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p(HGNC:MME)

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Entity

Name
MME
Namespace
HGNC
Namespace Version
20180215
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/namespace/hgnc/hgnc-20180215.belns

Appears in Networks 6

APP processing in Alzheimer's disease v1.0.1

APP processing in Alzheimer's disease

Proteolytic processing of Alzeimer's beta-amyloid precursor protein v1.0.1

Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0

Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0

Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 19

act(a(HBP:HBP00071), ma(tscript)) regulates p(HGNC:MME) View Subject | View Object

In a similar fashion, released AICD has been shown to possess transactivation activity and can regulate transcription of multiple genes including APP, GSK- 3b, KAI1, neprilysin, BACE1, p53, EGFR, and LRP1 [127-132] PubMed:21214928

Appears in Networks:
Annotations
MeSH
Endosomes
Confidence
Medium
MeSH
Neurons

complex(p(HBP:HBP00071), p(HGNC:APBB1), p(HGNC:KAT5)) regulates p(HGNC:MME) View Subject | View Object

Although Tip60 does not bind to AICD directly, an indirect interaction between AICD and Tip60 is mediated by Fe65. Upon forming this complex, AICD is stabilized and can be translocated into the nucleus to regulate expression of genes such as KAI1, Neprilysin, LRP1, p53, GSK-3b and EGF receptor (Baek et al. 2002; Kim et al. 2003; Cao and Sudhof 2004; Pardossi-Piquard et al. 2005; Alves da Costa et al. 2006; Liu et al. 2007; Zhang et al. 2007) PubMed:22122372

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Neurons

a(CHEBI:"GW 501516") increases p(HGNC:MME) View Subject | View Object

In a study reported by Kalinin et al., treatment of 5xFAD mice with the PPAR-d agonist, GW742, resulted in decreased plaque burden and an increase in the expression of two Ab proteases, neprilysin and IDE [72]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High

a(CHEBI:"(-)-epigallocatechin") increases p(HGNC:MME) View Subject | View Object

In regard to pharmacological manipulation, substances such as epigallocatechin and somatostatin promote the expression, secretion and (allosterically) catalytic activ- ity of IDE and neprilysin in parallel with an increase in the degradation of Aβ peptides 259,280 . PubMed:30116051

Appears in Networks:

a(CHEBI:"(-)-epigallocatechin") increases sec(p(HGNC:MME)) View Subject | View Object

In regard to pharmacological manipulation, substances such as epigallocatechin and somatostatin promote the expression, secretion and (allosterically) catalytic activ- ity of IDE and neprilysin in parallel with an increase in the degradation of Aβ peptides 259,280 . PubMed:30116051

Appears in Networks:

a(CHEBI:"(-)-epigallocatechin") increases act(p(HGNC:MME)) View Subject | View Object

In regard to pharmacological manipulation, substances such as epigallocatechin and somatostatin promote the expression, secretion and (allosterically) catalytic activ- ity of IDE and neprilysin in parallel with an increase in the degradation of Aβ peptides 259,280 . PubMed:30116051

Appears in Networks:

a(CHEBI:somatostatin) increases p(HGNC:MME) View Subject | View Object

In regard to pharmacological manipulation, substances such as epigallocatechin and somatostatin promote the expression, secretion and (allosterically) catalytic activ- ity of IDE and neprilysin in parallel with an increase in the degradation of Aβ peptides 259,280 . PubMed:30116051

Appears in Networks:

a(CHEBI:somatostatin) increases sec(p(HGNC:MME)) View Subject | View Object

In regard to pharmacological manipulation, substances such as epigallocatechin and somatostatin promote the expression, secretion and (allosterically) catalytic activ- ity of IDE and neprilysin in parallel with an increase in the degradation of Aβ peptides 259,280 . PubMed:30116051

Appears in Networks:

a(CHEBI:somatostatin) increases act(p(HGNC:MME)) View Subject | View Object

In regard to pharmacological manipulation, substances such as epigallocatechin and somatostatin promote the expression, secretion and (allosterically) catalytic activ- ity of IDE and neprilysin in parallel with an increase in the degradation of Aβ peptides 259,280 . PubMed:30116051

Appears in Networks:

p(HGNC:GRN) increases act(p(HGNC:MME)) View Subject | View Object

Furthermore, expression of progranulin in the hippocampus of AD mice reduces the density of amyloid plaques by enhanc- ing the activity of neprilysin 281 . PubMed:30116051

Appears in Networks:

path(MESH:"Alzheimer Disease") decreases p(HGNC:MME) View Subject | View Object

Similar to IDE, neprilysin catabolizes Aβ42, and its loss in mouse models of AD and in patients with AD alike also contributes to Aβ42 accumulation 253,256,260 . PubMed:30116051

Appears in Networks:

a(CHEBI:"ginsenoside Rg1") increases act(p(HGNC:MME)) View Subject | View Object

And ginsenoside Rg1 and granulocyte-colony stimulating factor may up-regulate activities of NEP in retinal cells in an AD mouse model to reduce tau protein pathology (He et al. 2014) (Doi et al.2014). PubMed:29626319

Appears in Networks:

a(CHEBI:atorvastatin) increases sec(p(HGNC:MME)) View Subject | View Object

Simvastatin and atorvastatin enhance extracellular Aβ degradation via increasing NEP secretion from astrocytes by activating MAPK/Erk1/2 (Yamamoto et al. 2016) PubMed:29626319

