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p(FPLX:PKC)

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Entity

Name
PKC
Namespace
FPLX
Namespace Version
20190217
Namespace URL
https://raw.githubusercontent.com/sorgerlab/famplex/d9ec0526c20795146a9a6aef17496efe1a36cac6/export/famplex.belns

Appears in Networks 10

Amyloid Precursor Protein Trafficking, Processing, and Function v1.0.0

Amyloid Precursor Protein Trafficking, Processing, and Function by Thinakaran, et al., 2008

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

Alzheimer's Disease: Targeting the Cholinergic System v1.0.0

M1 muscarinic acetylcholine receptor in Alzheimer’s disease v1.0.0

This file encodes the article M1 muscarinic acetylcholine receptor in Alzheimer’s disease by Jiang et al, 2014

Tau Biochemistry v1.2.5

Tau Biochemistry Section of NESTOR

The Spleen Tyrosine Kinase (Syk) Regulates Alzheimer Amyloid-β Production and Tau Hyperphosphorylation* v1.0.0

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0

In-Edges 10

a(CHEBI:nicotine) increases act(p(FPLX:PKC)) View Subject | View Object

An ever-growing body of evidence indicates that in CNS and parasympathetic nervous system neurons and in heterologous systems expressing specific nAChR subtypes, nicotine stimulates several Ca2+-dependent kinases, including PI3K, protein kinase C (PKC), protein kinase A (PKA), calmodulin-dependent protein kinase II (CAM kinase II), and extracellular signal-regulated kinases (ERKs; Refs. 108, 112, 146, 318, 469). PubMed:19126755

Appears in Networks:
Annotations
MeSH
Central Nervous System
MeSH
Parasympathetic Nervous System
Text Location
Review

composite(a(CHEBI:"3',5'-cyclic AMP"), p(FPLX:PKC)) hasComponent p(FPLX:PKC) View Subject | View Object

Appears in Networks:

act(p(HGNC:CHRM1)) increases act(p(FPLX:PKC)) View Subject | View Object

It has been shown that activation of M1 receptors decreases tau hyperphosphorylation via activation of PKC and inhibition of GSK-3β PubMed:26813123

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(p(HGNC:CHRM1)) increases act(p(FPLX:PKC)) View Subject | View Object

Interestingly, stimulation of M1 mAChR by agonists has been found to enhance sAPPalpha generation and reduce Abeta production[61-70]. Protein kinase C (PKC) is well-known to be activated upon stimulation of M1 mAChR. PKC may promote the activity of alpha-secretase[71] and the traffi cking of APP from the Golgi/ trans-Golgi network to the cell surface PubMed:24590577

Appears in Networks:

act(p(HGNC:CHRM1)) increases act(p(FPLX:PKC)) View Subject | View Object

When APP/PS1/tau triple transgenic (3×Tg) AD mice are treated with the selective M1 mAChR agonist AF267B, the endogenous level of BACE1 decreases via an unclear mechanism, accompanied by a decreased Abeta level[77]. However, another study found that stimulation of M1 mAChR upregulates BACE1 levels in SK-SH-SY5Y cells via the PKC and MAPK signaling cascades[78]. We recently found that M1 mAChR directly interacts with BACE1 and mediates its proteasomal degradation[79]. These results suggest that M1 mAChR modulates BACE1 in a mixed manner. PubMed:24590577

Appears in Networks:

act(p(HGNC:CHRM1)) increases act(p(FPLX:PKC)) View Subject | View Object

In addition to inhibiting Abeta generation, activation of M1 mAChR counteracts Abeta-induced neurotoxicity through the Wnt signaling pathway, as Abeta impairs the Wnt pathway and M1 mAChR stimulation inactivates GSK-3beta via PKC activation, stabilizes beta-catenin, and induces the expression of Wnt-targeting genes engrailed and cyclin-D1 for neuron survival PubMed:24590577

Appears in Networks:

a(CHEBI:"phorbol 13-acetate 12-myristate") increases act(p(FPLX:PKC)) View Subject | View Object

PMA is a known agonist of PKC, which leads to the activation of the PKC/RAS/RAF/MEK/MAPK pathway that ultimately induces NFkB activation (46–48) PubMed:25331948

Appears in Networks:

a(CHEBI:"amyloid-beta") regulates act(p(FPLX:PKC)) View Subject | View Object

Moreover, there is preponderance of data implicating Amyloid-β in the modulation of PKC signaling pathway [335-338] and the PI3K/Akt/mTOR signaling pathway [339-341], which are known to activate NF-κB signaling pathway PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

bp(GO:"calcium ion import") increases act(p(FPLX:PKC)) View Subject | View Object

In addition to CamKII, other kinases activated in response to a rise in cytosolic Ca2+ such as protein kinase C (PKC), phosphatidylinositol-3-kinase (PI3K), and Akt, also activate NF-κB signaling pathway by increasing the phosphorylation and activation of IKK PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"reactive oxygen species") increases act(p(FPLX:PKC)) View Subject | View Object

ROS activate various downstream signaling molecules, such as PKC and mitogen-activated protein kinases (MAPKs) that induce nuclear translocation of NF-B and the expression of pro-inflammatory genes [41]. PubMed:29179999

Appears in Networks:

Out-Edges 14

p(FPLX:PKC) increases sec(p(HGNC:APP)) View Subject | View Object

Activation of protein kinase C increases APPs α-secretion by mechanisms involving the formation and release of secretory vesicles from the TGN, thus enhancing APP (and possiblyα-secretase) trafficking to the cell surface. PubMed:18650430

