Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 Biomarker disease BEFREE Industrial Trans Fatty Acids Stimulate SREBP2-Mediated Cholesterogenesis and Promote Non-Alcoholic Fatty Liver Disease. 31327168 2019
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 Biomarker disease BEFREE RES prevented the development and progression of NAFLD and significantly improved insulin sensitivity through (1) inhibiting the proteolytic cleavage of SREBPs-1 and SREBPs-2 without affecting their precursor mRNA or protein levels, (2) inhibiting free fatty acid β-oxidation and generation of reactive oxygen species through significant inhibition of CPT-1 and UCP-2, and (3) decreasing activity of pancreatic lipase in vivo and in vitro. 28777914 2018
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 AlteredExpression disease BEFREE However, whether the regulation of SREBP‑2 restores dysfunctional autophagy in hepatocytes during NAFLD remains to be elucidated. 29336468 2018
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 Biomarker disease BEFREE The results suggest that consumption of a white corn/bean snack (70%/30% blend) attenuates weight gain, fat mass accumulation, adipocyte size and nonalcoholic fatty liver disease in HFD-fed mice by inhibiting PPARγ and SREBF2. 28965030 2017
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 AlteredExpression disease BEFREE Sulfated polysaccharides from Enteromorpha prolifera suppress SREBP-2 and HMG-CoA reductase expression and attenuate non-alcoholic fatty liver disease induced by a high-fat diet. 28429814 2017
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 AlteredExpression disease BEFREE In this study, we demonstrated that inhibition of SREBP-2 intracellular trafficking by site-1 protease (S1P) and site-2 protease (S2P) specific inhibitors, or shRNAs targeting S1P and S2P, upregulated gene and protein expression of autophagy markers, and improved the impaired autophagic flux induced in both cell and mouse models of NAFLD. 28011404 2017
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 GeneticVariation disease BEFREE Our results indicated that the GG genotype and G carrier (CG+GG) of rs2228314 G>C polymorphism in the SREBP-2 gene were strongly associated with susceptibility to NAFLD (both p<0.001). 24992162 2014
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 GeneticVariation disease BEFREE An SREBF-2 polymorphism predisposes individuals to NAFLD and associated cardiometabolic abnormalities and affects liver histology and glucose and lipid metabolism in biopsy-proven NAFLD. 23274901 2013
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 GeneticVariation disease BEFREE NAFLD was associated with increased SREBP-2 maturation, HMG CoA reductase (HMGCR) expression and decreased phosphorylation of HMGCR. 22560219 2012
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 AlteredExpression disease BEFREE We found that the LXRα gene and its lipogenic targets PPAR-γ (peroxisome-proliferator-activated receptor-γ), SREBP (sterol-regulatory-element-binding protein)-1c, SREBP-2 and FAS (fatty acid synthase) were overexpressed in the liver of NAFLD and HCV patients who had steatosis. 20929443 2011
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 GeneticVariation disease BEFREE This study aims to determine the association of the 1784G>C polymorphism in the SREBP-2 gene with NAFLD in Asian Indians in north India. 22182810 2011
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 AlteredExpression disease BEFREE Since hydroxymethylglutaryl-CoA (HMG-CoA) reductase is the key enzyme in cholesterol synthesis and transcriptionally controlled by SREBP-2 we measured its mRNA levels, being 3- to 4-fold higher in NAFLD compared to controls, without any difference between NASH and steatosis patients. 19231010 2009
CUI: C0400966
Disease: Non-alcoholic Fatty Liver Disease
Non-alcoholic Fatty Liver Disease
0.100 AlteredExpression disease BEFREE Although the expression of the LDL receptor, which acts on cholesterol uptake, and of SREBP-2, a positive key regulator of cholesterol, was suppressed, the expression of enzymes that promote cholesterol synthesis was uniformly increased in NAFLD. 19360318 2009