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a(CHEBI:"advanced glycation end-product")

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Entity

Name
advanced glycation end-product
Namespace
chebi
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/chebi-names.belns

Appears in Networks 2

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0

In-Edges 6

a(CHEBI:"D-ribose") increases a(CHEBI:"advanced glycation end-product") View Subject | View Object

Here, we show for the first time that the administration of D-ribose, the most active glycator among monosaccharides, produces high levels of advanced glycation end products (AGEs) and, importantly, triggers hyperphosphorylation of Tau in the brain of C57BL/6 mouse and neuroblastoma N2a cells. PubMed:26095350

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Uberon
brain

a(CHEBI:methylglyoxal) increases a(CHEBI:"advanced glycation end-product") View Subject | View Object

Here, we found that MG could induce tau hyperphosphorylation at multiple AD-related sites in neuroblastoma 2a cells under maintaining normal cell viability. MG treatment increased the level of advanced glycation end products (AGEs) and the receptor of AGEs (RAGE). PubMed:22798221

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a(HBP:"GA-AGE") isA a(CHEBI:"advanced glycation end-product") View Subject | View Object

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p(HGNC:MAPT, pmod(HBP:glycation)) increases a(CHEBI:"advanced glycation end-product") View Subject | View Object

Tau is rapidly glycated in the presence of D-ribose, resulting in oligomerization and polymerization with Glycated derivatives appearing after 24 h. Advanced glycation end-products (AGEs) were formed during initial stages of glycation. Thioflavin T-positive (ThT-positive) aggregations (day 4) indicated the globular-like features. Atomic force microscopy revealed that the surface morphology of ribosylated Tau40 was globular-like. PubMed:19517062

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a(CHEBI:pentosidine) isA a(CHEBI:"advanced glycation end-product") View Subject | View Object

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a(HBP:GLAP) isA a(CHEBI:"advanced glycation end-product") View Subject | View Object

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Out-Edges 13

a(CHEBI:"advanced glycation end-product") increases p(MGI:Mapt, pmod(Ph, Ser, 214)) View Subject | View Object

Thus, our results suggest that Tau hyperphosphorylation was a result of ribosylated AGEs, rather than due to a direct reaction involving D-ribose. PubMed:26095350

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a(CHEBI:"advanced glycation end-product") increases p(MGI:Mapt, pmod(Ph, Ser, 396)) View Subject | View Object

Thus, our results suggest that Tau hyperphosphorylation was a result of ribosylated AGEs, rather than due to a direct reaction involving D-ribose. PubMed:26095350

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a(CHEBI:"advanced glycation end-product") increases act(p(MGI:Gsk3b), ma(kin)) View Subject | View Object

Taken all together, we think that activation of GSK-3b and p38 should be responsible for MG-induced tau hyperphosphorylation. PubMed:22798221

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a(CHEBI:"advanced glycation end-product") directlyIncreases act(p(HGNC:AGER)) View Subject | View Object

Recently, Li et al. (2012b) have demonstrated in their study that AGEs can induce tau hyperphosphorylation through receptor for advanced glycation end product (RAGE)-mediated glycogen synthase kinase 3 (GSK-3) activation and targeting RAGE/GSK-3 pathway can improve AD-like changes. PubMed:24183963

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a(CHEBI:"advanced glycation end-product") increases p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

Recently, Li et al. (2012b) have demonstrated in their study that AGEs can induce tau hyperphosphorylation through receptor for advanced glycation end product (RAGE)-mediated glycogen synthase kinase 3 (GSK-3) activation and targeting RAGE/GSK-3 pathway can improve AD-like changes. PubMed:24183963

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a(CHEBI:"advanced glycation end-product") directlyIncreases act(p(HGNC:AGER)) View Subject | View Object

The levels of sRAGE consistently decreased with age (R = −0.264, p = <0.001) and with the indices of obesity, such as BMI. However, of special interest was the highly significant and previ-ously not reported independent correlation with fat free mass (p < 0.001). PubMed:25681682

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a(CHEBI:"advanced glycation end-product") increases act(p(MGI:Mapk14), ma(kin)) View Subject | View Object

Taken all together, we think that activation of GSK-3b and p38 should be responsible for MG-induced tau hyperphosphorylation. PubMed:22798221

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a(CHEBI:"advanced glycation end-product") decreases act(p(HGNC:MAPT)) View Subject | View Object

Glycation by AGE (Advanced Glycation End products) decreases MT binding, promotes aggregation, activates RAGE PubMed:8063802

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a(CHEBI:"advanced glycation end-product") increases bp(GO:"neurofibrillary tangle assembly") View Subject | View Object

Glycation by AGE (Advanced Glycation End products) decreases MT binding, promotes aggregation, activates RAGE PubMed:8063802

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a(CHEBI:"advanced glycation end-product") increases p(HGNC:MAPT, pmod(HBP:hyperphosphorylation)) View Subject | View Object

AGEs induce tau hyperphosphorylation, memory deterioration, decline of synaptic proteins, and impairment of long-term potentiation in rats [10]. PubMed:27288790

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a(CHEBI:"advanced glycation end-product") decreases bp(GO:memory) View Subject | View Object

AGEs induce tau hyperphosphorylation, memory deterioration, decline of synaptic proteins, and impairment of long-term potentiation in rats [10]. PubMed:27288790

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a(CHEBI:"advanced glycation end-product") increases bp(GO:"cellular protein catabolic process") View Subject | View Object

AGEs induce tau hyperphosphorylation, memory deterioration, decline of synaptic proteins, and impairment of long-term potentiation in rats [10]. PubMed:27288790

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MeSH
Synapses

a(CHEBI:"advanced glycation end-product") decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

AGEs induce tau hyperphosphorylation, memory deterioration, decline of synaptic proteins, and impairment of long-term potentiation in rats [10]. PubMed:27288790

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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.