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p(MGI:Mapt)

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Entity

Name
Mapt
Namespace
MGI
Namespace Version
20170725
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/namespace/mgi-mouse-genes/mgi-mouse-genes-20170725.belns

Appears in Networks 13

Interplay of pathogenic forms of human tau with different autophagic pathways v1.0.1

Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease v1.0.0

Adenosine A1 receptor antagonist 64627 alleviates axonopathy caused by human Tau ΔK280 v1.0.0

Anti-aggregant tau mutant promotes neurogenesis v1.0.0

TFEB enhances astroglial uptake of extracellular tau species and reduces tau spreading v1.0.0

Tau protein aggregation is associated with cellular senescence in the brain v1.0.0

Tau Antibody Targeting Pathological Species Blocks Neuronal Uptake and Interneuron Propagation of Tau in Vitro v1.0.0

This file encodes the article Tau Antibody Targeting Pathological Species Blocks Neuronal Uptake and Interneuron Propagation of Tau in Vitro by Nobuhara et. al. 2017

TAU and Interaction Partners v1.2.5

TAU Interactions Section of NESTOR

Tau Effect on Mitochondria v1.0.3

Tau and mitochondria section of NESTOR

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Tau interactome mapping based identification of Otub1 as Tau deubiquitinase involved in accumulation of pathological Tau forms in vitro and in vivo v1.0.0

The Spleen Tyrosine Kinase (Syk) Regulates Alzheimer Amyloid-β Production and Tau Hyperphosphorylation* v1.0.0

mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0

In-Edges 57

complex(a(GO:lysosome), p(MGI:Mapt)) hasComponent p(MGI:Mapt) View Subject | View Object

Appears in Networks:

a(GO:"late endosome") increases deg(p(MGI:Mapt)) View Subject | View Object

We found that WT tau was taken up and efficiently degraded by LE (Fig. 2c,d) PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain

a(HBP:HBP00054) decreases tloc(p(MGI:Mapt), fromLoc(MESH:"Extracellular Space"), toLoc(GO:lysosome)) View Subject | View Object

In contrast, once the first N-terminal insert is lost (in 0N3R tau), we observed a very pronounced decrease in tau uptake (Fig. 5b,c) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

a(HBP:HBP00055) increases tloc(p(MGI:Mapt), fromLoc(MESH:"Extracellular Space"), toLoc(GO:lysosome)) View Subject | View Object

Absence of the second N-terminal insert (in 1N3R tau) did not reduce CMA of tau, but instead this isoform displayed faster internalization (lower binding because of more efficient uptake) (Fig. 5b,c) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

a(HBP:HBP00055) decreases deg(p(MGI:Mapt)) View Subject | View Object

Absence of the second N-terminal insert also significantly reduced e-MI of tau (Fig. 5e,f) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

a(HBP:HBP00057) increases tloc(p(MGI:Mapt), fromLoc(MESH:"Extracellular Space"), toLoc(GO:lysosome)) View Subject | View Object

Analysis of their uptake by isolated CMA-active lysosomes revealed that 2N3R tau behaved similarly to 2N4R tau (which we have used in the rest of the study as control) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

bp(GO:"chaperone-mediated autophagy") increases deg(p(MGI:Mapt)) View Subject | View Object

In this study, we analyzed the contribution of three different types of autophagy, macroautophagy, chaperone-mediated autophagy, and endosomal microautophagy to the degradation of tau protein variants and tau mutations associated with this agerelated disease. We have found that the pathogenic P301L mutation inhibits degradation of tau by any of the three autophagic pathways, whereas the risk-associated tau mutation A152T reroutes tau for degradation through a different autophagy pathway PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Neurons

bp(GO:"chaperone-mediated autophagy") increases deg(p(MGI:Mapt)) View Subject | View Object

Taken together, our in vitro and cell-based studies argue that these two point mutations, A152T and P301L, reduce the normal degradation of tau by CMA, although the P301L mutation has a more pronounced inhibitory effect PubMed:29024336

Appears in Networks:
Annotations
MeSH
Lysosomes
Confidence
High
MeSH
Brain

bp(GO:"chaperone-mediated autophagy") increases deg(p(MGI:Mapt)) View Subject | View Object

