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Appears in Networks 2

In-Edges 4

act(complex(GO:"protein phosphatase type 2A complex")) negativeCorrelation p(FPLX:PPP2, pmod(Ph, Tyr, 307)) View Subject | View Object

Decreased expression levels of PTPA in AD brain tissue may also lead to inactivation of PP2A by indirectly increasing levels of PP2A phosphorylated at the Tyr-307 site (Luo et al.,2013). PubMed:24653673

act(p(HGNC:GSK3B)) increases p(FPLX:PPP2, pmod(Ph, Tyr, 307)) View Subject | View Object

For instance, activated GSK3β has been reported to induce PP2A inactivation via several mechanisms: phosphorylation of PP2A on Tyr307 (Yao et al.,2011); demethylation of PP2A on Leu309 through inhibition of LCMT1 and up-regulation of PME1 (Yao et al.,2012); and accumulation of I2 PP2A (Liu et al.,2008a). PubMed:24653673

p(HGNC:PTPA) decreases p(FPLX:PPP2, pmod(Ph, Tyr, 307)) View Subject | View Object

Decreased expression levels of PTPA in AD brain tissue may also lead to inactivation of PP2A by indirectly increasing levels of PP2A phosphorylated at the Tyr-307 site (Luo et al.,2013). PubMed:24653673

Out-Edges 3

p(FPLX:PPP2, pmod(Ph, Tyr, 307)) decreases act(p(FPLX:PPP2)) View Subject | View Object

Phosphorylation of Y307 by receptor associated tyrosine kinases effectively decreases the PP2A activity by inhibiting the interaction of PP2Ac with the PP2A-PR55/PR61 subunit [54]. PubMed:23454242

p(FPLX:PPP2, pmod(Ph, Tyr, 307)) negativeCorrelation act(complex(GO:"protein phosphatase type 2A complex")) View Subject | View Object

Decreased expression levels of PTPA in AD brain tissue may also lead to inactivation of PP2A by indirectly increasing levels of PP2A phosphorylated at the Tyr-307 site (Luo et al.,2013). PubMed:24653673

p(FPLX:PPP2, pmod(Ph, Tyr, 307)) decreases act(complex(GO:"protein phosphatase type 2A complex")) View Subject | View Object

For instance, activated GSK3β has been reported to induce PP2A inactivation via several mechanisms: phosphorylation of PP2A on Tyr307 (Yao et al.,2011); demethylation of PP2A on Leu309 through inhibition of LCMT1 and up-regulation of PME1 (Yao et al.,2012); and accumulation of I2 PP2A (Liu et al.,2008a). PubMed:24653673

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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.