Appears in Networks:
Annotations
Confidence
High

p(FPLX:PKC) increases p(HGNC:SLC18A3, pmod(Ph)) View Subject | View Object

Interestingly, PKC can phosphorylate VAChT and regulate its vesicular localization PubMed:26813123

Appears in Networks:

p(FPLX:PKC) increases p(FPLX:CHRN, pmod(Ph)) View Subject | View Object

It has been demonstrated that phosphorylation of nicotinic receptors by protein kinase A, protein kinase C, and tyrosine kinase can regulate receptor activity PubMed:26813123

Appears in Networks:

act(p(FPLX:PKC)) increases act(p(HGNC:ADAM10)) View Subject | View Object

Interestingly, stimulation of M1 mAChR by agonists has been found to enhance sAPPalpha generation and reduce Abeta production[61-70]. Protein kinase C (PKC) is well-known to be activated upon stimulation of M1 mAChR. PKC may promote the activity of alpha-secretase[71] and the traffi cking of APP from the Golgi/ trans-Golgi network to the cell surface PubMed:24590577

Appears in Networks:

act(p(FPLX:PKC)) increases tloc(p(HGNC:APP), fromLoc(GO:"Golgi apparatus"), toLoc(GO:"cell surface")) View Subject | View Object

Interestingly, stimulation of M1 mAChR by agonists has been found to enhance sAPPalpha generation and reduce Abeta production[61-70]. Protein kinase C (PKC) is well-known to be activated upon stimulation of M1 mAChR. PKC may promote the activity of alpha-secretase[71] and the traffi cking of APP from the Golgi/ trans-Golgi network to the cell surface PubMed:24590577

Appears in Networks:

act(p(FPLX:PKC)) increases p(HGNC:BACE1) View Subject | View Object

When APP/PS1/tau triple transgenic (3×Tg) AD mice are treated with the selective M1 mAChR agonist AF267B, the endogenous level of BACE1 decreases via an unclear mechanism, accompanied by a decreased Abeta level[77]. However, another study found that stimulation of M1 mAChR upregulates BACE1 levels in SK-SH-SY5Y cells via the PKC and MAPK signaling cascades[78]. We recently found that M1 mAChR directly interacts with BACE1 and mediates its proteasomal degradation[79]. These results suggest that M1 mAChR modulates BACE1 in a mixed manner. PubMed:24590577

Appears in Networks:

act(p(FPLX:PKC)) decreases act(p(HGNC:GSK3B)) View Subject | View Object

In addition to inhibiting Abeta generation, activation of M1 mAChR counteracts Abeta-induced neurotoxicity through the Wnt signaling pathway, as Abeta impairs the Wnt pathway and M1 mAChR stimulation inactivates GSK-3beta via PKC activation, stabilizes beta-catenin, and induces the expression of Wnt-targeting genes engrailed and cyclin-D1 for neuron survival PubMed:24590577

Appears in Networks:

p(FPLX:PKC) increases p(HGNC:MAPT, pmod(Ph, Ser, 214)) View Subject | View Object

A further potent detaching site is phosphoS214, which can be phosphorylated by PKA and other kinases of the AGC group (PKA/PKG/PKC group of protein kinases), and is up-regulated during mitosis (16, 63). Tau contains one or two cysteines in the repeat domain (C291 in R2, present in 4R isoforms, and C322 in R3), which can be engaged in intra- or intermolecular cross-linking affecting conformation, dimerization and aggregation (108). PubMed:17493042

Appears in Networks:
Annotations
Uberon
brain

act(p(FPLX:PKC)) increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

In addition to CamKII, other kinases activated in response to a rise in cytosolic Ca2+ such as protein kinase C (PKC), phosphatidylinositol-3-kinase (PI3K), and Akt, also activate NF-κB signaling pathway by increasing the phosphorylation and activation of IKK PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(p(FPLX:PKC)) increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

The three well characterized sensors of intracellular calcium – calmodulin/CamKII pathway, PI3K/ Akt pathway, and protein kinase C (PKC) pathway – are known to induce NF-κB activation and couple upstream signal transduction pathways that induce calcium dyshomeostasis to NF-κB activation PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(p(FPLX:PKC)) increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

Moreover, there is preponderance of data implicating Amyloid-β in the modulation of PKC signaling pathway [335-338] and the PI3K/Akt/mTOR signaling pathway [339-341], which are known to activate NF-κB signaling pathway PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(p(FPLX:PKC)) increases act(complex(GO:"IkappaB kinase complex")) View Subject | View Object

In addition to CamKII, other kinases activated in response to a rise in cytosolic Ca2+ such as protein kinase C (PKC), phosphatidylinositol-3-kinase (PI3K), and Akt, also activate NF-κB signaling pathway by increasing the phosphorylation and activation of IKK PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(p(FPLX:PKC)) increases p(MESH:"I-kappa B Kinase", pmod(Ph)) View Subject | View Object

In addition to CamKII, other kinases activated in response to a rise in cytosolic Ca2+ such as protein kinase C (PKC), phosphatidylinositol-3-kinase (PI3K), and Akt, also activate NF-κB signaling pathway by increasing the phosphorylation and activation of IKK PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(p(FPLX:PKC)) increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

Several kinase pathways including the calcium-calmodium dependent kinase-II (CaMK), the protein kinases-C (PKC) and the ras/phosphatidylinositol 3-kinase (PI3K) pathways have been implicated in activating neuronal NF-κB signaling PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons

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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.