Our previous studies and data presented in this work support substantial contribution of CMA to the degradation of wild-type unmodified tau (Wang et al., 2009) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

bp(GO:"late endosomal microautophagy") increases deg(p(MGI:Mapt)) View Subject | View Object

In this study, we analyzed the contribution of three different types of autophagy, macroautophagy, chaperone-mediated autophagy, and endosomal microautophagy to the degradation of tau protein variants and tau mutations associated with this agerelated disease. We have found that the pathogenic P301L mutation inhibits degradation of tau by any of the three autophagic pathways, whereas the risk-associated tau mutation A152T reroutes tau for degradation through a different autophagy pathway PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Neurons

bp(GO:"late endosomal microautophagy") increases deg(p(MGI:Mapt)) View Subject | View Object

Interestingly, although judging by the studies in intact cells the contribution of e-MI to tau degradation is small (Fig. 2a), our in vitro studies with isolated LE revealed a high efficiency for e-MI of tau (Fig. 2c) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

bp(GO:"protein oxidation") increases tloc(p(MGI:Mapt), fromLoc(MESH:"Extracellular Space"), toLoc(GO:"multivesicular body")) View Subject | View Object

Previous studies have demonstrated that oxidized proteins accumulate inside multivesicular bodies (Cannizzo et al., 2012), suggesting that oxidation may be a prerequisite to complete internalization of tau by e-MI, and that the LE environment may contribute to that modification PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

bp(GO:macroautophagy) increases deg(p(MGI:Mapt)) View Subject | View Object

In this study, we analyzed the contribution of three different types of autophagy, macroautophagy, chaperone-mediated autophagy, and endosomal microautophagy to the degradation of tau protein variants and tau mutations associated with this agerelated disease. We have found that the pathogenic P301L mutation inhibits degradation of tau by any of the three autophagic pathways, whereas the risk-associated tau mutation A152T reroutes tau for degradation through a different autophagy pathway PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Neurons

bp(GO:macroautophagy) decreases deg(p(MGI:Mapt)) View Subject | View Object

Macroautophagy blockage resulted in preferential accumulation of A152T, but not WT and P301L tau (Fig. 2e,f) PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain

p(MGI:Mapt, var("p.Ala152Thr")) decreases deg(p(MGI:Mapt)) View Subject | View Object

In this study, we analyzed the contribution of three different types of autophagy, macroautophagy, chaperone-mediated autophagy, and endosomal microautophagy to the degradation of tau protein variants and tau mutations associated with this agerelated disease. We have found that the pathogenic P301L mutation inhibits degradation of tau by any of the three autophagic pathways, whereas the risk-associated tau mutation A152T reroutes tau for degradation through a different autophagy pathway PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Neurons

p(MGI:Mapt, var("p.Ala152Thr")) increases p(MGI:Mapt) View Subject | View Object

An increase in overall tau levels has been observed in brains from patients bearing either P301L or A152T mutation on tau (Torres et al., 1998) PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain

p(MGI:Mapt, var("p.Ala152Thr")) decreases deg(p(MGI:Mapt)) View Subject | View Object

Taken together, our in vitro and cell-based studies argue that these two point mutations, A152T and P301L, reduce the normal degradation of tau by CMA, although the P301L mutation has a more pronounced inhibitory effect PubMed:29024336

Appears in Networks:
Annotations
MeSH
Lysosomes
Confidence
High
MeSH
Brain

p(MGI:Mapt, var("p.Ala152Thr")) decreases deg(p(MGI:Mapt)) View Subject | View Object

In summary, when comparing the pathogenic tau mutation P301L with the risk-associated mutation A152T, we found that both reduced normal turnover of tau by autophagy, but that the effect of the P301L mutation was more pronounced (summarized in Fig. 2g and Fig. S6, Supporting information) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

p(MGI:Mapt, var("p.Pro301Leu")) decreases deg(p(MGI:Mapt)) View Subject | View Object

In this study, we analyzed the contribution of three different types of autophagy, macroautophagy, chaperone-mediated autophagy, and endosomal microautophagy to the degradation of tau protein variants and tau mutations associated with this agerelated disease. We have found that the pathogenic P301L mutation inhibits degradation of tau by any of the three autophagic pathways, whereas the risk-associated tau mutation A152T reroutes tau for degradation through a different autophagy pathway PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Neurons

p(MGI:Mapt, var("p.Pro301Leu")) increases p(MGI:Mapt) View Subject | View Object

An increase in overall tau levels has been observed in brains from patients bearing either P301L or A152T mutation on tau (Torres et al., 1998) PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain

p(MGI:Mapt, var("p.Pro301Leu")) decreases deg(p(MGI:Mapt)) View Subject | View Object

