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Out-Edges 6

p(HGNC:DISC1, var("?")) increases path(MESH:Schizophrenia) View Subject | View Object

In addition, these findings strongly suggest that DISC1 alterations may increase the risk of schizophrenia by dysregulating DA release PubMed:30061532

p(HGNC:DISC1, var("?")) increases path(MESH:Schizophrenia) View Subject | View Object

Therefore, disruption of DISC1 activity, due to genetic rearrangements (i.e., balanced (1;11) (q42;q14) chromosomal translocation) or missense mutations, produces schizophrenic-like behavior, which is bound to enhanced Akt activity, over-activation of mTOR signaling, and depressed autophagy PubMed:30061532

p(HGNC:DISC1, var("?")) decreases sec(a(CHEBI:dopamine)) View Subject | View Object

In addition, these findings strongly suggest that DISC1 alterations may increase the risk of schizophrenia by dysregulating DA release PubMed:30061532

p(HGNC:DISC1, var("?")) increases act(p(FPLX:AKT)) View Subject | View Object

Therefore, disruption of DISC1 activity, due to genetic rearrangements (i.e., balanced (1;11) (q42;q14) chromosomal translocation) or missense mutations, produces schizophrenic-like behavior, which is bound to enhanced Akt activity, over-activation of mTOR signaling, and depressed autophagy PubMed:30061532

p(HGNC:DISC1, var("?")) increases act(p(HGNC:MTOR)) View Subject | View Object

Therefore, disruption of DISC1 activity, due to genetic rearrangements (i.e., balanced (1;11) (q42;q14) chromosomal translocation) or missense mutations, produces schizophrenic-like behavior, which is bound to enhanced Akt activity, over-activation of mTOR signaling, and depressed autophagy PubMed:30061532

p(HGNC:DISC1, var("?")) decreases bp(GO:autophagy) View Subject | View Object

Therefore, disruption of DISC1 activity, due to genetic rearrangements (i.e., balanced (1;11) (q42;q14) chromosomal translocation) or missense mutations, produces schizophrenic-like behavior, which is bound to enhanced Akt activity, over-activation of mTOR signaling, and depressed autophagy PubMed:30061532

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.