|
Arthritis, Psoriatic
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Additionally, 1,25(OH)2D significantly increased ATP levels and gene expression related to mitochondrial function such as carnitine palmitoyltransferase 1 (CPT1), peroxisome proliferator-activated receptor α (PPARα), very long-chain acyl-CoA dehydrogenase (VLCAD), long-chain acyl-CoA dehydrogenase (LCAD), medium-chain acyl-CoA dehydrogenase (MCAD), uncoupling protein 2 (UCP2), and UCP3 and the vitamin D pathway including 25-dihydroxyvitamin D3 24-hydroxylase (CYP24) and 25-hydroxyvitamin D3 1-alpha-hydroxylase (CYP27) in PA-treated C2C12 myotubes.
|
31744213 |
2019 |
|
Neuroblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Our findings indicate that the aurora kinase inhibitor could cause metabolic imbalance, possibly by disturbing carbohydrate and fatty acid metabolic pathways, and ACADM may be a potential target in MNA neuroblastoma.
|
31560547 |
2019 |
|
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Literature retrieval results showed the hub gene NDC80, CENPE and ACADM might be novel targets for the diagnosis, clinical treatment and prognosis of ccRCC.
|
31788359 |
2019 |
|
Carcinogenesis
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
Survival analysis showed the high expression of CENPE, KIF20A, KIF4A, MELK, NCAPG, NDC80, NUF2, TOP2A, TPX2 and UBE2C, and low expression of ACADM gene could be involved in the carcinogenesis, invasion or recurrence of ccRCC.
|
31788359 |
2019 |
|
Central neuroblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Our findings indicate that the aurora kinase inhibitor could cause metabolic imbalance, possibly by disturbing carbohydrate and fatty acid metabolic pathways, and ACADM may be a potential target in MNA neuroblastoma.
|
31560547 |
2019 |
|
Protein Misfolding Disorders
|
0.010 |
Biomarker
|
disease |
BEFREE |
Protein misfolding diseases caused due to defective mitochondrial PQC system include medium-chain acyl-CoA dehydrogenase (MCAD)/short-chain acyl-CoA dehydrogenase (SCAD) deficiency diseases, hereditary spastic paraplegia.
|
31187709 |
2019 |
|
Childhood Neuroblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Our findings indicate that the aurora kinase inhibitor could cause metabolic imbalance, possibly by disturbing carbohydrate and fatty acid metabolic pathways, and ACADM may be a potential target in MNA neuroblastoma.
|
31560547 |
2019 |
|
Renal carnitine transport defect
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Fourteen patients were diagnosed with FAODs by NBS at the age of 54.8 ± 4.8 days: 5 with very-long-chain acyl-CoA dehydrogenase (VLCAD) deficiency, 5 with medium chain acyl-CoA dehydrogenase (MCAD) deficiency, 1 with primary carnitine deficiency, 1 with carnitine palmitoyltransferase 1A (CPT1A) deficiency, 1 with long-chain 3-hydroxyacyl-CoA dehydrogenase or mitochondrial trifunctional protein (LCAHD/MTP) deficiency, and 1 with short chain acyl-CoA dehydrogenase (SCAD) deficiency.
|
29519241 |
2018 |
|
Neurodegenerative Disorders
|
0.010 |
Biomarker
|
group |
BEFREE |
Our work validates and extends the current knowledge of PINK1, identifies a novel function of MCAD, and illuminates the need for and effectiveness of metabolic profiling in models of neurodegenerative disease.
|
29563254 |
2018 |
|
Colorectal Carcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Survival analysis of patients in the CRC dataset from The Cancer Genome Atlas (TCGA) revealed that higher expression of these 7 genes, especially CPT2, ACAA2 and ACADM, was associated with better prognosis (<i>p</i> = 0.034, <i>p</i> = 0.00058, <i>p</i> = 0.039, <i>p</i> = 0.04).
|
28977850 |
2017 |
|
Phenylketonurias
|
0.010 |
Biomarker
|
group |
BEFREE |
This protocol outlines a study that will establish COS for each of two relatively common IMD in children, phenylketonuria (PKU) and medium-chain acyl-CoA dehydrogenase (MCAD) deficiency.