In contrast, the P301L mutation severely impaired lysosomal uptake of tau by CMA, resulting in a sixfold decrease in degradation when compared to WT tau protein (Fig. 1c,d) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Lysosomes
Confidence
High
MeSH
Brain

p(MGI:Mapt, var("p.Pro301Leu")) decreases deg(p(MGI:Mapt)) View Subject | View Object

Taken together, our in vitro and cell-based studies argue that these two point mutations, A152T and P301L, reduce the normal degradation of tau by CMA, although the P301L mutation has a more pronounced inhibitory effect PubMed:29024336

Appears in Networks:
Annotations
MeSH
Lysosomes
Confidence
High
MeSH
Brain

p(MGI:Mapt, var("p.Pro301Leu")) decreases deg(p(MGI:Mapt)) View Subject | View Object

In summary, when comparing the pathogenic tau mutation P301L with the risk-associated mutation A152T, we found that both reduced normal turnover of tau by autophagy, but that the effect of the P301L mutation was more pronounced (summarized in Fig. 2g and Fig. S6, Supporting information) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

p(HGNC:MAPT, var("p.Ala152Thr")) decreases deg(p(MGI:Mapt)) View Subject | View Object

Tau-A152T displayed very similar degradation dynamics, although this mutation slightly reduced tau’s rates of lysosomal degradation (20% inhibition) when compared with WT tau (Fig. 1a,b). PubMed:29024336

Appears in Networks:
Annotations
MeSH
Lysosomes
Confidence
High
MeSH
Brain

complex(a(GO:microtubule), p(MGI:Mapt)) hasComponent p(MGI:Mapt) View Subject | View Object

Appears in Networks:

composite(a(HP:"Argyrophilic inclusion bodies"), p(MGI:Mapt)) hasComponent p(MGI:Mapt) View Subject | View Object

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases p(MGI:Mapt) View Subject | View Object

In the controls and the antiaggregant TauRDΔKPP slices there was a uniform axonal distribution of Tau in the hippocampus (Fig. 5, A1 and 2) PubMed:29202785

Appears in Networks:
Annotations
MeSH
Axons
MeSH
Hippocampus

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases p(MGI:Mapt) View Subject | View Object

Surprisingly, there was an ~80% increase in the endogenous mouse Tau level in slices obtained from pups expressing anti-aggregant TauRDΔKPP (Fig. 5b lane 2 and 5c bar 2), compared with age matched non-transgenic controls and pro-aggregant TauRDΔK (Fig. 5b lane 1 and 3; and 5c lane 1 and 3) PubMed:29202785

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases tloc(p(MGI:Mapt), fromLoc(GO:axon), toLoc(GO:"somatodendritic compartment")) View Subject | View Object

In spite of this increase, there was little mislocalization of Tau (endogenous or exogenous) into the somatodendritic compartment in the anti-aggregant TauRDΔKPP (Fig. 5, A2) PubMed:29202785

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases p(MGI:Mapt) View Subject | View Object

From DIV15 until DIV30 the anti-aggregant slices were treated with DOX to switch off the expression of the anti-aggregant Tau. This lead to a strong reduction (~70%) of the endogenous mouse Tau (Fig. 10c, lane3) PubMed:29202785

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) increases tloc(p(MGI:Mapt), fromLoc(GO:axon), toLoc(GO:"somatodendritic compartment")) View Subject | View Object

The pro-aggregant TauRDΔK slices showed intense mislocalization of Tau in the somato-dendritic compartment, the most affected being the CA3 pyramidal neurons (Fig. 5, A3) PubMed:29202785

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) causesNoChange p(MGI:Mapt) View Subject | View Object

By contrast, pro-aggregant TauRDΔK slices showed no overall increase in endogenous mouse Tau (rather a 20% decrease), yet pronounced mislocalization (Fig. 5, A3). PubMed:29202785

