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Entity

Name
Hot Temperature
Namespace
MeSH
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/01c9daa61012b37dd0a1bc962521ba51a15b38f1/external/mesh-names.belns

Appears in Networks 2

TAU and Interaction Partners v1.2.5

TAU Interactions Section of NESTOR

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 2

p(HGNC:MAPT) negativeCorrelation bp(MESH:"Hot Temperature") View Subject | View Object

In this work, we demonstrate that acute oxidative stress and mild heat stress (HS) induce the accumulation of dephosphorylated Tau in neuronal nuclei. Using chromatin immunoprecipitation assays, we demonstrate that the capacity of endogenous Tau to interact with neuronal DNA increased following HS. Comet assays performed on both wildtype and Tau-deficient neuronal cultures showed that Tau fully protected neuronal genomic DNA against HS-induced damage. Interestingly, HS-induced DNA damage observed in Tau-deficient cells was completely rescued after the overexpression of human Tau targeted to the nucleus. PubMed:21131359

a(HBP:"O-GlcNAcylation") association bp(MESH:"Hot Temperature") View Subject | View Object

This post-translational modification is likely an indicator of good health since its intracellular level correlates with the availability of extracellular glucose. From a more practical point of view, it has been shown that O-GlcNAcylation impairments contribute to the etiology of cardiovascular diseases, type-2 diabetes and Alzheimer's disease (AD), three illnesses common in occidental societies. PubMed:19732809

Appears in Networks:

Out-Edges 6

bp(MESH:"Hot Temperature") increases complex(a(CHEBI:"double-stranded DNA"), p(HGNC:MAPT)) View Subject | View Object

In this work, we demonstrate that acute oxidative stress and mild heat stress (HS) induce the accumulation of dephosphorylated Tau in neuronal nuclei. Using chromatin immunoprecipitation assays, we demonstrate that the capacity of endogenous Tau to interact with neuronal DNA increased following HS. Comet assays performed on both wildtype and Tau-deficient neuronal cultures showed that Tau fully protected neuronal genomic DNA against HS-induced damage. Interestingly, HS-induced DNA damage observed in Tau-deficient cells was completely rescued after the overexpression of human Tau targeted to the nucleus. PubMed:21131359

bp(MESH:"Hot Temperature") increases tloc(p(HGNC:MAPT), fromLoc(GO:cytoplasm), toLoc(GO:nucleus)) View Subject | View Object

In this work, we demonstrate that acute oxidative stress and mild heat stress (HS) induce the accumulation of dephosphorylated Tau in neuronal nuclei. Using chromatin immunoprecipitation assays, we demonstrate that the capacity of endogenous Tau to interact with neuronal DNA increased following HS. Comet assays performed on both wildtype and Tau-deficient neuronal cultures showed that Tau fully protected neuronal genomic DNA against HS-induced damage. Interestingly, HS-induced DNA damage observed in Tau-deficient cells was completely rescued after the overexpression of human Tau targeted to the nucleus. PubMed:21131359

bp(MESH:"Hot Temperature") negativeCorrelation p(HGNC:MAPT) View Subject | View Object

In this work, we demonstrate that acute oxidative stress and mild heat stress (HS) induce the accumulation of dephosphorylated Tau in neuronal nuclei. Using chromatin immunoprecipitation assays, we demonstrate that the capacity of endogenous Tau to interact with neuronal DNA increased following HS. Comet assays performed on both wildtype and Tau-deficient neuronal cultures showed that Tau fully protected neuronal genomic DNA against HS-induced damage. Interestingly, HS-induced DNA damage observed in Tau-deficient cells was completely rescued after the overexpression of human Tau targeted to the nucleus. PubMed:21131359

bp(MESH:"Hot Temperature") decreases a(CHEBI:"double-stranded DNA") View Subject | View Object

In this work, we demonstrate that acute oxidative stress and mild heat stress (HS) induce the accumulation of dephosphorylated Tau in neuronal nuclei. Using chromatin immunoprecipitation assays, we demonstrate that the capacity of endogenous Tau to interact with neuronal DNA increased following HS. Comet assays performed on both wildtype and Tau-deficient neuronal cultures showed that Tau fully protected neuronal genomic DNA against HS-induced damage. Interestingly, HS-induced DNA damage observed in Tau-deficient cells was completely rescued after the overexpression of human Tau targeted to the nucleus. PubMed:21131359

bp(MESH:"Hot Temperature") increases p(HGNC:MAPT, pmod(HBP:hyperphosphorylation)) View Subject | View Object

>8 phosphates per tau molecules (vs 2 in adult healthy brain); can also be increased during development, hibernation and temperature, heat and oxydative stress These phosphorylated states are detected by specific antibodies and are targets of proline-directed kinases (SP motifs), non-proline kinases (KXGS motif) Weakens tau-MT interaction especially S261 in R1 and S214 in proline-rich domain PubMed:8226987

Appears in Networks:

bp(MESH:"Hot Temperature") association a(HBP:"O-GlcNAcylation") View Subject | View Object

This post-translational modification is likely an indicator of good health since its intracellular level correlates with the availability of extracellular glucose. From a more practical point of view, it has been shown that O-GlcNAcylation impairments contribute to the etiology of cardiovascular diseases, type-2 diabetes and Alzheimer's disease (AD), three illnesses common in occidental societies. PubMed:19732809

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.