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Appears in Networks 3

In-Edges 18

act(p(FPLX:PPP2)) association p(FPLX:PPP2, pmod(Me)) View Subject | View Object

Methylation [52] and phosphorylation [53] are two major modifications that have been shown to modulate PP2A catalytic efficiency. PubMed:23454242

a(CHEBI:folates) decreases p(FPLX:PPP2, pmod(Me)) View Subject | View Object

Dietary folate and B-vitamin deficiency (Sontag et al.,2008; Nicolia et al.,2010) and elevated homocysteine levels (Sontag et al.,2007, 2013; Zhang et al.,2008) lead to down-regulation of PP2A methylation and concomitant phosphorylation of tau and/or APP in vivo PubMed:24653673

a(CHEBI:homocysteine) negativeCorrelation p(FPLX:PPP2, pmod(Me)) View Subject | View Object

Dietary folate and B-vitamin deficiency (Sontag et al.,2008; Nicolia et al.,2010) and elevated homocysteine levels (Sontag et al.,2007, 2013; Zhang et al.,2008) lead to down-regulation of PP2A methylation and concomitant phosphorylation of tau and/or APP in vivo PubMed:24653673

bp(GO:"one-carbon metabolic process") association p(FPLX:PPP2, pmod(Me)) View Subject | View Object

The deregulation of PP2A methylation in AD is especially interesting, not only because it can lead to a loss of PP2A/Bα, a major tau regulator, but also because PP2A methylation state is intimately linked to the integrity of one-carbon metabolism, which regulates SAM supply (Reviewed in Fowler,2005). PubMed:24653673

p(HGNC:LCMT1) increases p(FPLX:PPP2, pmod(Me)) View Subject | View Object

Significantly, down-regulation of LCMT1 protein expression parallels the deficits in PP2A methylation observed in AD (Sontag et al.,2004a). PubMed:24653673

complex(p(HGNC:PPP2CA), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) positiveCorrelation p(FPLX:PPP2, pmod(Me)) View Subject | View Object

Notably, the loss of neuronal PP2A/Bα holoenzymes correlates with the down-regulation of PP2A methylation and severity of phosphorylated tau (P-tau) pathology in AD-affected brain regions (Sontag et al.,2004 a,b). PubMed:24653673

complex(p(HGNC:PPP2CA), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) association p(FPLX:PPP2, pmod(Me)) View Subject | View Object

As described earlier, it is especially significant that the biogenesis of PP2A/Bα holoenzymes is intimately related to the methylation state of PP2A PubMed:24653673

complex(p(HGNC:PPP2CA), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) positiveCorrelation p(FPLX:PPP2, pmod(Me)) View Subject | View Object

The deregulation of PP2A methylation in AD is especially interesting, not only because it can lead to a loss of PP2A/Bα, a major tau regulator, but also because PP2A methylation state is intimately linked to the integrity of one-carbon metabolism, which regulates SAM supply (Reviewed in Fowler,2005). PubMed:24653673

complex(p(HGNC:PPP2CB), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) positiveCorrelation p(FPLX:PPP2, pmod(Me)) View Subject | View Object

Notably, the loss of neuronal PP2A/Bα holoenzymes correlates with the down-regulation of PP2A methylation and severity of phosphorylated tau (P-tau) pathology in AD-affected brain regions (Sontag et al.,2004 a,b). PubMed:24653673

complex(p(HGNC:PPP2CB), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) association p(FPLX:PPP2, pmod(Me)) View Subject | View Object

As described earlier, it is especially significant that the biogenesis of PP2A/Bα holoenzymes is intimately related to the methylation state of PP2A PubMed:24653673

complex(p(HGNC:PPP2CB), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) positiveCorrelation p(FPLX:PPP2, pmod(Me)) View Subject | View Object

The deregulation of PP2A methylation in AD is especially interesting, not only because it can lead to a loss of PP2A/Bα, a major tau regulator, but also because PP2A methylation state is intimately linked to the integrity of one-carbon metabolism, which regulates SAM supply (Reviewed in Fowler,2005). PubMed:24653673

p(HGNC:APP, pmod(Ph)) negativeCorrelation p(FPLX:PPP2, pmod(Me)) View Subject | View Object

