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Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 7

a(CHEBI:harmine) decreases p(HGNC:DYRK1A) View Subject | View Object

Neprilysin, a major Aß-degrading enzyme, was downregulated in DS patient-derived fibroblasts. Treatment with harmine, a DYRK1A inhibitor and gene knockdown of DYRK1A, upregulated neprilysin in fibroblasts. PubMed:28250274

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MeSH
Down Syndrome

a(HBP:"ID-8") decreases act(p(HGNC:DYRK1A), ma(kin)) View Subject | View Object

ID-8 indeed showed selectivity against the CMGC kinase family, with DYRK1B, GSK3B and DYRK1A being the top three kinase targets. Although a biotinylated derivative of ID-8 bound DYRK2 and DYRK4 in affinity chromatography pull down assays (Hasegawa et al., 2012), ID-8 itself showed little activity against these kinases, or against DYRK3. Next we determined IC50 values for a subset of these kinase targets, using the same 33P incorporation assay (Table 1). PubMed:28884684

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bp(GO:"neuron differentiation") positiveCorrelation act(p(HGNC:DYRK1A), ma(kin)) View Subject | View Object

Here we present evidence that the indole compound ID-8 and a series of related molecules act to inhibit the neural specification of hESC through inhibition of DYRK1A. PubMed:28884684

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p(HBP:"NP_001387.2:p.Arg205del") decreases act(p(HGNC:DYRK1A)) View Subject | View Object

We conclude that the Dyrk1a dosage is critical for proper neurite and axonal outgrowth and that the two nonsense mutations, R205X and E239X, are loss-of-function mutants. PubMed:28167836

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p(HBP:"NP_001387.2:p.Glu239del") decreases act(p(HGNC:DYRK1A)) View Subject | View Object

We conclude that the Dyrk1a dosage is critical for proper neurite and axonal outgrowth and that the two nonsense mutations, R205X and E239X, are loss-of-function mutants. PubMed:28167836

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p(HGNC:MME) negativeCorrelation p(HGNC:DYRK1A) View Subject | View Object

Neprilysin, a major Aß-degrading enzyme, was downregulated in DS patient-derived fibroblasts. Treatment with harmine, a DYRK1A inhibitor and gene knockdown of DYRK1A, upregulated neprilysin in fibroblasts. PubMed:28250274

Appears in Networks:
Annotations
MeSH
Down Syndrome

Out-Edges 5

act(p(HGNC:DYRK1A), ma(kin)) positiveCorrelation bp(GO:"neuron differentiation") View Subject | View Object

Here we present evidence that the indole compound ID-8 and a series of related molecules act to inhibit the neural specification of hESC through inhibition of DYRK1A. PubMed:28884684

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p(HGNC:DYRK1A) negativeCorrelation p(HGNC:MME) View Subject | View Object

Neprilysin, a major Aß-degrading enzyme, was downregulated in DS patient-derived fibroblasts. Treatment with harmine, a DYRK1A inhibitor and gene knockdown of DYRK1A, upregulated neprilysin in fibroblasts. PubMed:28250274

Appears in Networks:
Annotations
MeSH
Down Syndrome

p(HGNC:DYRK1A) biomarkerFor path(MESH:"Alzheimer Disease") View Subject | View Object

Receiver-operating characteristic curves and logistic regression analyses showed that combined assessment of DYRK1A, BDNF and homocysteine has a sensitivity of 0.952, a specificity of 0.889 and an accuracy of 0.933 in testing for AD. The blood levels of these markers provide a diagnosis assessment profile. Combined assessment of these three markers outperforms most of the previous markers and could become a useful substitute to the current panel of AD biomarkers. PubMed:28632203

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Annotations
Uberon
blood plasma
MeSH
Alzheimer Disease

act(p(HGNC:DYRK1A)) regulates a(HBP:Neurites) View Subject | View Object

We conclude that the Dyrk1a dosage is critical for proper neurite and axonal outgrowth and that the two nonsense mutations, R205X and E239X, are loss-of-function mutants. PubMed:28167836

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act(p(HGNC:DYRK1A)) regulates a(GO:axon) View Subject | View Object

We conclude that the Dyrk1a dosage is critical for proper neurite and axonal outgrowth and that the two nonsense mutations, R205X and E239X, are loss-of-function mutants. PubMed:28167836

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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.