|
White Blood Cell Count procedure
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Lymphocyte Count measurement
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
The Allelic Landscape of Human Blood Cell Trait Variation and Links to Common Complex Disease.
|
27863252 |
2016 |
|
Diabetes
|
0.010 |
Biomarker
|
disease |
BEFREE |
These results identify the UBE2O/AMPKα2 axis as both a potent regulator of metabolic homeostasis in skeletal muscle and a therapeutic target in the treatment of diabetes and metabolic disorders.
|
31292296 |
2019 |
|
Diabetes Mellitus
|
0.010 |
Biomarker
|
group |
BEFREE |
These results identify the UBE2O/AMPKα2 axis as both a potent regulator of metabolic homeostasis in skeletal muscle and a therapeutic target in the treatment of diabetes and metabolic disorders.
|
31292296 |
2019 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.010 |
Biomarker
|
disease |
BEFREE |
Here we find that UBE2O is markedly upregulated in obese subjects with type 2 diabetes and show that whole-body disruption of Ube2o in mouse models in vivo results in improved metabolic profiles and resistance to high-fat diet-induced (HFD-induced) obesity and metabolic syndrome.
|
31292296 |
2019 |
|
Metabolic Diseases
|
0.010 |
Biomarker
|
group |
BEFREE |
These results identify the UBE2O/AMPKα2 axis as both a potent regulator of metabolic homeostasis in skeletal muscle and a therapeutic target in the treatment of diabetes and metabolic disorders.
|
31292296 |
2019 |
|
Neoplasms
|
0.010 |
GeneticVariation
|
group |
BEFREE |
Our meta-analysis showed that AMPK pathway had significant associations with progression-free survival (PFS; p < 0.001) and overall survival (OS; p < 0.001), but not with tumor response (TR; p = 0.220): PRKAA1 rs13361707 was significantly associated with favorable PFS (log HR = -0.219, SE = 0.073, p = 0.003), as well as PRKAA1 rs10074991 (log HR = -0.215, SE = 0.073, p = 0.003), and there were suggestive associations of PRKAG1 rs1138908 with unfavorable OS (log HR = 0.170, SE = 0.083, p = 0.041), and of UBE2O rs3803739 with unfavorable PFS (log HR = 0.137, SE = 0.068, p = 0.042) and OS (log HR = 0.210, SE = 0.077, p = 0.006), although these results were not significant after false discovery rate adjustment.
|
30856283 |
2019 |
|
Obesity
|
0.010 |
Biomarker
|
disease |
BEFREE |
Here we find that UBE2O is markedly upregulated in obese subjects with type 2 diabetes and show that whole-body disruption of Ube2o in mouse models in vivo results in improved metabolic profiles and resistance to high-fat diet-induced (HFD-induced) obesity and metabolic syndrome.
|
31292296 |
2019 |
|
Metabolic Syndrome X
|
0.010 |
Biomarker
|
disease |
BEFREE |
Here we find that UBE2O is markedly upregulated in obese subjects with type 2 diabetes and show that whole-body disruption of Ube2o in mouse models in vivo results in improved metabolic profiles and resistance to high-fat diet-induced (HFD-induced) obesity and metabolic syndrome.
|
31292296 |
2019 |
|
Malignant Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
In this review, we focus on recent insights into the pathogenetic roles of E2s (particularly the ubiquitin-conjugating enzyme E2O [UBE2O]) in debilitating diseases and cancer, and discuss the tantalizing prospect that E2s may someday serve as potential therapeutic targets for human diseases.
|
29562734 |
2018 |
|
Kidney Diseases
|
0.010 |
Biomarker
|
group |
BEFREE |
Gene expression studies highlighted the differential expression of several genes involved in prostaglandin metabolism (AKR1C18), heme and iron metabolism (HbA-A2, HMOX1, SCL25A37), electrolyte balance (SLC4A1, AQP6), immunity (RSAD2, C3, UBE2O), fatty acid metabolism (FASN), hypoxia hall-mark genes (GCK, SDC3, VEGFA, ETS1, CP, BCL2), as well as genes implicated in other forms of kidney disease (PODXL, ELMO1, FRMD3, MYH9, APOA1).
|
29476712 |
2018 |
|
Osteosarcoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Bioluminescence experiments disclosed that <i>UBE2O</i> knockdown elevates the amplitude of the circadian clock in human osteosarcoma U2OS cells.
|
29871923 |
2018 |
|
Osteosarcoma of bone
|
0.010 |
Biomarker
|
disease |
BEFREE |
Bioluminescence experiments disclosed that <i>UBE2O</i> knockdown elevates the amplitude of the circadian clock in human osteosarcoma U2OS cells.
|
29871923 |
2018 |
|
Primary malignant neoplasm
|
0.010 |
Biomarker
|
group |
BEFREE |
In this review, we focus on recent insights into the pathogenetic roles of E2s (particularly the ubiquitin-conjugating enzyme E2O [UBE2O]) in debilitating diseases and cancer, and discuss the tantalizing prospect that E2s may someday serve as potential therapeutic targets for human diseases.
|
29562734 |
2018 |
|
Childhood Osteosarcoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Bioluminescence experiments disclosed that <i>UBE2O</i> knockdown elevates the amplitude of the circadian clock in human osteosarcoma U2OS cells.
|
29871923 |
2018 |
|
Multiple Myeloma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
UBE2O was found to interact with c-Maf, a critical transcription factor in MM, by the affinity purification/tandem mass spectrometry assay and co-immunoprecipitation assays.
|
28673317 |
2017 |
|
Carcinogenesis
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Finally, pharmacological blockade of UBE2O inhibits tumorigenesis through the restoration of AMPKα2, suggesting the UBE2O-AMPKα2 axis as a potential cancer therapeutic target.
|
28162974 |
2017 |
|
Tumor Initiation
|
0.010 |
GeneticVariation
|
phenotype |
BEFREE |
Here we show that Ube2o deletion in MMTV-PyVT or TRAMP mice profoundly impairs tumor initiation, growth, and metastasis, while switching off the metabolic reprogramming of tumor cells.
|
28162974 |
2017 |
|
MIXED LINEAGE LEUKEMIA
|
0.010 |
Biomarker
|
disease |
BEFREE |
We report that UBE2O functions in regulating the stability of wild-type MLL in response to interleukin-1 signaling.
|
28065413 |
2017 |