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) increases tloc(p(MGI:Mapt), fromLoc(GO:axon), toLoc(GO:"somatodendritic compartment")) View Subject | View Object

By contrast, pro-aggregant TauRDΔK slices showed no overall increase in endogenous mouse Tau (rather a 20% decrease), yet pronounced mislocalization (Fig. 5, A3). PubMed:29202785

Appears in Networks:

p(MGI:Tfeb) decreases p(MGI:Mapt) View Subject | View Object

In the insoluble fraction, phospho- and total tau species were all reduced in the TFEB mice, as demonstrated by Western blot PubMed:30108137

Appears in Networks:
Annotations
Cell Ontology (CL)
astrocyte

a(HBP:"Tau antibody, 40E8") decreases p(MGI:Mapt, loc(GO:cell)) View Subject | View Object

Among the seven antibodies, Tau13 and 6C5 most efficiently removed tau (>85% reduction) from rTg4510 brain extracts on immunodepletion (Figure 2A). HT7 showed an intermediate effect (72% reduction), whereas the other four antibodies (40E8, 4E4, p396, and Tau46) removed only a small fraction of tau (5.6%, 16.6%, 8.4%, and 18% reductions, respectively) (Figure 2A). PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(HBP:"Tau antibody, 40E8") decreases tloc(p(MGI:Mapt), fromLoc(GO:"extracellular region"), toLoc(GO:intracellular)) View Subject | View Object

The 40E8, 4E4, and p396 antibodies also reduced neuronal tau uptake by 40% to 80%, despite their low-immunodepletion efficiency (Figure 2). This finding suggests that they interacted with tau species that are prone to cellular uptake, which account for only a small fraction of all soluble tau species in the brain extract. Notably, Tau46 had little effect on tau uptake (Figure 2, B and C). PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(HBP:"Tau antibody, 4E4") decreases p(MGI:Mapt, loc(GO:cell)) View Subject | View Object

Among the seven antibodies, Tau13 and 6C5 most efficiently removed tau (>85% reduction) from rTg4510 brain extracts on immunodepletion (Figure 2A). HT7 showed an intermediate effect (72% reduction), whereas the other four antibodies (40E8, 4E4, p396, and Tau46) removed only a small fraction of tau (5.6%, 16.6%, 8.4%, and 18% reductions, respectively) (Figure 2A). PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(HBP:"Tau antibody, 4E4") decreases tloc(p(MGI:Mapt), fromLoc(GO:"extracellular region"), toLoc(GO:intracellular)) View Subject | View Object

The 40E8, 4E4, and p396 antibodies also reduced neuronal tau uptake by 40% to 80%, despite their low-immunodepletion efficiency (Figure 2). This finding suggests that they interacted with tau species that are prone to cellular uptake, which account for only a small fraction of all soluble tau species in the brain extract. Notably, Tau46 had little effect on tau uptake (Figure 2, B and C). PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(HBP:"Tau antibody, 6C5") decreases p(MGI:Mapt, loc(GO:cell)) View Subject | View Object

Among the seven antibodies, Tau13 and 6C5 most efficiently removed tau (>85% reduction) from rTg4510 brain extracts on immunodepletion (Figure 2A). HT7 showed an intermediate effect (72% reduction), whereas the other four antibodies (40E8, 4E4, p396, and Tau46) removed only a small fraction of tau (5.6%, 16.6%, 8.4%, and 18% reductions, respectively) (Figure 2A). PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(HBP:"Tau antibody, 6C5") decreases tloc(p(MGI:Mapt), fromLoc(GO:"extracellular region"), toLoc(GO:intracellular)) View Subject | View Object

Confocal FRET image analysis showed robust tau aggregation in primary neurons treated with control IgG-immunodepleted rTg4510 brain extracts (Figure 2, B and C).The 6C5 antibody most successfully reduced tau uptake by immunodepletion (>90% reduction), and Tau13 and HT7 showed intermediate effects (approximately 60% reductions) (Figure 2, B and C) PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(HBP:"Tau antibody, HT7") decreases p(MGI:Mapt, loc(GO:cell)) View Subject | View Object

