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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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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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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.