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p(HGNC:DKK1)

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Entity

Name
DKK1
Namespace
hgnc
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/hgnc-symbols.belns

Appears in Networks 3

A role for APP in Wnt signalling links synapse loss with β-amyloid production. v1.0.0

TAU and Interaction Partners v1.2.5

TAU Interactions Section of NESTOR

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 8

composite(a(CHEBI:"fasudil hydrochloride"), p(HGNC:DKK1)) hasComponent p(HGNC:DKK1) View Subject | View Object

Appears in Networks:

p(HGNC:APP) increases act(p(HGNC:DKK1)) View Subject | View Object

Overexpression of APP enhanced the inhibitory effects of Dkk1 on Wnt3a induced Wnt-β-catenin signalling, counteracting the enhanced activity resulting from APP overexpression and reducing the IC50 of Dkk1 to 122ng/mL from 173ng/mL in the absence of APP (Fig. 2f) . PubMed:30232325

Appears in Networks:
Annotations
Confidence
Medium

p(HGNC:APP) increases act(p(HGNC:DKK1)) View Subject | View Object

In contrast, the stimulatory effects of Dkk1 on WntPCP signalling induced by Wnt5a were enhanced by APP overexpression, decreasing the EC50 of Dkk1 to 599ng/ mL from 1405ng/mL (Fig. 2g). PubMed:30232325

Appears in Networks:
Annotations
Confidence
High

composite(p(HGNC:APP), p(HGNC:DKK1)) hasComponent p(HGNC:DKK1) View Subject | View Object

Appears in Networks:

bp(GO:"inflammatory response") increases p(HGNC:DKK1) View Subject | View Object

For example, ongoing inflammation can trigger various cell stress-response pathways, including overexpression of the secreted glycoprotein Dickopff-1 (DKK-1). DKK-1 up-regulates GSK-3β activity, promotes tau hyper-phosphorylation, NFT formation and neuronal degeneration. Thus, DKK-1 inhibits Wnt signalling in a manner similar to Aβ, and thereby fosters a self-sustaining feedback loop resulting in cellular injury PubMed:18494933

Appears in Networks:

p(FPLX:JNK) increases p(HGNC:DKK1) View Subject | View Object

Utilizing Western blot, electrophoretic mobility shift assay, supershift and reverse transcriptase-polymerase chain reaction techniques, it has been demonstrated that micromolar S100B concentrations stimulate c-Jun N-terminal kinase (JNK) phosphorylation through the receptor for advanced glycation ending products, and subsequently activate nuclear AP-1/cJun transcription, in cultured human neural stem cells. In addition, as revealed by Western blot, small interfering RNA and immunofluorescence analysis, S100B-induced JNK activation increased expression of Dickopff-1 that, in turn, promoted glycogen synthase kinase 3β phosphorylation and β-catenin degradation, causing canonical Wnt pathway disruption and tau protein hyperphosphorylation. These findings propose a previously unrecognized link between S100B and tau hyperphosphorylation, suggesting S100B can contribute to NFT formation in AD and in all other conditions in which neuroinflammation may have a crucial role. PubMed:18494933

Appears in Networks:

act(p(FPLX:JNK)) increases p(HGNC:DKK1) View Subject | View Object

In addition, as revealed by Western blot, small interfering RNA and immunofluorescence analysis, S100B-induced JNK activation increased expression of Dickopff-1 that, in turn, promoted glycogen synthase kinase 3-beta phosphorylation and beta-catenin degradation, causing canonical Wnt pathway disruption and tau protein hyperphosphorylation. PubMed:18494933

Appears in Networks:

deg(p(HGNC:CTNNB1)) positiveCorrelation p(HGNC:DKK1) View Subject | View Object

In addition, as revealed by Western blot, small interfering RNA and immunofluorescence analysis, S100B-induced JNK activation increased expression of Dickopff-1 that, in turn, promoted glycogen synthase kinase 3-beta phosphorylation and beta-catenin degradation, causing canonical Wnt pathway disruption and tau protein hyperphosphorylation. PubMed:18494933

Appears in Networks:

Out-Edges 13

p(HGNC:DKK1) decreases a(MESH:"Dendritic Spines") View Subject | View Object

Dkk1 resulted in substantial loss of dendritic spines, which was blocked by 10µM fasudil treatment (Fig. 3e, f). PubMed:30232325

Appears in Networks:
Annotations
Confidence
High

act(p(HGNC:DKK1)) decreases act(p(HGNC:WNT3A)) View Subject | View Object

Overexpression of APP enhanced the inhibitory effects of Dkk1 on Wnt3a induced Wnt-β-catenin signalling, counteracting the enhanced activity resulting from APP overexpression and reducing the IC50 of Dkk1 to 122ng/mL from 173ng/mL in the absence of APP (Fig. 2f) . PubMed:30232325