Among the seven antibodies, Tau13 and 6C5 most efficiently removed tau (>85% reduction) from rTg4510 brain extracts on immunodepletion (Figure 2A). HT7 showed an intermediate effect (72% reduction), whereas the other four antibodies (40E8, 4E4, p396, and Tau46) removed only a small fraction of tau (5.6%, 16.6%, 8.4%, and 18% reductions, respectively) (Figure 2A). PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(HBP:"Tau antibody, HT7") decreases tloc(p(MGI:Mapt), fromLoc(GO:"extracellular region"), toLoc(GO:intracellular)) View Subject | View Object

Confocal FRET image analysis showed robust tau aggregation in primary neurons treated with control IgG-immunodepleted rTg4510 brain extracts (Figure 2, B and C).The 6C5 antibody most successfully reduced tau uptake by immunodepletion (>90% reduction), and Tau13 and HT7 showed intermediate effects (approximately 60% reductions) (Figure 2, B and C) PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(HBP:"Tau antibody, Tau-13") decreases p(MGI:Mapt, loc(GO:cell)) View Subject | View Object

Among the seven antibodies, Tau13 and 6C5 most efficiently removed tau (>85% reduction) from rTg4510 brain extracts on immunodepletion (Figure 2A). HT7 showed an intermediate effect (72% reduction), whereas the other four antibodies (40E8, 4E4, p396, and Tau46) removed only a small fraction of tau (5.6%, 16.6%, 8.4%, and 18% reductions, respectively) (Figure 2A). PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(HBP:"Tau antibody, Tau-13") decreases tloc(p(MGI:Mapt), fromLoc(GO:"extracellular region"), toLoc(GO:intracellular)) View Subject | View Object

Confocal FRET image analysis showed robust tau aggregation in primary neurons treated with control IgG-immunodepleted rTg4510 brain extracts (Figure 2, B and C).The 6C5 antibody most successfully reduced tau uptake by immunodepletion (>90% reduction), and Tau13 and HT7 showed intermediate effects (approximately 60% reductions) (Figure 2, B and C) PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(HBP:"Tau antibody, pS396") decreases p(MGI:Mapt, loc(GO:cell)) View Subject | View Object

Among the seven antibodies, Tau13 and 6C5 most efficiently removed tau (>85% reduction) from rTg4510 brain extracts on immunodepletion (Figure 2A). HT7 showed an intermediate effect (72% reduction), whereas the other four antibodies (40E8, 4E4, p396, and Tau46) removed only a small fraction of tau (5.6%, 16.6%, 8.4%, and 18% reductions, respectively) (Figure 2A). PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(HBP:"Tau antibody, pS396") decreases tloc(p(MGI:Mapt), fromLoc(GO:"extracellular region"), toLoc(GO:intracellular)) View Subject | View Object

The 40E8, 4E4, and p396 antibodies also reduced neuronal tau uptake by 40% to 80%, despite their low-immunodepletion efficiency (Figure 2). This finding suggests that they interacted with tau species that are prone to cellular uptake, which account for only a small fraction of all soluble tau species in the brain extract. Notably, Tau46 had little effect on tau uptake (Figure 2, B and C). PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

a(CHEBI:"2-bromohexadecanoic acid") negativeCorrelation p(MGI:Mapt) View Subject | View Object

A rapid but transient increase was found in the amount of fyn detected in DRMs on ADDL exposure for 2 min that was partially reduced after 10 min exposure. Mirroring the movement of fyn into the DRM, tau content of DRMs increased in response to ADDLs. To further test a putative association between fyn and tau levels in DRMs, we treated cells with 2-bromopalmitate, an inhibitor of protein palmitoylation, which is required for fyn’s localization in DRMs. This treatment resulted in a progressive reduction in both fyn and tau in DRMs, demonstrating that the association of tau with DRMs may be directly regulated by fyn (Supplemental Fig. 2). PubMed:18096814

Appears in Networks:
Annotations
MeSH
Hippocampus

a(HBP:"amyloid-beta derived diffusible ligands") increases tloc(p(MGI:Mapt), fromLoc(GO:cytoplasm), toLoc(GO:"membrane raft")) View Subject | View Object

