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p(HGNC:PPP2CB)

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

Entity

Name
PPP2CB
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 2

Phosphatase: PP2A structural importance, regulation and its aberrant expression in cancer v1.0.0

Protein phosphatase 2A dysfunction in Alzheimer’s disease v1.0.0

In-Edges 18

a(MESH:"Cell Nucleus") association p(HGNC:PPP2CB) View Subject | View Object

The isoform C α is predominantly expressed in the plasma membrane and C β in the cytoplasm and nucleus. PubMed:23454242

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a(MESH:Cytosol) association p(HGNC:PPP2CB) View Subject | View Object

The isoform C α is predominantly expressed in the plasma membrane and C β in the cytoplasm and nucleus. PubMed:23454242

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p(FPLX:PPP2C) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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complex(p(HGNC:LCMT1), p(HGNC:PPP2CB)) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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act(complex(GO:"protein phosphatase type 2A complex")) association p(HGNC:PPP2CB) View Subject | View Object

Deficits in PP2A activity are in line with the reported down-regulation of PP2A catalytic C subunit at the gene (Loring et al.,2001), mRNA (Vogelsberg-Ragaglia et al.,2001) and protein (Sontag et al.,2004b) expression levels in AD. PubMed:24653673

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complex(a(CHEBI:"okadaic acid"), p(HGNC:PPP2CB)) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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complex(a(PUBCHEM:5311365), p(HGNC:PPP2CB)) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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complex(a(PUBCHEM:6913994), p(HGNC:PPP2CB)) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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complex(p(HGNC:ANP32A), p(HGNC:PPP2CB)) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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complex(p(HGNC:IGBP1), p(HGNC:PPP2CB)) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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complex(p(HGNC:MAPT), p(HGNC:PPP2CB), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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complex(p(HGNC:PPME1), p(HGNC:PPP2CB)) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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complex(p(HGNC:PPP2CB), p(HGNC:PPP2R1A)) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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complex(p(HGNC:PPP2CB), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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complex(p(HGNC:PPP2CB), p(HGNC:PTPA)) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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complex(p(HGNC:PPP2CB), p(HGNC:SET)) hasComponent p(HGNC:PPP2CB) View Subject | View Object

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p(HGNC:IGBP1, frag("?")) positiveCorrelation deg(p(HGNC:PPP2CB)) View Subject | View Object

Lastly, increased calpain-mediated cleavage of alpha4, which critically modulates PP2A stability, could be responsible for increased degradation of PP2A catalytic subunit in AD (Watkins et al., 2012). PubMed:24653673

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") negativeCorrelation p(HGNC:PPP2CB) View Subject | View Object

Deficits in PP2A activity are in line with the reported down-regulation of PP2A catalytic C subunit at the gene (Loring et al.,2001), mRNA (Vogelsberg-Ragaglia et al.,2001) and protein (Sontag et al.,2004b) expression levels in AD. PubMed:24653673

Appears in Networks:

Out-Edges 9

p(HGNC:PPP2CB) association a(MESH:Cytosol) View Subject | View Object

The isoform C α is predominantly expressed in the plasma membrane and C β in the cytoplasm and nucleus. PubMed:23454242

Appears in Networks:

p(HGNC:PPP2CB) association a(MESH:"Cell Nucleus") View Subject | View Object

The isoform C α is predominantly expressed in the plasma membrane and C β in the cytoplasm and nucleus. PubMed:23454242

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p(HGNC:PPP2CB) hasVariant p(HGNC:PPP2CB, pmod(Me, Leu, 309)) View Subject | View Object

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p(HGNC:PPP2CB) hasVariant p(HGNC:PPP2CB, pmod(Ph, Tyr, 307)) View Subject | View Object

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p(HGNC:PPP2CB) hasVariant p(HGNC:PPP2CB, var("p.Leu309Ala")) View Subject | View Object

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p(HGNC:PPP2CB) association act(complex(GO:"protein phosphatase type 2A complex")) View Subject | View Object

Deficits in PP2A activity are in line with the reported down-regulation of PP2A catalytic C subunit at the gene (Loring et al.,2001), mRNA (Vogelsberg-Ragaglia et al.,2001) and protein (Sontag et al.,2004b) expression levels in AD. PubMed:24653673

Appears in Networks:

p(HGNC:PPP2CB) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Deficits in PP2A activity are in line with the reported down-regulation of PP2A catalytic C subunit at the gene (Loring et al.,2001), mRNA (Vogelsberg-Ragaglia et al.,2001) and protein (Sontag et al.,2004b) expression levels in AD. PubMed:24653673

Appears in Networks:

deg(p(HGNC:PPP2CB)) positiveCorrelation p(HGNC:IGBP1, frag("?")) View Subject | View Object

Lastly, increased calpain-mediated cleavage of alpha4, which critically modulates PP2A stability, could be responsible for increased degradation of PP2A catalytic subunit in AD (Watkins et al., 2012). PubMed:24653673

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:PPP2CB) decreases p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

Knock-down of PP2A catalytic subunit (Kins et al.,2001) or PP2A B’δ (or PPP2R5D) regulatory subunit (Louis et al.,2011), and expression of the methylation-site L309A C subunit mutant (Schild et al.,2006) all induce AD-like tau phosphorylation in transgenic mice 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.