Dietary folate and B-vitamin deficiency (Sontag et al.,2008; Nicolia et al.,2010) and elevated homocysteine levels (Sontag et al.,2007, 2013; Zhang et al.,2008) lead to down-regulation of PP2A methylation and concomitant phosphorylation of tau and/or APP in vivo PubMed:24653673

p(HGNC:MAPT, pmod(Ph)) negativeCorrelation p(FPLX:PPP2, pmod(Me)) View Subject | View Object

Dietary folate and B-vitamin deficiency (Sontag et al.,2008; Nicolia et al.,2010) and elevated homocysteine levels (Sontag et al.,2007, 2013; Zhang et al.,2008) lead to down-regulation of PP2A methylation and concomitant phosphorylation of tau and/or APP in vivo PubMed:24653673

path(MESH:"Alzheimer Disease") negativeCorrelation p(FPLX:PPP2, pmod(Me)) View Subject | View Object

Significantly, down-regulation of LCMT1 protein expression parallels the deficits in PP2A methylation observed in AD (Sontag et al.,2004a). PubMed:24653673

path(MESH:"Alzheimer Disease") negativeCorrelation p(FPLX:PPP2, pmod(Me)) View Subject | View Object

Conversely, decreased PP2A methylation and PP2A/Bα levels in AD will disrupt normal PP2A-tau interactions (Sontag et al., 2007), thereby preventing PP2A-mediated tau dephosphorylation while allowing for enhanced binding of Fyn kinase or other regulators to the tau proteins. PubMed:24653673

path(MESH:"Alzheimer Disease") negativeCorrelation p(FPLX:PPP2, pmod(Me)) View Subject | View Object

The deregulation of PP2A methylation in AD is especially interesting, not only because it can lead to a loss of PP2A/Bα, a major tau regulator, but also because PP2A methylation state is intimately linked to the integrity of one-carbon metabolism, which regulates SAM supply (Reviewed in Fowler,2005). PubMed:24653673

path(MESH:"Vitamin B Deficiency") decreases p(FPLX:PPP2, pmod(Me)) View Subject | View Object

Dietary folate and B-vitamin deficiency (Sontag et al.,2008; Nicolia et al.,2010) and elevated homocysteine levels (Sontag et al.,2007, 2013; Zhang et al.,2008) lead to down-regulation of PP2A methylation and concomitant phosphorylation of tau and/or APP in vivo PubMed:24653673

Out-Edges 18

p(FPLX:PPP2, pmod(Me)) association act(p(FPLX:PPP2)) View Subject | View Object

Methylation [52] and phosphorylation [53] are two major modifications that have been shown to modulate PP2A catalytic efficiency. PubMed:23454242

p(FPLX:PPP2, pmod(Me)) regulates bp(GO:"cell cycle") View Subject | View Object

It had also been demonstrated that methylation levels of PP2A changed during a cell cycle, suggesting a critical role of methylation in cell cycle regulation PubMed:19277525

p(FPLX:PPP2, pmod(Me)) positiveCorrelation complex(p(HGNC:PPP2CA), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) View Subject | View Object

Notably, the loss of neuronal PP2A/Bα holoenzymes correlates with the down-regulation of PP2A methylation and severity of phosphorylated tau (P-tau) pathology in AD-affected brain regions (Sontag et al.,2004 a,b). PubMed:24653673

p(FPLX:PPP2, pmod(Me)) association complex(p(HGNC:PPP2CA), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) View Subject | View Object

As described earlier, it is especially significant that the biogenesis of PP2A/Bα holoenzymes is intimately related to the methylation state of PP2A PubMed:24653673

p(FPLX:PPP2, pmod(Me)) negativeCorrelation a(CHEBI:homocysteine) View Subject | View Object

Dietary folate and B-vitamin deficiency (Sontag et al.,2008; Nicolia et al.,2010) and elevated homocysteine levels (Sontag et al.,2007, 2013; Zhang et al.,2008) lead to down-regulation of PP2A methylation and concomitant phosphorylation of tau and/or APP in vivo PubMed:24653673

p(FPLX:PPP2, pmod(Me)) positiveCorrelation complex(p(HGNC:PPP2CA), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) View Subject | View Object

The deregulation of PP2A methylation in AD is especially interesting, not only because it can lead to a loss of PP2A/Bα, a major tau regulator, but also because PP2A methylation state is intimately linked to the integrity of one-carbon metabolism, which regulates SAM supply (Reviewed in Fowler,2005). PubMed:24653673

p(FPLX:PPP2, pmod(Me)) positiveCorrelation complex(p(HGNC:PPP2CB), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) View Subject | View Object

