Hyperbiliverdinemia
|
0.610 |
GermlineCausalMutation
|
disease |
ORPHANET |
This is the first report of a homozygous BLVRA inactivating mutation indicating that the complete absence of BVRα activity is a non-lethal condition, the most evident phenotypic characteristic of which is the appearance of green jaundice accompanying cholestasis episodes.
|
21278388 |
2011 |
Hyperbiliverdinemia
|
0.610 |
GeneticVariation
|
disease |
BEFREE |
Hyperbiliverdinaemia (green jaundice) with green plasma and urine may be caused by a genetic defect in the BVR-A gene in conjunction with decompensated liver cirrhosis.
|
19580635 |
2009 |
Hyperbiliverdinemia
|
0.610 |
Biomarker
|
disease |
CTD_human |
|
|
|
Hyperbiliverdinemia
|
0.610 |
CausalMutation
|
disease |
CLINVAR |
|
|
|
Cholestasis
|
0.400 |
Biomarker
|
disease |
CTD_human |
When cholestasis was induced in pregnant rats, BVR alpha, SVCT1 and SVCT2 expression in maternal and fetal livers was stimulated, and this was further enhanced by UDCA treatment.
|
18706437 |
2008 |
Cholestasis
|
0.400 |
Biomarker
|
disease |
HPO |
|
|
|
Liver Cirrhosis, Experimental
|
0.300 |
Biomarker
|
disease |
CTD_human |
Systems level analysis and identification of pathways and networks associated with liver fibrosis.
|
25380136 |
2014 |
Cholelithiasis
|
0.100 |
Biomarker
|
disease |
HPO |
|
|
|
Decreased liver function
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
Green urine
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
Alzheimer's Disease
|
0.080 |
Biomarker
|
disease |
BEFREE |
Biliverdin Reductase-A Mediates the Beneficial Effects of Intranasal Insulin in Alzheimer Disease.
|
30073505 |
2019 |
Alzheimer's Disease
|
0.080 |
PosttranslationalModification
|
disease |
BEFREE |
Loss of biliverdin reductase-A favors Tau hyper-phosphorylation in Alzheimer's disease.
|
30738142 |
2019 |
Alzheimer's Disease
|
0.080 |
Biomarker
|
disease |
BEFREE |
Biliverdin reductase-A impairment links brain insulin resistance with increased Aβ production in an animal model of aging: Implications for Alzheimer disease.
|
29981845 |
2018 |
Alzheimer's Disease
|
0.080 |
AlteredExpression
|
disease |
BEFREE |
Our results show that OS-induced impairment of BVR-A kinase activity is an early event, which starts prior the accumulation of Aβ and tau pathology or the elevation of TNF-α, and that greatly contribute to the onset of BIR along the progression of AD pathology in 3xTg-Ad mice.
|
26698666 |
2016 |
Alzheimer's Disease
|
0.080 |
Biomarker
|
disease |
BEFREE |
The above data support the hypothesis that the dysregulation of HO-1/BVR-A system contributes to the early increase of oxidative stress in DS and provide potential mechanistic paths involved in the neurodegenerative process and AD development.
|
25391381 |
2015 |
Alzheimer's Disease
|
0.080 |
GeneticVariation
|
disease |
BEFREE |
We previously reported alterations in BVR activity along with decreased phosphorylation and increased oxidative/nitrosative posttranslational modifications in the brain of subjects with AD and those with mild cognitive impairment (MCI).
|
22549002 |
2012 |
Alzheimer's Disease
|
0.080 |
Biomarker
|
disease |
BEFREE |
In conclusion, nitrosative stress-induced modifications on hippocampal BVR-A are an early event in the pathogenesis of AD since they appear also in MCI subjects and could contribute to the antioxidant and metabolic derangement characteristic of these neurodegenerative disorders.
|
21483094 |
2011 |
Alzheimer's Disease
|
0.080 |
Biomarker
|
disease |
BEFREE |
Consequently, not just the increased levels of biliverdin reductase-A, but also its changed activity and phosphorylation state, should be taken into account when considering potential biomarkers for Alzheimer disease and mild cognitive impairment.
|
21241799 |
2011 |
Mild cognitive disorder
|
0.040 |
Biomarker
|
disease |
BEFREE |
We evaluated changes of BVR-A, Akt, GSK-3β, oxidative stress and Tau phosphorylation levels: (a) in brain from young (6-months) and old (12-months) 3xTg-AD mice; and (b) in post-mortem inferior parietal lobule (IPL) samples from amnestic mild cognitive impairment (MCI), from AD and from age-matched controls.
|
30738142 |
2019 |
Mild cognitive disorder
|
0.040 |
GeneticVariation
|
disease |
BEFREE |
We previously reported alterations in BVR activity along with decreased phosphorylation and increased oxidative/nitrosative posttranslational modifications in the brain of subjects with AD and those with mild cognitive impairment (MCI).
|
22549002 |
2012 |
Mild cognitive disorder
|
0.040 |
Biomarker
|
disease |
BEFREE |
In conclusion, nitrosative stress-induced modifications on hippocampal BVR-A are an early event in the pathogenesis of AD since they appear also in MCI subjects and could contribute to the antioxidant and metabolic derangement characteristic of these neurodegenerative disorders.
|
21483094 |
2011 |
Mild cognitive disorder
|
0.040 |
Biomarker
|
disease |
BEFREE |
Consequently, not just the increased levels of biliverdin reductase-A, but also its changed activity and phosphorylation state, should be taken into account when considering potential biomarkers for Alzheimer disease and mild cognitive impairment.
|
21241799 |
2011 |
Liver Cirrhosis
|
0.020 |
Biomarker
|
disease |
BEFREE |
FOXD2-AS1/miR-139-5p/BLVRA or CYTH2 axis might be the underlying molecular mechanism that dissects HCC development caused by cirrhosis.
|
31758243 |
2020 |
Fatty Liver Disease
|
0.020 |
Biomarker
|
disease |
BEFREE |
In vitro studies have demonstrated that BVR-A is a substrate of the insulin receptor and regulates IRS1 by avoiding its aberrant activation, and in animal model of obesity the loss of hepatic BVR-A has been associated with glucose/insulin alterations and fatty liver disease.However, no studies exist in humans.
|
30826467 |
2019 |
Fatty Liver Disease
|
0.020 |
Biomarker
|
disease |
BEFREE |
In conclusion, our data demonstrate a critical role for BVRA in protecting against lipid accumulation and oxidative stress in hepatocytes, which may serve as a future therapeutic target for NAFLD and its progression to NASH.
|
31422074 |
2019 |