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p(HGNC:GRIA1)

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Entity

Name
GRIA1
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 3

Amyloid β oligomers (AβOs) in Alzheimer’s disease v1.0.0

Activity-dependent tau protein translocation to excitatory synapse is disrupted by exposure to amyloid-beta oligomers v1.0.0

Extracellular low-n oligomers of tau cause selective synaptotoxicity without affecting cell viability v1.0.0

In-Edges 6

a(HBP:HBP00074) regulates tloc(p(HGNC:GRIA1), fromLoc(GO:"extracellular region"), toLoc(GO:intracellular)) View Subject | View Object

Soluble AβOs, but not monomers, mediate the internalization of the GluA1/GluA2 subunits by endocytosis (Zhang et al. 2011), leading to synaptic dysfunction (Hsieh et al. 2006). PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
Medium

a(HBP:"amyloid-beta oligomers") increases p(HGNC:GRIA1) View Subject | View Object

Abetao exposure induced a translocation of tau into the PSD fraction (***p  0.0002, 2-tailed Student’s t test; control 20.12  1228 vs Abetao 29.74  1.748, N  12 independent culture). There was also an increase of PSD-95 (***p0.0006, 2-tailed Student’s t test; control 19.10  2.557 vs Abetao 33.3  2153, N  9 independent culture), GluA1 (**p  0.0078, 2-tailed Student’s t test; control 18.841.930 vs Abetao 26.221.475,N9 independent culture) and fyn (**p  0.0041, 2-tailed Student’s t test; control 19.42  1.337 vs Abetao 29.67  2.181, N  6 independent cultures; Fig. 6D). PubMed:24760868

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Text Location
Results

a(MESH:jasplakinolide) increases p(HGNC:GRIA1) View Subject | View Object

We analyzed actin and tau in the PSD-enriched fraction from primary cortical neurons treated with jasplakinolide (Fig. 5E). We observed that increased neuronal F-actin content promotes concurrent tau enrichment (*p0.0150, 2-tailed Student’s t test; control 17.49  0.7755 vs jasplakinolide 27.02  2719, N  4 independent cultures; Fig. 5F). GLUA1, the membrane trafficking of which is known to be actin dependent, was increased (*p 0.0279, 2-tailed Student’s t test; control 16.91  1015 vs jasplakinolide 31.00  4.778, N  4 independent cultures). The amount of Fyn in the PSD was decreased (*p  0.0265, 2-tailed Student’s t test; control 27.25 5.003 vs jasplakinolide 11.71  1.786, N  4 independent cultures). PubMed:24760868

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Text Location
Results

bp(GO:"long-term synaptic potentiation") positiveCorrelation p(HGNC:GRIA1, loc(GO:synapse)) View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

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Text Location
Results

bp(GO:"long-term synaptic potentiation") positiveCorrelation p(HGNC:GRIA1) View Subject | View Object

We observed a similar LTPinduced increase in tau content within the PSD-enriched fraction from CA1 synaptosomes (29.86 +-4.86 to 70.15 +- 4.86, **p = 0.0011; Fig. 3B). As expected, actin and GluA1 were also increased, strengthening the idea that tau is involved in synaptic reorganization processes necessary for synaptic plasticity PubMed:24760868

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Text Location
Results

p(HBP:"Tau oligomers", var("p.Lys280del")) decreases p(HGNC:GRIA1) View Subject | View Object

Similarly, the GluR1 subunits of a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (characteristic of mature spines and necessary for LTP and calcium signaling) decreased in the oligomer-treated samples up to 60%. PubMed:28528849

Appears in Networks:

Out-Edges 2

p(HGNC:GRIA1, loc(GO:synapse)) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

Therefore, during a long-lasting synaptic activation, we observed an increase in tau, fyn, actin, GluA1, and PSD-95 content in the PSD-positive fraction, which is consistent with the characteristic features of synaptic plasticity (Ehlers, 2003). PubMed:24760868

Appears in Networks:
Annotations
Text Location
Results

p(HGNC:GRIA1) positiveCorrelation bp(GO:"long-term synaptic potentiation") View Subject | View Object

We observed a similar LTPinduced increase in tau content within the PSD-enriched fraction from CA1 synaptosomes (29.86 +-4.86 to 70.15 +- 4.86, **p = 0.0011; Fig. 3B). As expected, actin and GluA1 were also increased, strengthening the idea that tau is involved in synaptic reorganization processes necessary for synaptic plasticity PubMed:24760868

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Text Location
Results

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.