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complex(p(HGNC:APP), p(HGNC:HSD17B10))

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Components

Appears in Networks 1

Amyloid-Binding Alcohol Dehydrogenase (ABAD) Inhibitors for the Treatment of Alzheimer’s Disease v1.0.0

In-Edges 2

a(CHEBI:"methylene blue") decreases complex(p(HGNC:APP), p(HGNC:HSD17B10)) View Subject | View Object

In mechanistic studies, it was proposed that methylene blue inhibits the Aβ-ABAD interaction and decreases mitochondrial dysfunction by decreasing the expression of ABAD levels, in addition to decreasing Aβ levels. PubMed:30444369

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a(PUBCHEM:33334) decreases complex(p(HGNC:APP), p(HGNC:HSD17B10)) View Subject | View Object

Frentizole, an FDA approved immunosuppressant drug, was identified as an Aβ-ABAD interaction inhibitor (IC 50 = 200 M) using an ELISA-based screening assay. PubMed:30444369

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MeSH
Neurons

Out-Edges 16

complex(p(HGNC:APP), p(HGNC:HSD17B10)) hasComponent p(HGNC:APP) View Subject | View Object

Appears in Networks:

complex(p(HGNC:APP), p(HGNC:HSD17B10)) hasComponent p(HGNC:HSD17B10) View Subject | View Object

Appears in Networks:

complex(p(HGNC:APP), p(HGNC:HSD17B10)) decreases act(p(HGNC:HSD17B10)) View Subject | View Object

However, it is well established that Aβ binding to ABAD induces a conformational change in the enzyme that prevents the binding of NAD + , preventing the enzyme performing its role in the oxidation of substrates, leading to changes in mitochondrial membrane permeability, which in turn has deleterious effects on mitochondrial enzymes. PubMed:30444369

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MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) increases path(MESH:"Alzheimer Disease") View Subject | View Object

Binding of Aβ to ABAD has been implicated in the development of AD, recent studies detected elevated ABAD levels in the regions of the hippocampus and cerebral cortex which are generally affected by AD pathology PubMed:30444369

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complex(p(HGNC:APP), p(HGNC:HSD17B10)) increases bp(GO:"response to oxidative stress") View Subject | View Object

Neurons from these animals exhibited increased oxidative stress, increased generation of ROS, DNA fragmentation, neuronal apoptosis, and impairment in learning, compared to single-transgenic mAPP mice. PubMed:30444369

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MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Neurons from these animals exhibited increased oxidative stress, increased generation of ROS, DNA fragmentation, neuronal apoptosis, and impairment in learning, compared to single-transgenic mAPP mice. PubMed:30444369

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MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) increases a(CHEBI:"reactive oxygen species") View Subject | View Object

In another study, neurons from Tg mAPP/ABAD mice were shown to exhibit decreased activity of cyclooxygenase (COX) enzyme, spontaneous release of ROS, loss of mitochondrial membrane potential, a decrease in ATP production and release of cytochrome c from mitochondria with subsequent induction of caspase-3-like activity followed by apoptotic cell death. PubMed:30444369

Appears in Networks:
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MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) increases bp(GO:"apoptotic DNA fragmentation") View Subject | View Object

Neurons from these animals exhibited increased oxidative stress, increased generation of ROS, DNA fragmentation, neuronal apoptosis, and impairment in learning, compared to single-transgenic mAPP mice. PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) increases bp(GO:"neuron death") View Subject | View Object

Neurons from these animals exhibited increased oxidative stress, increased generation of ROS, DNA fragmentation, neuronal apoptosis, and impairment in learning, compared to single-transgenic mAPP mice. PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) decreases bp(GO:learning) View Subject | View Object

Neurons from these animals exhibited increased oxidative stress, increased generation of ROS, DNA fragmentation, neuronal apoptosis, and impairment in learning, compared to single-transgenic mAPP mice. PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) decreases act(p(FPLX:COX)) View Subject | View Object

In another study, neurons from Tg mAPP/ABAD mice were shown to exhibit decreased activity of cyclooxygenase (COX) enzyme, spontaneous release of ROS, loss of mitochondrial membrane potential, a decrease in ATP production and release of cytochrome c from mitochondria with subsequent induction of caspase-3-like activity followed by apoptotic cell death. PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) decreases bp(GO:"regulation of mitochondrial membrane potential") View Subject | View Object

In another study, neurons from Tg mAPP/ABAD mice were shown to exhibit decreased activity of cyclooxygenase (COX) enzyme, spontaneous release of ROS, loss of mitochondrial membrane potential, a decrease in ATP production and release of cytochrome c from mitochondria with subsequent induction of caspase-3-like activity followed by apoptotic cell death. PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) decreases a(CHEBI:ATP) View Subject | View Object

In another study, neurons from Tg mAPP/ABAD mice were shown to exhibit decreased activity of cyclooxygenase (COX) enzyme, spontaneous release of ROS, loss of mitochondrial membrane potential, a decrease in ATP production and release of cytochrome c from mitochondria with subsequent induction of caspase-3-like activity followed by apoptotic cell death. PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) increases act(p(HGNC:CASP3)) View Subject | View Object

In another study, neurons from Tg mAPP/ABAD mice were shown to exhibit decreased activity of cyclooxygenase (COX) enzyme, spontaneous release of ROS, loss of mitochondrial membrane potential, a decrease in ATP production and release of cytochrome c from mitochondria with subsequent induction of caspase-3-like activity followed by apoptotic cell death. PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) increases bp(GO:"apoptotic process") View Subject | View Object

In another study, neurons from Tg mAPP/ABAD mice were shown to exhibit decreased activity of cyclooxygenase (COX) enzyme, spontaneous release of ROS, loss of mitochondrial membrane potential, a decrease in ATP production and release of cytochrome c from mitochondria with subsequent induction of caspase-3-like activity followed by apoptotic cell death. PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

complex(p(HGNC:APP), p(HGNC:HSD17B10)) decreases complex(a(CHEBI:"NAD(+)"), p(HGNC:HSD17B10)) View Subject | View Object

However, it is well established that Aβ binding to ABAD induces a conformational change in the enzyme that prevents the binding of NAD + , preventing the enzyme performing its role in the oxidation of substrates, leading to changes in mitochondrial membrane permeability, which in turn has deleterious effects on mitochondrial enzymes. PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.