1. Catalog
  2. Nodes
  3. p(HGNC:CASP1)

p(HGNC:CASP1)

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

Entity

Name
CASP1
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 7

Tau Protein Hyperphosphorylation and Aggregation in Alzheimer’s Disease and Other Tauopathies, and Possible Neuroprotective Strategies v1.0.0

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Inflammasome activation and innate immunity in Alzheimer’s disease v1.0.2

Activation and regulation of the inflammasomes v1.0.0

The role of inflammasome in Alzheimer’s disease v1.0.3

Inflammasome Involvement in Alzheimer’s Disease v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 34

a(CHEBI:"methylene blue") decreases act(p(HGNC:CASP1)) View Subject | View Object

MB is a phenothiazine that crosses the blood brain barrier and acts as a redox cycler. Moreover, besides its beneficial properties as being able to improve energy metabolism and to act as an antioxidant, it is also able to reduce tau protein aggregation PubMed:26751493

Appears in Networks:

a(CHEBI:"amyloid-beta") increases act(p(HGNC:CASP1)) View Subject | View Object

Further data, showing “neuronal pyroptosis” of Abeta exposed neurons in a NLRP1- dependent and caspase-1-mediated manner may point to a vicious cycle, by which NLRP1 is causing neurodegeneration in response to increased Abeta production (14) PubMed:28019679

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Neurons
NeuroMMSigDB
Apoptosis signaling subgraph
NeuroMMSigDB
Caspase subgraph

a(CHEBI:paraquat) increases p(HGNC:CASP1) View Subject | View Object

Using the herbizide, N,N0-dimethyl-4,40-bipyridinium dichloride (paraquat) as a mitochondrial toxin, which is known to induce oxidative stress, Chen et al. found increased levels of caspase-1 and IL-1b in brain of wild type and APP/PS1 transgenic mice (2), suggesting that those were due to NLRP3 inflammasome activation PubMed:28019679

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons
NeuroMMSigDB
Caspase subgraph

complex(GO:"NLRP1 inflammasome complex") increases act(p(HGNC:CASP1)) View Subject | View Object

Recently, Kaushal et al. described the involvement of NLRP1 inflammasome activation in neurons. In these experiments, serum deprivation induced NLRP1-dependent caspase-1 activity and ASC speck formation, which resulted in caspase-6 activation and an increase in the Ab42/total Ab ratio (11) PubMed:28019679

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

complex(GO:"NLRP3 inflammasome complex") increases act(p(HGNC:CASP1)) View Subject | View Object

NLRP3 inflammasome formation and subsequent activation of caspase-1 cleavage capacity was instrumental for Abeta-induced nitric oxide production and TNF-a release PubMed:28019679

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

act(complex(GO:"NLRP3 inflammasome complex")) increases p(HGNC:CASP1) View Subject | View Object

Using the herbizide, N,N0-dimethyl-4,40-bipyridinium dichloride (paraquat) as a mitochondrial toxin, which is known to induce oxidative stress, Chen et al. found increased levels of caspase-1 and IL-1b in brain of wild type and APP/PS1 transgenic mice (2), suggesting that those were due to NLRP3 inflammasome activation PubMed:28019679

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons
NeuroMMSigDB
Caspase subgraph

complex(GO:"IPAF inflammasome complex") increases act(p(HGNC:CASP1)) View Subject | View Object

NLRC4 and NLRP1 can both activate caspase 1 through their CARDs without recruiting ASC; however, the recruitment of ASC greatly enhances the formation of the complex and the processing of IL-1β7,13–16. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

complex(GO:"NLRP1 inflammasome complex") increases act(p(HGNC:CASP1)) View Subject | View Object

NLRC4 and NLRP1 can both activate caspase 1 through their CARDs without recruiting ASC; however, the recruitment of ASC greatly enhances the formation of the complex and the processing of IL-1β7,13–16. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

complex(GO:"inflammasome complex") hasComponent p(HGNC:CASP1) View Subject | View Object

Appears in Networks:

complex(GO:"inflammasome complex") increases act(p(HGNC:CASP1)) View Subject | View Object

Once the protein complexes have formed, the inflammasomes activate caspase 1, which proteolytically activates the pro-inflammatory cytokines interleukin-1β (IL-1β)3 and IL-18. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

complex(GO:"inflammasome complex") increases act(p(HGNC:CASP1)) View Subject | View Object

Indeed, inflammasomes (which induce pyroptosis through caspase 1 or caspase 11 activation) and apoptosomes (which activate caspase 9 in response to cytochrome c release from mitochondria) are two mechanisms by which compromised cells are eliminated. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Apoptosis signaling subgraph
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
XIAP subgraph

complex(p(HGNC:CASP1), p(HGNC:CASP1)) hasComponent p(HGNC:CASP1) View Subject | View Object

