|
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 |
|
Malignant neoplasm of stomach
|
0.010 |
Biomarker
|
disease |
BEFREE |
Our study revealed that ANGPTL6 is an important driver gene of angiogenesis in AFPGC development.
|
31146977 |
2019 |
|
Stomach Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Our study revealed that ANGPTL6 is an important driver gene of angiogenesis in AFPGC development.
|
31146977 |
2019 |
|
Primary malignant neoplasm
|
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 |
|
Non-alcoholic Fatty Liver Disease
|
0.010 |
Biomarker
|
disease |
BEFREE |
The effects of ANGPTL2 and ANGPTL6 in the pathogenesis of NAFLD should be investigated further.
|
30002695 |
2018 |
|
Familial (FPAH)
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Rare Coding Variants in ANGPTL6 Are Associated with Familial Forms of Intracranial Aneurysm.
|
29304371 |
2018 |
|
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 |
|
Intermittent Claudication
|
0.010 |
AlteredExpression
|
phenotype |
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 |
|
Obesity, Morbid
|
0.010 |
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 |
|
Polycystic Ovary Syndrome
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Cardiovascular risk markers such as ADMA, CRP, Hcy, PAI-1, VEGF and ANGPTL6 levels are elevated in women with PCOS.
|
27425379 |
2017 |
|
Peripheral Vascular Diseases
|
0.010 |
Biomarker
|
group |
BEFREE |
Besides, this study analyzed AGF levels in LEPAD patients according to disease severity and evaluated the prognostic value of AGF for amputation and mortality in LEPAD patients after a follow-up period of 1.7years.
|
27866700 |
2017 |
|
Amputated structure (morphologic abnormality)
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Besides, this study analyzed AGF levels in LEPAD patients according to disease severity and evaluated the prognostic value of AGF for amputation and mortality in LEPAD patients after a follow-up period of 1.7years.
|
27866700 |
2017 |
|
Carcinoma of 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 |
|
Tumor Cell Invasion
|
0.010 |
AlteredExpression
|
phenotype |
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 |
|
Peripheral Arterial Diseases
|
0.010 |
Biomarker
|
group |
BEFREE |
Besides, this study analyzed AGF levels in LEPAD patients according to disease severity and evaluated the prognostic value of AGF for amputation and mortality in LEPAD patients after a follow-up period of 1.7years.
|
27866700 |
2017 |
|
Peripheral arterial stenosis
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Our results suggested that lower extremity peripheral artery disease was positively associated with AGF serum levels.
|
27866700 |
2017 |
|
Psoriasis
|
0.010 |
Biomarker
|
disease |
BEFREE |
We conclude that the K14-Angptl6 Tg mouse is useful to investigate psoriasis pathogenesis and for preclinical testing of new therapeutics.
|
27698489 |
2016 |
|
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 |
|
Secondary malignant neoplasm of liver
|
0.010 |
Biomarker
|
disease |
BEFREE |
We demonstrate that an interaction between hepatic angiopoietin-like 6 and tumoural α(6) integrin/E-cadherin drives liver homing and colonization by CRC cells, and that CGIYRLRSC inhibits liver metastasis through interference with this ligand/receptor system.
|
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 |
|
Glioblastoma Multiforme
|
0.010 |
Biomarker
|
disease |
BEFREE |
Addition of exogenous miRNA-128 to CRL-1690 and CRL-2610 GBM cell lines (a) restored 'homeostatic' ARP5 (ANGPTL6), Bmi-1 and E2F-3a expression, and (b) significantly decreased the proliferation of CRL-1690 and CRL-2610 cell lines.
|
19941032 |
2010 |
|
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 |