1. Catalog
  2. Nodes
  3. p(HGNC:MAPT, pmod(Ph, Thr, 181))

p(HGNC:MAPT, pmod(Ph, Thr, 181))

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

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

Appears in Networks 3

Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers v1.0.0

This document contains the bel code for the Article Alzheimer’s disease-type neuronal tau hyperphosphorylation induced by Abeta oligomers by De Felice et al

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage from Shafiei et al., 2017

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 18

a(HBP:"amyloid-beta derived diffusible ligands") increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

Verification of the findings from immunofluorescence microscopy was provided by Western blot analysis of hippocampal neuronal lysates with P404, P231 and P181 antiphosphotau antibodies. A 4 h exposure to 500nM ADDLs resulted in a significant increase in tau phosphorylated at the three epitopes, to levels similar to those observed after exposure to 10 M Abeta fibrils (Fig. 4A–D). PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

a(HBP:"amyloid-beta fibrils") increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

Verification of the findings from immunofluorescence microscopy was provided by Western blot analysis of hippocampal neuronal lysates with P404, P231 and P181 antiphosphotau antibodies. A 4 h exposure to 500nM ADDLs resulted in a significant increase in tau phosphorylated at the three epitopes, to levels similar to those observed after exposure to 10 M Abeta fibrils (Fig. 4A–D). PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

p(HGNC:MAPT) hasVariant p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

Appears in Networks:

a(MESH:Exosomes) association p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

In support, tau associated with exosomes and phosphorylated at Thr-181 (AT270+ tau) has been identified in human CSF samples of AD patients PubMed:28420982

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebrospinal Fluid
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

More recently, patients affected with FTD and AD, were found to have high levels of total tau and phosphorylated tau (p-T181 and p-S396; Saman et al., 2012) PubMed:28420982

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebrospinal Fluid
MeSH
Alzheimer Disease

path(MESH:"Frontotemporal Dementia") positiveCorrelation p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

More recently, patients affected with FTD and AD, were found to have high levels of total tau and phosphorylated tau (p-T181 and p-S396; Saman et al., 2012) PubMed:28420982

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebrospinal Fluid
MeSH
Alzheimer Disease

a(CHEBI:"D-ribose") increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) 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

Appears in Networks:

a(CHEBI:"D-ribose") positiveCorrelation p(HGNC:MAPT, pmod(Ph, Thr, 181)) 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:28176663

Appears in Networks:

a(CHEBI:glyceraldehyde) increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

Aβ 42 in the medium decreased in a GA dose-dependent manner (Fig. 3a). In contrast, GA significantly increased tau and its phosphorylated form, p-tauT181 (Fig. 3b,c) in the medium. In addition, VEGF (Fig. 3e) and TGF-β (Fig. 3f), which are also AD biomarkers, were increased when the concentration of GA added was greater than 0.7 mM. PubMed:26304819

Appears in Networks:

a(HBP:"advanced glycation end product") increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) 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:28176663

Appears in Networks:

act(p(HGNC:CDK5)) increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

Here, we found that prephosphorylation by PKA promotes GSK-3beta-catalyzed tau phosphorylation at Thr181, Ser199, Ser202, Thr205, Thr217, Thr231, Ser396 and Ser422, but inhibits its phosphorylation at Thr212 and Ser404. In contrast, the prephosphorylation had no significant effect on its subsequent phosphorylation by cdk5 at Thr181, Ser199, Thr205, Thr231 and Ser422; inhibited it at Ser202, Thr212, Thr217 and Ser404; and slightly promoted it at Ser396. PubMed:17078951

Appears in Networks:

p(HGNC:MAPK13) increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

All five SAP kinases generated the AT270 epitope, indicative of phosphorylation of T181 in tau. PubMed:11943212

Appears in Networks:

p(FPLX:PKA) positiveCorrelation p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