Appears in Networks:
Annotations
Confidence
Medium

act(p(HGNC:DKK1)) decreases bp(GO:"canonical Wnt signaling pathway") View Subject | View Object

Overexpression of APP enhanced the inhibitory effects of Dkk1 on Wnt3a induced Wnt-β-catenin signalling, counteracting the enhanced activity resulting from APP overexpression and reducing the IC50 of Dkk1 to 122ng/mL from 173ng/mL in the absence of APP (Fig. 2f) . PubMed:30232325

Appears in Networks:
Annotations
Confidence
Medium

act(p(HGNC:DKK1)) increases act(p(HGNC:WNT5A)) View Subject | View Object

In contrast, the stimulatory effects of Dkk1 on WntPCP signalling induced by Wnt5a were enhanced by APP overexpression, decreasing the EC50 of Dkk1 to 599ng/ mL from 1405ng/mL (Fig. 2g). PubMed:30232325

Appears in Networks:
Annotations
Confidence
High

act(p(HGNC:DKK1)) increases bp(GO:"Wnt signaling pathway, planar cell polarity pathway") View Subject | View Object

In contrast, the stimulatory effects of Dkk1 on WntPCP signalling induced by Wnt5a were enhanced by APP overexpression, decreasing the EC50 of Dkk1 to 599ng/ mL from 1405ng/mL (Fig. 2g). PubMed:30232325

Appears in Networks:
Annotations
Confidence
High

p(HGNC:DKK1) increases bp(HBP:HBP00061) View Subject | View Object

Aβ synaptoxicity is Dkk1-dependent12,24 and also appears to be APP-dependent25. PubMed:30232325

Appears in Networks:
Annotations
Confidence
High

p(HGNC:DKK1) decreases a(MESH:"Dendritic Spines") View Subject | View Object

In addition to causing a significant reduction in the numbers of dendritic spines, Dkk1 treatment also resulted a substantial increase in levels of all three Aβ species (Fig. 3g). PubMed:30232325

Appears in Networks:
Annotations
Confidence
Medium

p(HGNC:DKK1) increases a(CHEBI:"amyloid-beta") View Subject | View Object

In addition to causing a significant reduction in the numbers of dendritic spines, Dkk1 treatment also resulted a substantial increase in levels of all three Aβ species (Fig. 3g). PubMed:30232325

Appears in Networks:
Annotations
Confidence
Medium

p(HGNC:DKK1) increases bp(GO:"amyloid-beta formation") View Subject | View Object

Notably, in parallel with the protective effect of fasudil on synapses (Fig. 3e, f), treatment with fasudil reversed the stimulatory effects of Dkk1 on Aβ production (Fig. 3g). PubMed:30232325

Appears in Networks:
Annotations
Confidence
Medium

p(HGNC:DKK1) increases act(p(HGNC:GSK3B)) View Subject | View Object

For example, ongoing inflammation can trigger various cell stress-response pathways, including overexpression of the secreted glycoprotein Dickopff-1 (DKK-1). DKK-1 up-regulates GSK-3β activity, promotes tau hyper-phosphorylation, NFT formation and neuronal degeneration. Thus, DKK-1 inhibits Wnt signalling in a manner similar to Aβ, and thereby fosters a self-sustaining feedback loop resulting in cellular injury PubMed:18494933

Appears in Networks:

p(HGNC:DKK1) decreases bp(GO:"Wnt signaling pathway") View Subject | View Object

For example, ongoing inflammation can trigger various cell stress-response pathways, including overexpression of the secreted glycoprotein Dickopff-1 (DKK-1). DKK-1 up-regulates GSK-3β activity, promotes tau hyper-phosphorylation, NFT formation and neuronal degeneration. Thus, DKK-1 inhibits Wnt signalling in a manner similar to Aβ, and thereby fosters a self-sustaining feedback loop resulting in cellular injury PubMed:18494933

Appears in Networks:

p(HGNC:DKK1) increases act(p(HGNC:GSK3B), ma(kin)) View Subject | View Object

In addition, as revealed by Western blot, small interfering RNA and immunofluorescence analysis, S100B-induced JNK activation increased expression of Dickopff-1 that, in turn, promoted glycogen synthase kinase 3-beta phosphorylation and beta-catenin degradation, causing canonical Wnt pathway disruption and tau protein hyperphosphorylation. PubMed:18494933

Appears in Networks:

p(HGNC:DKK1) positiveCorrelation deg(p(HGNC:CTNNB1)) View Subject | View Object

In addition, as revealed by Western blot, small interfering RNA and immunofluorescence analysis, S100B-induced JNK activation increased expression of Dickopff-1 that, in turn, promoted glycogen synthase kinase 3-beta phosphorylation and beta-catenin degradation, causing canonical Wnt pathway disruption and tau protein hyperphosphorylation. PubMed:18494933

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.