A rapid but transient increase was found in the amount of fyn detected in DRMs on ADDL exposure for 2 min that was partially reduced after 10 min exposure. Mirroring the movement of fyn into the DRM, tau content of DRMs increased in response to ADDLs. To further test a putative association between fyn and tau levels in DRMs, we treated cells with 2-bromopalmitate, an inhibitor of protein palmitoylation, which is required for fyn’s localization in DRMs. This treatment resulted in a progressive reduction in both fyn and tau in DRMs, demonstrating that the association of tau with DRMs may be directly regulated by fyn (Supplemental Fig. 2). PubMed:18096814

Appears in Networks:
Annotations
MeSH
Hippocampus

p(MGI:Fyn) regulates tloc(p(MGI:Mapt), fromLoc(GO:cytoplasm), toLoc(GO:"membrane raft")) View Subject | View Object

A rapid but transient increase was found in the amount of fyn detected in DRMs on ADDL exposure for 2 min that was partially reduced after 10 min exposure. Mirroring the movement of fyn into the DRM, tau content of DRMs increased in response to ADDLs. To further test a putative association between fyn and tau levels in DRMs, we treated cells with 2-bromopalmitate, an inhibitor of protein palmitoylation, which is required for fyn’s localization in DRMs. This treatment resulted in a progressive reduction in both fyn and tau in DRMs, demonstrating that the association of tau with DRMs may be directly regulated by fyn (Supplemental Fig. 2). PubMed:18096814

Appears in Networks:
Annotations
MeSH
Hippocampus

complex(p(HGNC:FYN), p(MGI:Mapt)) hasComponent p(MGI:Mapt) View Subject | View Object

Appears in Networks:

complex(p(MGI:Dapk1), p(MGI:Mapt)) hasComponent p(MGI:Mapt) View Subject | View Object

Appears in Networks:

p(MGI:Dapk1) association p(MGI:Mapt) View Subject | View Object

Direct interaction of DAPK1 with Tau causes spine loss and subsequently neuronal death. DAPK1 phosphorylates Tau protein at Ser262 (pS(262)) in cortical neurons of stroke mice. PubMed:25995053

Appears in Networks:
Annotations
MeSH
Stroke

p(MGI:Dyrk1a) negativeCorrelation p(MGI:Mapt) View Subject | View Object

Normalizing the gene dosage of Dyrk1A in the TS mouse rescued the density of senescent cells in the cingulate cortex, hippocampus and septum, prevented cholinergic neuron degeneration, and reduced App expression in the hippocampus, Aß load in the cortex and hippocampus, the expression of phosphorylated tau at the Ser202 residue in the hippocampus and cerebellum and the levels of total tau in the cortex, hippocampus and cerebellum. PubMed:29221819

Appears in Networks:
Annotations
Uberon
cerebellum
Uberon
cerebral cortex
Uberon
hippocampal formation
MeSH
Alzheimer Disease
MeSH
Down Syndrome

complex(p(MGI:Dpysl2, pmod(Ph)), p(MGI:Mapt), p(MGI:Wasf1, pmod(Ph))) hasComponent p(MGI:Mapt) View Subject | View Object

Appears in Networks:

p(MGI:Mapt, pmod(HBP:nitration, Tyr, 488)) causesNoChange act(p(MGI:Mapt)) View Subject | View Object

It was possible to find nitrated Tyr 488 (numbers refer to mouse tau P10637 in the Swiss-Prot/ThEMBL data bank) which corresponds to Tyr 507 in rat tau (Table 1) in accordance with the data reported above for tau in PC12 cells. PubMed:17768677

Appears in Networks:

p(MGI:Syk) positiveCorrelation p(MGI:Mapt) View Subject | View Object

Interestingly, Syk upregulation in SH-SY5Y cells leads to a significant increase (1.7-fold) in phosphorylated tau at Y18 (Fig. 14c, p < 0.01) and at S396/404 (Fig. 14d, 3-fold, p < 0.0001) compared to control cells. Total tau levels are also significantly increased following Syk overexpression (Fig. 14e, 4.2-fold, p < 0.0001). PubMed:28877763

Appears in Networks:

p(MGI:Otub1) increases p(MGI:Mapt) View Subject | View Object

This revealed a significant increase of monomeric Tau and oligomeric Tau in AAV– Otub1-injected mice compared with AAV–GFP-injected mice (Fig. 7c). PubMed:28083634

Appears in Networks:

Out-Edges 59

p(MGI:Mapt) hasVariant p(MGI:Mapt, var("p.Ala152Thr")) View Subject | View Object