Here, we found that prephosphorylation by PKA promotes GSK-3beta-catalyzed tau phosphorylation at Thr181, Ser199, Ser202, Thr205, Thr217, Thr231, Ser396 and Ser422, but inhibits its phosphorylation at Thr212 and Ser404. In contrast, the prephosphorylation had no significant effect on its subsequent phosphorylation by cdk5 at Thr181, Ser199, Thr205, Thr231 and Ser422; inhibited it at Ser202, Thr212, Thr217 and Ser404; and slightly promoted it at Ser396. PubMed:17078951

Appears in Networks:

act(p(HGNC:GSK3B), ma(kin)) increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

Here, we found that prephosphorylation by PKA promotes GSK-3beta-catalyzed tau phosphorylation at Thr181, Ser199, Ser202, Thr205, Thr217, Thr231, Ser396 and Ser422, but inhibits its phosphorylation at Thr212 and Ser404. In contrast, the prephosphorylation had no significant effect on its subsequent phosphorylation by cdk5 at Thr181, Ser199, Thr205, Thr231 and Ser422; inhibited it at Ser202, Thr212, Thr217 and Ser404; and slightly promoted it at Ser396. PubMed:17078951

Appears in Networks:

p(HGNC:MAPK11) increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

All five SAP kinases generated the AT270 epitope, indicative of phosphorylation of T181 in tau. PubMed:11943212

Appears in Networks:

p(HGNC:MAPK12) increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

All five SAP kinases generated the AT270 epitope, indicative of phosphorylation of T181 in tau. PubMed:11943212

Appears in Networks:

p(HGNC:MAPK14) increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

All five SAP kinases generated the AT270 epitope, indicative of phosphorylation of T181 in tau. PubMed:11943212

Appears in Networks:

p(HGNC:MAPK8) increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

All five SAP kinases generated the AT270 epitope, indicative of phosphorylation of T181 in tau. PubMed:11943212

Appears in Networks:

Out-Edges 6

p(HGNC:MAPT, pmod(Ph, Thr, 181)) association a(MESH:Exosomes) View Subject | View Object

In support, tau associated with exosomes and phosphorylated at Thr-181 (AT270+ tau) has been identified in human CSF samples of AD patients PubMed:28420982

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebrospinal Fluid
MeSH
Alzheimer Disease

p(HGNC:MAPT, pmod(Ph, Thr, 181)) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

More recently, patients affected with FTD and AD, were found to have high levels of total tau and phosphorylated tau (p-T181 and p-S396; Saman et al., 2012) PubMed:28420982

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebrospinal Fluid
MeSH
Alzheimer Disease

p(HGNC:MAPT, pmod(Ph, Thr, 181)) positiveCorrelation path(MESH:"Frontotemporal Dementia") View Subject | View Object

More recently, patients affected with FTD and AD, were found to have high levels of total tau and phosphorylated tau (p-T181 and p-S396; Saman et al., 2012) PubMed:28420982

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebrospinal Fluid
MeSH
Alzheimer Disease

p(HGNC:MAPT, pmod(Ph, Thr, 181)) positiveCorrelation a(CHEBI:"D-ribose") 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:28176663

Appears in Networks:

p(HGNC:MAPT, pmod(Ph, Thr, 181)) positiveCorrelation p(FPLX:PKA) View Subject | View Object

Here, we found that prephosphorylation by PKA promotes GSK-3beta-catalyzed tau phosphorylation at Thr181, Ser199, Ser202, Thr205, Thr217, Thr231, Ser396 and Ser422, but inhibits its phosphorylation at Thr212 and Ser404. In contrast, the prephosphorylation had no significant effect on its subsequent phosphorylation by cdk5 at Thr181, Ser199, Thr205, Thr231 and Ser422; inhibited it at Ser202, Thr212, Thr217 and Ser404; and slightly promoted it at Ser396. PubMed:17078951

Appears in Networks:

p(HGNC:MAPT, pmod(Ph, Thr, 181)) partOf p(HBP:"Tau epitope, AT270") View Subject | View Object

Appears in Networks:

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.