Appears in Networks:

complex(p(HGNC:CASP1), p(HGNC:CASP1)) increases act(p(HGNC:CASP1)) View Subject | View Object

Using its CARD, ASC brings monomers of procaspase 1 into close proximity, which initiates caspase 1 self- cleavage and the formation of the active heterotetrameric caspase 1. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

composite(complex(GO:"NLRP1 inflammasome complex"), p(HGNC:PYCARD)) increases act(p(HGNC:CASP1)) View Subject | View Object

NLRC4 and NLRP1 can both activate caspase 1 through their CARDs without recruiting ASC; however, the recruitment of ASC greatly enhances the formation of the complex and the processing of IL-1β7,13–16. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

complex(p(HGNC:CASP1), p(MGI:Casp12)) hasComponent p(HGNC:CASP1) View Subject | View Object

Appears in Networks:

complex(p(HGNC:CASP1), p(MGI:Casp12)) decreases act(p(HGNC:CASP1)) View Subject | View Object

Similarly, mouse caspase 12, which is a paralogue of caspase 1, interacts with caspase 1 to reduce its activity110 PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
MeSH
Extracellular Space
NeuroMMSigDB
Caspase subgraph

composite(complex(GO:"IPAF inflammasome complex"), p(HGNC:PYCARD)) increases act(p(HGNC:CASP1)) View Subject | View Object

NLRC4 and NLRP1 can both activate caspase 1 through their CARDs without recruiting ASC; however, the recruitment of ASC greatly enhances the formation of the complex and the processing of IL-1β7,13–16. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

p(HGNC:CARD16) decreases act(p(HGNC:CASP1)) View Subject | View Object

CARD-only proteins (COPs) can also inhibit caspase 1 activation112. CARD18 (also known as ICEBERG) and CARD16 (also known as pseudoICE and COP1) were the first ‘decoy’ COPs to be described113. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
MeSH
Extracellular Space
NeuroMMSigDB
Caspase subgraph

p(HGNC:CARD18) decreases act(p(HGNC:CASP1)) View Subject | View Object

CARD-only proteins (COPs) can also inhibit caspase 1 activation112. CARD18 (also known as ICEBERG) and CARD16 (also known as pseudoICE and COP1) were the first ‘decoy’ COPs to be described113. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
MeSH
Extracellular Space
NeuroMMSigDB
Caspase subgraph

p(HGNC:CASP1, pmod(NO)) decreases act(p(HGNC:CASP1)) View Subject | View Object

By contrast, nitrosylation of caspase 9 inhibits its function94. Similarly, caspase 1 can be inhibited by nitrosylation95, which suggests that modification by reactive molecules is a general mechanism for the regulation of caspase activity. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
MeSH
Extracellular Space
NeuroMMSigDB
Caspase subgraph

act(p(HGNC:RIPK3)) increases act(p(HGNC:CASP1)) View Subject | View Object

The formation of this complex activates RIP3, which is necessary for the cleavage of pro-IL-1β by both the NLRP3-caspase 1 and the caspase 8 pathways56 (FIG. 1). PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

complex(GO:"NLRP1 inflammasome complex") hasComponent p(HGNC:CASP1) View Subject | View Object

Appears in Networks:

complex(GO:"NLRP3 inflammasome complex") hasComponent p(HGNC:CASP1) View Subject | View Object

Appears in Networks:

act(complex(GO:"inflammasome complex")) increases act(p(HGNC:CASP1)) View Subject | View Object

Like IL-1β, in most cases, the mature secretable form of IL-18 is generated by caspase-1 through the activation of inflammasome PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

complex(p(HGNC:CASP1), p(HGNC:NLRP1), p(HGNC:PYCARD)) hasComponent p(HGNC:CASP1) View Subject | View Object

Appears in Networks:

complex(p(HGNC:CASP1), p(HGNC:NLRP3), p(HGNC:PYCARD)) hasComponent p(HGNC:CASP1) View Subject | View Object

Appears in Networks:

composite(complex(GO:"inflammasome complex"), p(HGNC:NLRP2)) association p(HGNC:CASP1) View Subject | View Object

ATP, a danger-associated molecular pattern that is released from damaged cells after brain injury, activates the NLRP2 inflammasome, which consists of the NLRP2 receptor, ASC and caspase-1, in human astrocytes (Minkiewicz et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

complex(GO:"NLRP3 inflammasome complex") increases p(HGNC:CASP1) View Subject | View Object