Appears in Networks:

p(MGI:Mapt) hasVariant p(MGI:Mapt, var("p.Pro301Leu")) View Subject | View Object

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p(MGI:Mapt) decreases bp(GO:"late endosomal microautophagy") View Subject | View Object

In the presence of any of the tau proteins, we found some sequestration of the probe in the multivesicular bodies, albeit significantly less in cells expressing the WT and A152T protein PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 202), pmod(Ph, Thr, 205)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 214), pmod(Ph, Thr, 212)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 214), var("p.P301S")) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Thr, 212), var("p.P301S")) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Thr, 231)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, var("p.P301L")) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, var("p.P301S")) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 262), pmod(Ph, Ser, 356)) View Subject | View Object

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p(MGI:Mapt) increases bp(GO:"neuron maturation") View Subject | View Object

This suggests that the expression of anti-aggregant TauRDΔKPP is needed for the increased proliferation of newborn neurons, and since these new born neurons need endogenous mouse Tau for their migration, differentiation, and maturation, there is enhanced expression of endogenous mouse Tau PubMed:29202785

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p(MGI:Mapt) increases bp(GO:"neuron migration") View Subject | View Object

This suggests that the expression of anti-aggregant TauRDΔKPP is needed for the increased proliferation of newborn neurons, and since these new born neurons need endogenous mouse Tau for their migration, differentiation, and maturation, there is enhanced expression of endogenous mouse Tau PubMed:29202785

Appears in Networks:

p(MGI:Mapt) increases bp(GO:"neuron differentiation") View Subject | View Object

This suggests that the expression of anti-aggregant TauRDΔKPP is needed for the increased proliferation of newborn neurons, and since these new born neurons need endogenous mouse Tau for their migration, differentiation, and maturation, there is enhanced expression of endogenous mouse Tau PubMed:29202785

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p(MGI:Mapt) increases a(GO:"neurofibrillary tangle") View Subject | View Object

However, genetically ablating endogenous mouse tau (microtubule associated protein tau, Mapt) reduces NFT pathology and neurodegeneration in tauNFT mice (tauNFT-Mapt0/0) (Wegmann et al., 2015) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

p(MGI:Mapt) increases bp(HP:Neurodegeneration) View Subject | View Object

However, genetically ablating endogenous mouse tau (microtubule associated protein tau, Mapt) reduces NFT pathology and neurodegeneration in tauNFT mice (tauNFT-Mapt0/0) (Wegmann et al., 2015) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

p(MGI:Mapt) increases p(MGI:Cdkn2a) View Subject | View Object

The reduced tau pathology corresponded with 60% lower Cdkn2a expression (P = 0.0041, Figure 4a), decreased SASP (Figure S4) and decreased brain atrophy (tauNFT-Mapt0/0: 0.4058 ± 0.009 versus age-matched tauNFT Maptwt/wt: 0.3451 ± 0.0116; 17.5% difference, P = 0.0143, Figure 4b) PubMed:30126037

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

p(MGI:Mapt) increases bp(GO:"cellular senescence") View Subject | View Object

The reduced tau pathology corresponded with 60% lower Cdkn2a expression (P = 0.0041, Figure 4a), decreased SASP (Figure S4) and decreased brain atrophy (tauNFT-Mapt0/0: 0.4058 ± 0.009 versus age-matched tauNFT Maptwt/wt: 0.3451 ± 0.0116; 17.5% difference, P = 0.0143, Figure 4b) PubMed:30126037

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

p(MGI:Mapt) increases path(HP:"Brain atrophy") View Subject | View Object

The reduced tau pathology corresponded with 60% lower Cdkn2a expression (P = 0.0041, Figure 4a), decreased SASP (Figure S4) and decreased brain atrophy (tauNFT-Mapt0/0: 0.4058 ± 0.009 versus age-matched tauNFT Maptwt/wt: 0.3451 ± 0.0116; 17.5% difference, P = 0.0143, Figure 4b) PubMed:30126037

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

tloc(p(MGI:Mapt), fromLoc(GO:"extracellular region"), toLoc(GO:intracellular)) increases a(HBP:"Tau aggregates") View Subject | View Object

