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p(HGNC:TTBK2, var("p.Glu450*"))

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

Entity

Name
TTBK2
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 1

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 2

p(HGNC:TTBK2) hasVariant p(HGNC:TTBK2, var("p.Glu450*")) View Subject | View Object

Appears in Networks:

path(HBP:"Spinocerebellar Ataxia 11") positiveCorrelation p(HGNC:TTBK2, var("p.Glu450*")) View Subject | View Object

SCA11 truncating mutations promote TTBK2 protein expression, suppress kinase activity and lead to enhanced nuclear localization. Using a SCA11-mutation-carrying knockin mouse we show that this leads to inhibition of endogenous TTBK2 protein kinase activity. PubMed:21548880

Appears in Networks:

Out-Edges 3

p(HGNC:TTBK2, var("p.Glu450*")) positiveCorrelation path(HBP:"Spinocerebellar Ataxia 11") View Subject | View Object

SCA11 truncating mutations promote TTBK2 protein expression, suppress kinase activity and lead to enhanced nuclear localization. Using a SCA11-mutation-carrying knockin mouse we show that this leads to inhibition of endogenous TTBK2 protein kinase activity. PubMed:21548880

Appears in Networks:

p(HGNC:TTBK2, var("p.Glu450*")) increases p(HGNC:TTBK2) View Subject | View Object

SCA11 truncating mutations promote TTBK2 protein expression, suppress kinase activity and lead to enhanced nuclear localization. Using a SCA11-mutation-carrying knockin mouse we show that this leads to inhibition of endogenous TTBK2 protein kinase activity. PubMed:21548880

Appears in Networks:

p(HGNC:TTBK2, var("p.Glu450*")) decreases act(p(HGNC:TTBK2), ma(kin)) View Subject | View Object

SCA11 truncating mutations promote TTBK2 protein expression, suppress kinase activity and lead to enhanced nuclear localization. Using a SCA11-mutation-carrying knockin mouse we show that this leads to inhibition of endogenous TTBK2 protein kinase activity. PubMed:21548880

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.