The NLRP3 inflammasome has a role in AD by increas- ing caspase-1 expression levels in AD brains [13, 23]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph

act(complex(GO:"inflammasome complex")) increases act(p(HGNC:CASP1)) View Subject | View Object

Post activation of the inflammasome, caspase 1 enzyme initiates the maturation of pro-inflammatory cytokines particularly interleukin (IL)-1beta, IL-18, and IL-33 [4] (Fig. 1),and inflammation mediated cell death occurs via the nucleotide-binding domain and leucine-rich repeat(NLR) family of proteins [5]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

complex(GO:"inflammasome complex") increases act(p(HGNC:CASP1)) View Subject | View Object

Both IL-1 beta and IL-18 are generated in their mature secreted form by caspase-1 through activa- tion of the inflammasome. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

composite(complex(GO:"NLRP3 inflammasome complex"), p(HGNC:CASP1), p(HGNC:PYCARD)) hasComponent p(HGNC:CASP1) View Subject | View Object

Appears in Networks:

composite(complex(GO:"NLRP3 inflammasome complex"), p(HGNC:CASP1), p(HGNC:PYCARD)) increases act(p(HGNC:CASP1)) View Subject | View Object

In the NLRP3 inflammasome, the NLR pro- tein recruits the inflammasome-adaptor protein apoptosis-associated speck-like protein containing CARD (ASC), which in turn interacts with caspase- 1 leading to its activation [7]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph

act(p(HGNC:NLRP3)) increases sec(p(HGNC:CASP1)) View Subject | View Object

In AD, microglial cells and astrocytes express NLRP3, which in turn can detect A beta plaques and act by secreting caspase-1 to activate IL-1 beta and IL- 18 [23–25]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:NLRP3) positiveCorrelation p(HGNC:CASP1) View Subject | View Object

As a component of inflammasome, NLRP3 is the best characterized member of NLRs, which recruits and activates caspase-1 via the adapter molecule ASC (apoptosis- associated speck-like protein containing caspase activation and recruitment domain) [8, 9]. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

Out-Edges 29

p(HGNC:CASP1) increases act(p(HGNC:IL18)) View Subject | View Object

Activation of NLRP3 leads to the generation of interleukin-1b (IL-1b) and interleukin 18 (IL-18), which are being cleaved by caspase-1 from their inactive precursors and subsequently PubMed:28019679

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:CASP1) increases act(p(HGNC:IL1B)) View Subject | View Object

Activation of NLRP3 leads to the generation of interleukin-1b (IL-1b) and interleukin 18 (IL-18), which are being cleaved by caspase-1 from their inactive precursors and subsequently PubMed:28019679

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases a(CHEBI:"nitric oxide") View Subject | View Object

NLRP3 inflammasome formation and subsequent activation of caspase-1 cleavage capacity was instrumental for Abeta-induced nitric oxide production and TNF-a release PubMed:28019679

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Nitric oxide subgraph

act(p(HGNC:CASP1)) increases sec(p(HGNC:TNF)) View Subject | View Object

NLRP3 inflammasome formation and subsequent activation of caspase-1 cleavage capacity was instrumental for Abeta-induced nitric oxide production and TNF-a release PubMed:28019679

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Tumor necrosis factor subgraph

act(p(HGNC:CASP1)) increases bp(GO:pyroptosis) View Subject | View Object

Further data, showing “neuronal pyroptosis” of Abeta exposed neurons in a NLRP1- dependent and caspase-1-mediated manner may point to a vicious cycle, by which NLRP1 is causing neurodegeneration in response to increased Abeta production (14) PubMed:28019679

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Neurons
NeuroMMSigDB
Apoptosis signaling subgraph
NeuroMMSigDB
Caspase subgraph

p(HGNC:CASP1) hasVariant p(HGNC:CASP1, pmod(NO)) View Subject | View Object

Appears in Networks:

act(p(HGNC:CASP1)) increases act(p(HGNC:IL1B)) View Subject | View Object

Once the protein complexes have formed, the inflammasomes activate caspase 1, which proteolytically activates the pro-inflammatory cytokines interleukin-1β (IL-1β)3 and IL-18. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL1B)) View Subject | View Object

Active caspase 1 proteolytically activates a number of proteins8, including pro-IL-1β and pro-IL-18 (REFS 9,10), and induces their release via a non-classical secretion pathway11. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases sec(p(HGNC:IL1B)) View Subject | View Object

Active caspase 1 proteolytically activates a number of proteins8, including pro-IL-1β and pro-IL-18 (REFS 9,10), and induces their release via a non-classical secretion pathway11. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL1B)) View Subject | View Object

Caspase 1mediated activation of members of the IL-1β cytokine family leads to the recruitment and the activation of other immune cells, such as neutrophils, at the site of infection and/or tissue damage. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