Notably, the loss of neuronal PP2A/Bα holoenzymes correlates with the down-regulation of PP2A methylation and severity of phosphorylated tau (P-tau) pathology in AD-affected brain regions (Sontag et al.,2004 a,b). PubMed:24653673

p(FPLX:PPP2, pmod(Me)) association complex(p(HGNC:PPP2CB), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) View Subject | View Object

As described earlier, it is especially significant that the biogenesis of PP2A/Bα holoenzymes is intimately related to the methylation state of PP2A PubMed:24653673

p(FPLX:PPP2, pmod(Me)) positiveCorrelation complex(p(HGNC:PPP2CB), p(HGNC:PPP2R1A), p(INTERPRO:"Protein phosphatase 2A regulatory subunit PR55")) View Subject | View Object

The deregulation of PP2A methylation in AD is especially interesting, not only because it can lead to a loss of PP2A/Bα, a major tau regulator, but also because PP2A methylation state is intimately linked to the integrity of one-carbon metabolism, which regulates SAM supply (Reviewed in Fowler,2005). PubMed:24653673

p(FPLX:PPP2, pmod(Me)) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Significantly, down-regulation of LCMT1 protein expression parallels the deficits in PP2A methylation observed in AD (Sontag et al.,2004a). PubMed:24653673

p(FPLX:PPP2, pmod(Me)) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Conversely, decreased PP2A methylation and PP2A/Bα levels in AD will disrupt normal PP2A-tau interactions (Sontag et al., 2007), thereby preventing PP2A-mediated tau dephosphorylation while allowing for enhanced binding of Fyn kinase or other regulators to the tau proteins. PubMed:24653673

p(FPLX:PPP2, pmod(Me)) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

The deregulation of PP2A methylation in AD is especially interesting, not only because it can lead to a loss of PP2A/Bα, a major tau regulator, but also because PP2A methylation state is intimately linked to the integrity of one-carbon metabolism, which regulates SAM supply (Reviewed in Fowler,2005). PubMed:24653673

p(FPLX:PPP2, pmod(Me)) association bp(GO:"one-carbon metabolic process") View Subject | View Object

The deregulation of PP2A methylation in AD is especially interesting, not only because it can lead to a loss of PP2A/Bα, a major tau regulator, but also because PP2A methylation state is intimately linked to the integrity of one-carbon metabolism, which regulates SAM supply (Reviewed in Fowler,2005). PubMed:24653673

p(FPLX:PPP2, pmod(Me)) negativeCorrelation p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

Dietary folate and B-vitamin deficiency (Sontag et al.,2008; Nicolia et al.,2010) and elevated homocysteine levels (Sontag et al.,2007, 2013; Zhang et al.,2008) lead to down-regulation of PP2A methylation and concomitant phosphorylation of tau and/or APP in vivo PubMed:24653673

p(FPLX:PPP2, pmod(Me)) negativeCorrelation p(HGNC:APP, pmod(Ph)) View Subject | View Object

Dietary folate and B-vitamin deficiency (Sontag et al.,2008; Nicolia et al.,2010) and elevated homocysteine levels (Sontag et al.,2007, 2013; Zhang et al.,2008) lead to down-regulation of PP2A methylation and concomitant phosphorylation of tau and/or APP in vivo PubMed:24653673

p(FPLX:PPP2, pmod(Me)) regulates bp(HBP:"APP processing") View Subject | View Object

In cultured cells, deregulation of PP2A methylation also affects APP processing (Sontag et al.,2007), neurite outgrowth (Sontag et al.,2010) and tau distribution (Sontag et al.,2013). PubMed:24653673

p(FPLX:PPP2, pmod(Me)) regulates bp(MESH:"Neuronal Outgrowth") View Subject | View Object

In cultured cells, deregulation of PP2A methylation also affects APP processing (Sontag et al.,2007), neurite outgrowth (Sontag et al.,2010) and tau distribution (Sontag et al.,2013). PubMed:24653673

p(FPLX:PPP2, pmod(Me)) regulates p(HGNC:MAPT) View Subject | View Object

In cultured cells, deregulation of PP2A methylation also affects APP processing (Sontag et al.,2007), neurite outgrowth (Sontag et al.,2010) and tau distribution (Sontag et al.,2013). PubMed:24653673

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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.