Appears in Networks:
Annotations
MeSH
Astrocytes

a(CHEBI:nobiletin) increases act(p(HGNC:MME)) View Subject | View Object

Nobiletin, a flavone from citrus depressa, leads to gene expression and improves the protein level and activity of NEP in SK-N-SH cells, thus reducing Aβ levels (Fujiwara et al. 2014) PubMed:29626319

Appears in Networks:

a(CHEBI:simvastatin) increases sec(p(HGNC:MME)) View Subject | View Object

Simvastatin and atorvastatin enhance extracellular Aβ degradation via increasing NEP secretion from astrocytes by activating MAPK/Erk1/2 (Yamamoto et al. 2016) PubMed:29626319

Appears in Networks:
Annotations
MeSH
Astrocytes

a(MESH:"Granulocyte Colony-Stimulating Factor") increases act(p(HGNC:MME)) View Subject | View Object

And ginsenoside Rg1 and granulocyte-colony stimulating factor may up-regulate activities of NEP in retinal cells in an AD mouse model to reduce tau protein pathology (He et al. 2014) (Doi et al.2014). PubMed:29626319

Appears in Networks:

p(HGNC:ANXA1) increases act(p(HGNC:MME)) View Subject | View Object

Anti-inflammatory mediator annexin A1 (ANXA1) can reduce Aβ content by increasing its degradation by NEP (Ries et al. 2016) PubMed:29626319

Appears in Networks:

a(CHEBI:harmine) increases p(HGNC:MME) View Subject | View Object

Neprilysin, a major Aß-degrading enzyme, was downregulated in DS patient-derived fibroblasts. Treatment with harmine, a DYRK1A inhibitor and gene knockdown of DYRK1A, upregulated neprilysin in fibroblasts. PubMed:28250274

Appears in Networks:
Annotations
MeSH
Down Syndrome

p(HGNC:DYRK1A) negativeCorrelation p(HGNC:MME) View Subject | View Object

Neprilysin, a major Aß-degrading enzyme, was downregulated in DS patient-derived fibroblasts. Treatment with harmine, a DYRK1A inhibitor and gene knockdown of DYRK1A, upregulated neprilysin in fibroblasts. PubMed:28250274

Appears in Networks:
Annotations
MeSH
Down Syndrome

Out-Edges 10

p(HGNC:MME) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

They were able to show that the lipidation of ApoE enhanced the degradation of soluble species of Ab by neprilysin in the endolytic compartments of microglia as well as extracellularly through the actions of the insulindegrading enzyme (IDE) [13]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High
MeSH
Microglia

p(HGNC:MME) increases deg(a(CHEBI:"amyloid-beta polypeptide 42")) View Subject | View Object

Similar to IDE, neprilysin catabolizes Aβ42, and its loss in mouse models of AD and in patients with AD alike also contributes to Aβ42 accumulation 253,256,260 . PubMed:30116051

Appears in Networks:

p(HGNC:MME) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Extracellular Aβ degrading enzymes include neprilysin (NEP), insulin-degrading enzyme (IDE), matrix metalloproteinases (MMPs), angiotensin converting enzyme (ACE), endothelin-converting enzyme (ECE), and plasmin (Baranello et al. 2015) PubMed:29626319

Appears in Networks:

p(HGNC:MME) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

NEP, plasma membrane glycoprotein, is a zinc metalloendopeptidase and the most efficient hydrolytic enzyme in degrading Aβ in vitro (Shirotani et al. 2001) PubMed:29626319

Appears in Networks:

p(HGNC:MME) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

And in APP transgenic mice, long-term gene therapy of NEP ameliorates behavior by lowering the levels of Aβ (Spencer et al. 2008) PubMed:29626319

Appears in Networks:

p(HGNC:MME) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Exercise training can increase extracellular Aβ clearance in the brains of Tg2576 mice in a dose-dependent manner through up-regulating NEP, IDE, MMP9, LRP1, and HSP70 (Moore et al. 2016) PubMed:29626319

Appears in Networks:

act(p(HGNC:MME)) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Anti-inflammatory mediator annexin A1 (ANXA1) can reduce Aβ content by increasing its degradation by NEP (Ries et al. 2016) PubMed:29626319

Appears in Networks:

p(HGNC:MME) increases bp(GO:behavior) View Subject | View Object

And in APP transgenic mice, long-term gene therapy of NEP ameliorates behavior by lowering the levels of Aβ (Spencer et al. 2008) PubMed:29626319

Appears in Networks:

p(HGNC:MME) negativeCorrelation p(HGNC:DYRK1A) View Subject | View Object

Neprilysin, a major Aß-degrading enzyme, was downregulated in DS patient-derived fibroblasts. Treatment with harmine, a DYRK1A inhibitor and gene knockdown of DYRK1A, upregulated neprilysin in fibroblasts. PubMed:28250274

Appears in Networks:
Annotations
MeSH
Down Syndrome

p(HGNC:MME) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Neprilysin, a major Aß-degrading enzyme, was downregulated in DS patient-derived fibroblasts. Treatment with harmine, a DYRK1A inhibitor and gene knockdown of DYRK1A, upregulated neprilysin in fibroblasts. PubMed:28250274

Appears in Networks:
Annotations
MeSH
Down Syndrome

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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.