|
29258568 |
2017 |
|
Tumor Progression
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Therefore, targeting the caspase-1/PPARγ/MCAD pathway might be a promising therapeutic approach to prevent tumor progression.Tumor associated macrophages (TAMs) promote cancer progression.
|
28974683 |
2017 |
|
Breast Carcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Here, the author show that caspase-1 promotes TAMs differentiation by attenuating medium-chain acyl-CoA dehydrogenase activity and that inhibition of this axis results in suppression of tumour growth in a transgenic mouse model of breast cancer.
|
28974683 |
2017 |
|
Glycogen Storage Disease
|
0.010 |
Biomarker
|
group |
BEFREE |
Abnormal liver function, hypoglycemia and muscle weakness are observed in various genetic diseases, including medium-chain acyl-CoA dehydrogenase (MCAD) deficiency and glycogen storage diseases.
|
25451272 |
2014 |
|
Paresis
|
0.010 |
GeneticVariation
|
phenotype |
BEFREE |
Abnormal liver function, hypoglycemia and muscle weakness are observed in various genetic diseases, including medium-chain acyl-CoA dehydrogenase (MCAD) deficiency and glycogen storage diseases.
|
25451272 |
2014 |
|
Muscle Weakness
|
0.010 |
GeneticVariation
|
phenotype |
BEFREE |
Abnormal liver function, hypoglycemia and muscle weakness are observed in various genetic diseases, including medium-chain acyl-CoA dehydrogenase (MCAD) deficiency and glycogen storage diseases.
|
25451272 |
2014 |
|
Liver diseases
|
0.010 |
GeneticVariation
|
group |
BEFREE |
Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency (OMIM 201450) is the most common inherited disorder of fatty acid metabolism presenting with hypoglycaemia, hepatopathy and Reye-like symptoms during catabolism.
|
23028790 |
2012 |
|
anaphylaxis
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
In addition, although both patients with ISMs(-) and patients with nc-MCAD presented with idiopathic and allergen-induced anaphylaxis, the former showed a higher frequency of men, cardiovascular symptoms, and insect bite as a trigger, together with greater sBt.
|
20434205 |
2010 |
|
Fatty acid oxidation defects
|
0.010 |
AlteredExpression
|
group |
BEFREE |
Hypoglycemia as one major clinical sign in all fatty acid oxidation defects occurs due to a reduced hepatic glucose output and an enhanced peripheral glucose uptake rather than to transcriptional changes that are also observed simultaneously, as presented in medium-chain acyl-CoA dehydrogenase (MCAD)-deficient mice.
|
20532823 |
2010 |
|
Lactic acidemia
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Biochemical testing identified metabolites characteristic of medium-chain acyl-CoA dehydrogenase (MCAD) deficiency (hexanoylglycine and suberylglycine), but also severe lactic acidemia (10-25 mM) and, in urine, excess of lactic acid, intermediates of the citric cycle, and marked ketonuria, suggesting mitochondrial dysfunction.
|
18203188 |
2008 |
|
Liver Failure, Acute
|
0.010 |
GeneticVariation
|
disease |
LHGDN |
We describe acute liver failure associated with an undiagnosed maternal medium-chain acyl-CoA dehydrogenase (MCAD) deficiency.
|
17186412 |
2007 |
|
Long QT Syndrome
|
0.010 |
Biomarker
|
disease |
BEFREE |
It is necessary to distinguish between lethal mutations leading to diseases such as MCAD and LQTS, and polymorphisms (for instance, in the IL-10 gene and mtDNA) that are normal gene variants but might be suboptimal in critical situations and thus predispose infants to sudden infant death.
|
15466077 |
2004 |
|
Left Ventricular Hypertrophy
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
MCAD mRNA levels are downregulated (>70%) during both the LVH and HF stages in the SHHF rats compared with controls.
|
9852194 |
1998 |
|
Reye-Like Syndrome
|
0.010 |
Biomarker
|
disease |
BEFREE |
Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is an autosomal recessive disorder which is known to cause Reye-like syndrome in children and sudden infant death.
|
1601002 |
1992 |
|
Hypoglycemic coma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is an inborn error of fatty-acid oxidation that is characterized by fasting intolerance and recurrent episodes of hypoglycemic coma which can be fatal.
|
1684086 |
1991 |