1. Catalog
  2. Nodes
  3. p(HGNC:UNC5C, var("p.Thr835Met"))

p(HGNC:UNC5C, var("p.Thr835Met"))

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

Entity

Name
UNC5C
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 1

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 4

p(HGNC:CALML5) decreases p(HGNC:UNC5C, var("p.Thr835Met")) View Subject | View Object

Overexpression of wild-type UNC5C causes low-grade death, intensified by an AD-linked mutation T835M inhibited by a AD-linked survival factor, calmodulin-like skin protein (CLSP), and a natural ligand of UNC5C, netrin1. T835M-UNC5C-induced neuronal cell death is mediated by an intracellular death-signaling cascade, consisting of DAPK1/protein kinase D/apoptosis signal-regulating kinase 1 (ASK1)/JNK/NADPH oxidase/caspases, which merges at ASK1 with a death-signaling cascade, mediated by amyloid ß precursor protein (APP). PubMed:27068745

Appears in Networks:

p(HGNC:NTN1) decreases p(HGNC:UNC5C, var("p.Thr835Met")) View Subject | View Object

Overexpression of wild-type UNC5C causes low-grade death, intensified by an AD-linked mutation T835M inhibited by a AD-linked survival factor, calmodulin-like skin protein (CLSP), and a natural ligand of UNC5C, netrin1. T835M-UNC5C-induced neuronal cell death is mediated by an intracellular death-signaling cascade, consisting of DAPK1/protein kinase D/apoptosis signal-regulating kinase 1 (ASK1)/JNK/NADPH oxidase/caspases, which merges at ASK1 with a death-signaling cascade, mediated by amyloid ß precursor protein (APP). PubMed:27068745

Appears in Networks:

act(p(HGNC:PRKD1)) positiveCorrelation p(HGNC:UNC5C, var("p.Thr835Met")) View Subject | View Object

Overexpression of wild-type UNC5C causes low-grade death, intensified by an AD-linked mutation T835M inhibited by a AD-linked survival factor, calmodulin-like skin protein (CLSP), and a natural ligand of UNC5C, netrin1. T835M-UNC5C-induced neuronal cell death is mediated by an intracellular death-signaling cascade, consisting of DAPK1/protein kinase D/apoptosis signal-regulating kinase 1 (ASK1)/JNK/NADPH oxidase/caspases, which merges at ASK1 with a death-signaling cascade, mediated by amyloid ß precursor protein (APP). PubMed:27068745

Appears in Networks:

p(HGNC:UNC5C) hasVariant p(HGNC:UNC5C, var("p.Thr835Met")) View Subject | View Object

Appears in Networks:

Out-Edges 2

p(HGNC:UNC5C, var("p.Thr835Met")) increases bp(GO:"neuron apoptotic process") View Subject | View Object

Overexpression of wild-type UNC5C causes low-grade death, intensified by an AD-linked mutation T835M inhibited by a AD-linked survival factor, calmodulin-like skin protein (CLSP), and a natural ligand of UNC5C, netrin1. T835M-UNC5C-induced neuronal cell death is mediated by an intracellular death-signaling cascade, consisting of DAPK1/protein kinase D/apoptosis signal-regulating kinase 1 (ASK1)/JNK/NADPH oxidase/caspases, which merges at ASK1 with a death-signaling cascade, mediated by amyloid ß precursor protein (APP). PubMed:27068745

Appears in Networks:

p(HGNC:UNC5C, var("p.Thr835Met")) positiveCorrelation act(p(HGNC:PRKD1)) View Subject | View Object

Overexpression of wild-type UNC5C causes low-grade death, intensified by an AD-linked mutation T835M inhibited by a AD-linked survival factor, calmodulin-like skin protein (CLSP), and a natural ligand of UNC5C, netrin1. T835M-UNC5C-induced neuronal cell death is mediated by an intracellular death-signaling cascade, consisting of DAPK1/protein kinase D/apoptosis signal-regulating kinase 1 (ASK1)/JNK/NADPH oxidase/caspases, which merges at ASK1 with a death-signaling cascade, mediated by amyloid ß precursor protein (APP). PubMed:27068745

Appears in Networks:

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.