 |
2011 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
This study aimed to find whether long-term glycemic control (glycated hemoglobin [HbA<sub>1c</sub>]) has any correlation with serum ANGPTL6 levels in patients of type 2 diabetes mellitus.
|
29033485 |
2018 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
VLCD decreased ANGPTL6 levels only in obese patients with T2DM.
|
27135654 |
2017 |
|
Metabolic Diseases
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Despite its beneficial effects on metabolism, human studies have shown a paradoxical increase in ANGPTL6 level in the serum of patients with metabolic diseases, which has been interpreted as a compensatory upregulation.
|
29852166 |
2018 |
|
Metabolic Diseases
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Collectively, our data suggest that serum ANGPTL6 levels and ANGPTL6 mRNA expression in SAT are affected by metabolic disorders and their treatment but do not appear to directly reflect nutritional status.
|
27135654 |
2017 |
|
Metabolic Syndrome X
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, serum AGF levels were paradoxically increased in metabolic syndrome, in comparison with data from animal experiments and data on sex, age, and waist circumference.
|
20673930 |
2011 |
|
Metabolic Syndrome X
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
The use of ANGPTL6 levels in addition to the conventional components improved the prediction of new-onset metabolic syndrome (area under the receiver operating characteristic curve: 0.775 vs. 0.807, <i>P</i>=0.036).
|
30968619 |
2019 |
|
Limb ischemia
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Among LEPAD patients, those with critical limb ischemia (n=43) showed higher AGF levels (124.9±73.9 vs. 88.98±53.26ng/mL, P=0.01) compared with those with intermittent claudication (n=62).
|
27866700 |
2017 |
|
Limb ischemia
|
0.020 |
Biomarker
|
disease |
BEFREE |
Our goal was to determine whether AGF enhances blood flow in a mouse hind-limb ischemia model and to define molecular mechanisms underlying AGF signaling in endothelial cells.
|
18258819 |
2008 |
|
Anorexia Nervosa
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
ANGPTL6 levels of AN patients were increased relative to the control group (68.6 ± 9.9 ng/ml) and decreased from 110.2 ± 13.3 to 73.6 ± 7.1 ng/ml (p = 0.004) after partial realimentation.
|
27135654 |
2017 |
|
Malignant neoplasm of urinary bladder
|
0.010 |
Biomarker
|
disease |
BEFREE |
At IC50 for HAase activity inhibition (5-20 μg/ml [0.4-1.7 μM]), sHA-F significantly inhibited proliferation, motility and invasion of HYAL-1 expressing BCa cells (253J-Lung, HT1376, UMUC-3), P<0.001. sHA-F did not affect the growth of HYAL-1 non-expressing BCa (5637, RT4, T24, TCCSUP) and normal urothelial (Urotsa, SV-HUC1) cells. sHA-F treatment induced apoptosis by death receptor pathway. sHA-F downregulated transcript and/or protein levels of HA receptors (CD44, RHAMM), p-AKT, β-catenin, pβ-Catenin(S552), Snail and Twist but increased levels of pβ-Catenin(T41/S45), pGSK-3α/β(S21/S9) and E-cadherin. sHA-F also inhibited CD44/Phosphoinositide 3-kinase (PI-3K) complex formation and PI-3K activity.
|
27419371 |
2017 |
|
Bladder Neoplasm
|
0.010 |
Biomarker
|
disease |
BEFREE |
At IC50 for HAase activity inhibition (5-20 μg/ml [0.4-1.7 μM]), sHA-F significantly inhibited proliferation, motility and invasion of HYAL-1 expressing BCa cells (253J-Lung, HT1376, UMUC-3), P<0.001. sHA-F did not affect the growth of HYAL-1 non-expressing BCa (5637, RT4, T24, TCCSUP) and normal urothelial (Urotsa, SV-HUC1) cells. sHA-F treatment induced apoptosis by death receptor pathway. sHA-F downregulated transcript and/or protein levels of HA receptors (CD44, RHAMM), p-AKT, β-catenin, pβ-Catenin(S552), Snail and Twist but increased levels of pβ-Catenin(T41/S45), pGSK-3α/β(S21/S9) and E-cadherin. sHA-F also inhibited CD44/Phosphoinositide 3-kinase (PI-3K) complex formation and PI-3K activity.
|
27419371 |
2017 |
|
Malignant Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
ANGPTL6 promotes endothelial cell migration and tube formation, Moreover, ANGPTL6 knockdown inhibits cancer cell apoptosis and invasiveness.
|
31146977 |
2019 |
|
Intracranial Aneurysm
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Altogether, our results indicate that rare coding variants in ANGPTL6 are causally related to familial forms of IA.
|
29304371 |
2018 |
|
Colorectal Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
We identify angiopoietin-like 6 protein as a peptide-mimicked natural ligand enriched in hepatic blood vessels of CRC patients.
|
23070965 |
2012 |
|
Diabetes
|
0.010 |
Biomarker
|
disease |
BEFREE |
Although the physiologic functions of human AGF have not yet been identified, serum levels of AGF displayed up-regulation in groups with diseases including preeclampsia and diabetes; and there was little association between genetic variability of AGF and metabolic syndrome-related phenotypes.
|
20673930 |
2011 |