Confocal FRET image analysis showed robust tau aggregation in primary neurons treated with control IgG-immunodepleted rTg4510 brain extracts (Figure 2, B and C).The 6C5 antibody most successfully reduced tau uptake by immunodepletion (>90% reduction), and Tau13 and HT7 showed intermediate effects (approximately 60% reductions) (Figure 2, B and C) PubMed:28408124

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Tauopathies
Text Location
Results

p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 202)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 214)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 214), pmod(Ph, Ser, 396)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 235)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 239)) View Subject | View Object

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p(MGI:Mapt) negativeCorrelation a(CHEBI:"2-bromohexadecanoic acid") View Subject | View Object

A rapid but transient increase was found in the amount of fyn detected in DRMs on ADDL exposure for 2 min that was partially reduced after 10 min exposure. Mirroring the movement of fyn into the DRM, tau content of DRMs increased in response to ADDLs. To further test a putative association between fyn and tau levels in DRMs, we treated cells with 2-bromopalmitate, an inhibitor of protein palmitoylation, which is required for fyn’s localization in DRMs. This treatment resulted in a progressive reduction in both fyn and tau in DRMs, demonstrating that the association of tau with DRMs may be directly regulated by fyn (Supplemental Fig. 2). PubMed:18096814

Appears in Networks:
Annotations
MeSH
Hippocampus

p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 262)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 301)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 396)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 400)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 404)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 422)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Thr, 149)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Thr, 153)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Thr, 175)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Thr, 176)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Thr, 205)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Thr, 217)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Thr, 220)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Thr, 403)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Tyr, 18)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ac)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ac, Lys, 174)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ac, Lys, 280)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(HBP:"O-GlcNAcylation")) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(HBP:hyperphosphorylation)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(HBP:nitration, Tyr, 488)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(HBP:nitration, Tyr, 507)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 178)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 195)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 198)) View Subject | View Object

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Ser, 199)) View Subject | View Object

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p(MGI:Mapt) increases complex(p(MGI:Dpysl2, pmod(Ph)), p(MGI:Mapt), p(MGI:Wasf1, pmod(Ph))) View Subject | View Object

First, we verified the colocalization of p-WAVE1 and pCRMP2 with aggregated hyperphosphorylated tau in the hippocampus at 23 months of age. Biochemical analysis revealed the inclusion of p-WAVE1, p-CRMP2, and tau in the sarkosyl-insoluble fractions of hippocampal homogenates PubMed:26400044

Appears in Networks:
Annotations
Uberon
hippocampal formation

p(MGI:Mapt) association p(MGI:Dapk1) View Subject | View Object

Direct interaction of DAPK1 with Tau causes spine loss and subsequently neuronal death. DAPK1 phosphorylates Tau protein at Ser262 (pS(262)) in cortical neurons of stroke mice. PubMed:25995053

Appears in Networks:
Annotations
MeSH
Stroke

p(MGI:Mapt) partOf complex(p(MGI:Dapk1), p(MGI:Mapt)) View Subject | View Object

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p(MGI:Mapt) negativeCorrelation p(MGI:Dyrk1a) View Subject | View Object

Normalizing the gene dosage of Dyrk1A in the TS mouse rescued the density of senescent cells in the cingulate cortex, hippocampus and septum, prevented cholinergic neuron degeneration, and reduced App expression in the hippocampus, Aß load in the cortex and hippocampus, the expression of phosphorylated tau at the Ser202 residue in the hippocampus and cerebellum and the levels of total tau in the cortex, hippocampus and cerebellum. PubMed:29221819

Appears in Networks:
Annotations
Uberon
cerebellum
Uberon
cerebral cortex
Uberon
hippocampal formation
MeSH
Alzheimer Disease
MeSH
Down Syndrome

p(MGI:Mapt) positiveCorrelation p(MGI:Syk) View Subject | View Object

Interestingly, Syk upregulation in SH-SY5Y cells leads to a significant increase (1.7-fold) in phosphorylated tau at Y18 (Fig. 14c, p < 0.01) and at S396/404 (Fig. 14d, 3-fold, p < 0.0001) compared to control cells. Total tau levels are also significantly increased following Syk overexpression (Fig. 14e, 4.2-fold, p < 0.0001). PubMed:28877763

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p(MGI:Mapt) hasVariant p(MGI:Mapt, pmod(Ph, Tyr, 231)) View Subject | View Object

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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.