Once the protein complexes have formed, the inflammasomes activate caspase 1, which proteolytically activates the pro-inflammatory cytokines interleukin-1β (IL-1β)3 and IL-18. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

Active caspase 1 proteolytically activates a number of proteins8, including pro-IL-1β and pro-IL-18 (REFS 9,10), and induces their release via a non-classical secretion pathway11. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases sec(p(HGNC:IL18)) View Subject | View Object

Active caspase 1 proteolytically activates a number of proteins8, including pro-IL-1β and pro-IL-18 (REFS 9,10), and induces their release via a non-classical secretion pathway11. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases bp(GO:pyroptosis) View Subject | View Object

Indeed, inflammasomes (which induce pyroptosis through caspase 1 or caspase 11 activation) and apoptosomes (which activate caspase 9 in response to cytochrome c release from mitochondria) are two mechanisms by which compromised cells are eliminated. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Apoptosis signaling subgraph
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
XIAP subgraph

p(HGNC:CASP1) increases p(HGNC:IL1B) View Subject | View Object

Caspase-1 is the protease that cleaves the precursor of the proinflammatory molecules to form their mature form, such as IL-1β and IL-18 (Schroder and Tschopp, 2010) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:CASP1) increases p(HGNC:IL18) View Subject | View Object

Caspase-1 is the protease that cleaves the precursor of the proinflammatory molecules to form their mature form, such as IL-1β and IL-18 (Schroder and Tschopp, 2010) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:CASP1) increases p(HGNC:IL18) View Subject | View Object

Like IL-1β, in most cases, the mature secretable form of IL-18 is generated by caspase-1 through the activation of inflammasome PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:CASP1) association composite(complex(GO:"inflammasome complex"), p(HGNC:NLRP2)) View Subject | View Object

ATP, a danger-associated molecular pattern that is released from damaged cells after brain injury, activates the NLRP2 inflammasome, which consists of the NLRP2 receptor, ASC and caspase-1, in human astrocytes (Minkiewicz et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL1B)) View Subject | View Object

Post activation of the inflammasome, caspase 1 enzyme initiates the maturation of pro-inflammatory cytokines particularly interleukin (IL)-1beta, IL-18, and IL-33 [4] (Fig. 1),and inflammation mediated cell death occurs via the nucleotide-binding domain and leucine-rich repeat(NLR) family of proteins [5]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL33)) View Subject | View Object

Post activation of the inflammasome, caspase 1 enzyme initiates the maturation of pro-inflammatory cytokines particularly interleukin (IL)-1beta, IL-18, and IL-33 [4] (Fig. 1),and inflammation mediated cell death occurs via the nucleotide-binding domain and leucine-rich repeat(NLR) family of proteins [5]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

sec(p(HGNC:CASP1)) increases act(p(HGNC:IL1B)) View Subject | View Object

In AD, microglial cells and astrocytes express NLRP3, which in turn can detect A beta plaques and act by secreting caspase-1 to activate IL-1 beta and IL- 18 [23–25]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL1B)) View Subject | View Object

Both IL-1 beta and IL-18 are generated in their mature secreted form by caspase-1 through activa- tion of the inflammasome. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL1B)) View Subject | View Object

Once activated, caspase-1 promotes the maturation of the proin- flammatory cytokines IL-1 beta , IL-18, and IL-33. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

Post activation of the inflammasome, caspase 1 enzyme initiates the maturation of pro-inflammatory cytokines particularly interleukin (IL)-1beta, IL-18, and IL-33 [4] (Fig. 1),and inflammation mediated cell death occurs via the nucleotide-binding domain and leucine-rich repeat(NLR) family of proteins [5]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

sec(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

In AD, microglial cells and astrocytes express NLRP3, which in turn can detect A beta plaques and act by secreting caspase-1 to activate IL-1 beta and IL- 18 [23–25]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

Both IL-1 beta and IL-18 are generated in their mature secreted form by caspase-1 through activa- tion of the inflammasome. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

Once activated, caspase-1 promotes the maturation of the proin- flammatory cytokines IL-1 beta , IL-18, and IL-33. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL33)) View Subject | View Object

Once activated, caspase-1 promotes the maturation of the proin- flammatory cytokines IL-1 beta , IL-18, and IL-33. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:CASP1) positiveCorrelation p(HGNC:NLRP3) View Subject | View Object

As a component of inflammasome, NLRP3 is the best characterized member of NLRs, which recruits and activates caspase-1 via the adapter molecule ASC (apoptosis- associated speck-like protein containing caspase activation and recruitment domain) [8, 9]. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

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.