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p(HGNC:MMP2)

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Entity

Name
MMP2
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 5

MMP-9 and MMP-2 Contribute to Neuronal Cell Death in iPSC Models of Frontotemporal Dementia with MAPT Mutations v1.0.0

Clearance systems in the brain-implications for Alzheimer disease. v1.0.1

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

Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation v1.0.0

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

In-Edges 12

a(CHEBI:"2-(2-amino-3-methoxyphenyl)chromen-4-one") causesNoChange act(p(HGNC:MMP2)) View Subject | View Object

Interestingly, the level and activity of MMP-2 was not affected after the PD98059 treatment in tau-A152T neurons (Figure 4B) and MAPT IVS10+16 neurons (Figure 4C) PubMed:27594586

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Frontotemporal Dementia

a(CHEBI:"2-(2-amino-3-methoxyphenyl)chromen-4-one") causesNoChange p(HGNC:MMP2) View Subject | View Object

Interestingly, the level and activity of MMP-2 was not affected after the PD98059 treatment in tau-A152T neurons (Figure 4B) and MAPT IVS10+16 neurons (Figure 4C) PubMed:27594586

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Frontotemporal Dementia

p(HGNC:MAPT, var("p.Ala152Thr")) increases sec(p(HGNC:MMP2)) View Subject | View Object

The level of secreted MMP-9 and MMP-2 was also increased in cortical neurons derived from a published iPSC line with the tau-A152T mutation (Fong et al., 2013) (Figures 2E and 2F) PubMed:27594586

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Frontotemporal Dementia

p(HGNC:MAPT, var("p.Ala152Thr")) increases act(p(HGNC:MMP2)) View Subject | View Object

It is worth noting that the level and activity of secreted MMP-9 in tau- A152T neurons is also substantially higher than that in MAPT IVS10+16 neurons (Figure 2) PubMed:27594586

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Frontotemporal Dementia

p(HGNC:MAPT, var("p.Ala152Thr")) increases sec(p(HGNC:MMP2)) View Subject | View Object

It is worth noting that the level and activity of secreted MMP-9 in tau- A152T neurons is also substantially higher than that in MAPT IVS10+16 neurons (Figure 2) PubMed:27594586

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Frontotemporal Dementia

p(HBP:HBP00045, var("p.Ala152Thr")) increases sec(p(HGNC:MMP2)) View Subject | View Object

Taken together, these findings strongly suggest that 4R tau-A152T activates the ERK pathway more strongly, which in turn increases the level and activity of secreted MMP-9. 4R tau-A152T expression (Figures 4E and 4F) but not inhibition of ERK activity (Figures 4B and 4C) also increases the total activity of secreted MMP-2, suggesting that tau-A152T increases the level and activity of secreted MMP-2, likely through an ERK-independent pathway PubMed:27594586

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
HEK293
Confidence
High
MeSH
Frontotemporal Dementia

p(HBP:HBP00045, var("p.Ala152Thr")) increases act(p(HGNC:MMP2)) View Subject | View Object

Taken together, these findings strongly suggest that 4R tau-A152T activates the ERK pathway more strongly, which in turn increases the level and activity of secreted MMP-9. 4R tau-A152T expression (Figures 4E and 4F) but not inhibition of ERK activity (Figures 4B and 4C) also increases the total activity of secreted MMP-2, suggesting that tau-A152T increases the level and activity of secreted MMP-2, likely through an ERK-independent pathway PubMed:27594586

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
HEK293
Confidence
High
MeSH
Frontotemporal Dementia

path(MESH:"Alzheimer Disease") increases p(HGNC:MMP2) View Subject | View Object

Although overall matrix metallo- proteinase 2 expression is increased in AD,58 its activity is reduced in astrocytes that surround Aβ plaques. PubMed:26195256

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Temporal Lobe

a(CHEBI:"amyloid-beta") increases act(p(HGNC:MMP2)) View Subject | View Object

Among MMPs, MMP-2, -3 and -9, stimulated by Aβ, play important roles in degrading Aβ (Wang et al. 2014) PubMed:29626319

Appears in Networks:

a(PUBCHEM:135316034) decreases p(HGNC:MMP2) View Subject | View Object

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

Appears in Networks:
Annotations
MeSH
Atherosclerosis

path(MESH:Atherosclerosis) increases p(HGNC:MMP2) View Subject | View Object

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

Appears in Networks:

a(PUBCHEM:164676) decreases act(p(HGNC:MMP2)) View Subject | View Object

It inhibited the activation of iNOS, matrix metalloproteinase 2 (MMP2), and NF-Bp65 and consequently prevent AD in the brain [229–231]. PubMed:29179999

Appears in Networks:

Out-Edges 3

act(p(HGNC:MMP2)) increases bp(GO:"neuron death") View Subject | View Object

To examine the contributions of increased MMP-9 and MMP-2 to neuronal cell death, we used two compounds that are known to inhibit MMP-9 and MMP-2 activity (catalog #444278 and #444244, Calbiochem). We found that this treatment partially rescued the increased sensitivity to rapamycin and improved survival (Figure 3B) PubMed:27594586

Appears in Networks:
Annotations
MeSH
Extracellular Space
Confidence
High
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Frontotemporal Dementia

p(HGNC:MMP2) increases bp(GO:"neuron death") View Subject | View Object

MMP-2 and MMP-9 seem to induce cell death directly, since this treatment also increased the TUNEL signal in iPSC-derived neurons (Figures S3D and S3E) PubMed:27594586

Appears in Networks:
Annotations
MeSH
Extracellular Space
Confidence
High
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Frontotemporal Dementia

act(p(HGNC:MMP2)) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Among MMPs, MMP-2, -3 and -9, stimulated by Aβ, play important roles in degrading Aβ (Wang et al. 2014) PubMed:29626319

Appears in Networks:

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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.