Table of Contents

Regulatory Pairs 1

These pairs of nodes represent motifs like A increases B and B decreases A.

Node A Node B
p(HGNC:PIN1) p(HGNC:SMAD2)

Contradictory Statements 4

These pairs of nodes have a contradiction in their causal relationships, meaning they have more than one of INCREASES, DECREASES, or CAUSES NO CHANGE. This may be due to different experimental conditions, so these statements need to be carefully considered in analyses.

Source Relations Target
a(CHEBI:"methylene blue") decreases, increases p(HGNC:MARK4)
p(HGNC:TTBK2, var("p.Tyr448*")) decreases, increases p(HGNC:TTBK2)
p(HGNC:TTBK2, var("p.Glu450*")) decreases, increases p(HGNC:TTBK2)
p(HGNC:TTBK2, var("p.Asp449*")) decreases, increases p(HGNC:TTBK2)

Unstable Pairs 1

Chaotic Pairs
Nodes that mutually increase each other, such as when both A increases B and B increases A.
Dampened Pairs
Nodes that mutually decrease each other, such as when both A decreases B and B decreases A.

While neither chaotic nor dampened pairs are biologically invalid, they require additional context to understand their regulation.

Type Node A Node B
Chaotic complex(p(HGNC:CDK5), p(HGNC:CDK5R1)) p(HGNC:CDK5)

Contradictory Triplets 24

Analysis of triple stability comes from a deep graph theoretic background. It identifies triangles within the graph that have logically inconsistent relations.

Separately Unstable Triplet
When both A positiveCorrelation B, B negativeCorrelation C, but C positiveCorrelation A.
Mutually Unstable Triplets
When both A negativeCorrelation B, B negativeCorrelation C, and C negativeCorrelation A.
Jens Contradictory Triplet
When A increases B, A decreases C, and C positiveCorrelation A.
Increase Mismatch Triplet
When A increases B, A increases C, and C negativeCorrelation A.
Decrease Mismatch Triplet
When A decreases B, A decreases C, and C negativeCorrelation A.
Type Node A Node B Node C
Jens p(HGNC:MAPT, pmod(Ac, Lys, 280)) p(HGNC:MAPT, pmod(Ph, Ser, 262)) path(MESH:"Alzheimer Disease")
Jens a(HBP:"Tau aggregates") a(HBP:"Tau aggregates") a(HBP:"Tau aggregates")
Jens a(CHEBI:"D-ribose") a(CHEBI:"advanced glycation end-product") p(MGI:Mapt, pmod(Ph, Ser, 214))
Jens a(CHEBI:rolipram) complex(GO:"proteasome complex") p(FPLX:PKA)
Jens a(CHEBI:"D-ribose") a(HBP:"advanced glycation end product") p(HGNC:MAPT, pmod(Ph, Ser, 396))
Jens bp(GO:"microtubule polymerization") p(HGNC:DAPK1) p(HGNC:MAPT)
Jens a(CHEBI:"okadaic acid") p(HGNC:MAPT, pmod(Ph, Ser, 202)) p(HGNC:MAPT, pmod(Sumo, Lys, 340))
Jens a(CHEBI:resveratrol) p(HGNC:MID1) p(HGNC:PPP2CA)
Jens a(GO:mitochondrion) bp(MESH:"Oxidative Stress") p(HGNC:GLP1R)
Jens a(CHEBI:"D-ribose") a(HBP:"advanced glycation end product") p(HGNC:MAPT, pmod(Ph, Thr, 181))
Jens a(CHEBI:"D-ribose") a(HBP:"advanced glycation end product") p(HGNC:MAPT, pmod(Ph, Ser, 214))
Jens a(CHEBI:"trichostatin A") p(FPLX:HDAC) p(HGNC:MAPT, pmod(Ac))
Jens a(HBP:"Tau aggregates") a(HBP:"Tau aggregates") p(MGI:Crhr1)
Jens p(HGNC:DAPK1) p(HGNC:MAPT) p(HGNC:PIN1, pmod(Ph, Ser, 71))
Jens a(HBP:"Tau epitope, PHF1") p(HGNC:GSK3B) p(HGNC:MAPT, pmod(Ph, Ser, 396))
Jens p(HBP:"CDK5R1 p25") p(HBP:"Tau epitope, AT8") p(MGI:Cdk5)
Jens a(HBP:"granulovacuolar degeneration") p(HGNC:MAPT, pmod(Ph, Ser, 262)) p(HGNC:MARK4, pmod(Ph))
Jens a(CHEBI:"D-ribose") a(CHEBI:"advanced glycation end-product") p(MGI:Mapt, pmod(Ph, Ser, 396))
Jens p(FPLX:CALM) p(HBP:"DAPK, basic loop (BL) motif") p(HGNC:DAPK2)
Jens p(HGNC:GSK3B) p(HGNC:GSK3B, pmod(Ph, Ser, 9)) p(HGNC:PPP1CA)
Increase Mismatch p(HBP:"APOE e4") p(MGI:Cdk5) p(MGI:Cdk5r1)
Increase Mismatch p(HGNC:DAPK1) p(HGNC:MAPT, pmod(Ph, Ser, 262)) bp(GO:"apoptotic process")
Increase Mismatch p(HGNC:DAPK1) bp(GO:"apoptotic process") p(HGNC:MAPT, pmod(Ph, Ser, 396))
Increase Mismatch p(HGNC:DAPK1) bp(GO:"apoptotic process") p(HGNC:MAPT, pmod(Ph, Thr, 231))

Causal Pathologies 14

Pathologies are more dogmatically the result of molecular and physical processes, and do not necessarily make sense as the subject of causal statements.

Source Relation Target
path(MESH:"Alzheimer Disease") increases p(ECCODE:"3.1.1.89")
path(MESH:"Alzheimer Disease") increases p(HGNC:ITPKB)
path(MESH:"Alzheimer Disease") decreases p(HGNC:LCMT1)
path(MESH:"Alzheimer Disease") increases p(HGNC:MAPK1)
path(MESH:"Alzheimer Disease") increases p(HGNC:PRKCB)
path(MESH:"Alzheimer Disease") increases p(HGNC:TGM2)
path(MESH:"Supranuclear Palsy, Progressive") increases p(ECCODE:"3.1.1.89")
path(MESH:"Supranuclear Palsy, Progressive") decreases p(HGNC:LCMT1)
path(MESH:"Supranuclear Palsy, Progressive") increases p(HGNC:TGM1)
path(MESH:"Supranuclear Palsy, Progressive") increases r(HBP:"TGM2 Isoform 3 (349 aa)")
path(MESH:"Supranuclear Palsy, Progressive") increases r(HGNC:TGM1)
path(MESH:"Supranuclear Palsy, Progressive") increases r(HGNC:TGM2)
path(MESH:Fasting) decreases p(MGI:Mapt, pmod(HBP:"O-GlcNAcylation"))
path(MESH:Fasting) increases p(MGI:Mapt, pmod(Ph))

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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.