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bp(GO:phagocytosis)

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Entity

Name
phagocytosis
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 6

Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease v1.0.0

Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0

Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1

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

Alzheimer’s disease and the autophagic-lysosomal system v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 12

a(CHEBI:"GW 3965") increases bp(GO:phagocytosis) View Subject | View Object

Similarly, stimulation of microglia with the LXR agonist, GW3965, acts simultaneously to suppress inflammation and promote fibrillar Ab stimulated phagocytosis [47]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
Medium

act(a(HBP:HBP00038)) increases bp(GO:phagocytosis) View Subject | View Object

Similarly, stimulation of microglia with the LXR agonist, GW3965, acts simultaneously to suppress inflammation and promote fibrillar Ab stimulated phagocytosis [47]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
Medium

act(a(MESH:Microglia)) increases bp(GO:phagocytosis) View Subject | View Object

On the other hand, they may show beneficial effects via facilitating aberrant protein clearance by means of microglial migration to the damaged, aberrant area, and phagocytosis of unnecessary materials in the early stages of AD PubMed:29626319

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(MESH:Microglia) increases bp(GO:phagocytosis) View Subject | View Object

Microglial cells, the key immune cells of the brain, play an important part in the phagocytosis of Aβ PubMed:29626319

Appears in Networks:

p(HGNC:ABCA7) association bp(GO:phagocytosis) View Subject | View Object

In addition, triggering receptor expressed on myeloid cells 2 (TREM2), ATP-binding cassette transporter A7, and CD33 also play key roles in microglial phagocytosis PubMed:29626319

Appears in Networks:

p(HGNC:ABCA7) regulates bp(GO:phagocytosis) View Subject | View Object

A recent study has shown that ABCA7, mainly expressed in human microglial cells, also regulates microglial phagocytic function and decreases Aβ deposition (Zhao et al. 2015a) PubMed:29626319

Appears in Networks:
Annotations
Cell Ontology (CL)
microglial cell

p(HGNC:CD33) association bp(GO:phagocytosis) View Subject | View Object

In addition, triggering receptor expressed on myeloid cells 2 (TREM2), ATP-binding cassette transporter A7, and CD33 also play key roles in microglial phagocytosis PubMed:29626319

Appears in Networks:

p(HGNC:TREM2) association bp(GO:phagocytosis) View Subject | View Object

In addition, triggering receptor expressed on myeloid cells 2 (TREM2), ATP-binding cassette transporter A7, and CD33 also play key roles in microglial phagocytosis PubMed:29626319

Appears in Networks:

act(p(HGNC:TREM2)) increases bp(GO:phagocytosis) View Subject | View Object

In addition, Aβ1–42 can increase the expression of TREM2, a surface signaling receptor in microglia, and the up-regulation of TRME2 can facilitate microglial phagocytosis of Aβ1–42 PubMed:29626319

Appears in Networks:

a(CHEBI:"amyloid-beta") increases bp(GO:phagocytosis) View Subject | View Object

Phagocytosis and subsequent lysosomal damage trigger by Aβ initiate the activation of the NLRP3 inflammasome in the microglia (Halle et al., 2008) PubMed:24561250

Appears in Networks:
Annotations
Cell Ontology (CL)
microglial cell
Confidence
High
NeuroMMSigDB
Amyloidogenic subgraph

p(HGNC:BECN1) increases bp(GO:phagocytosis) View Subject | View Object

For example, Beclin 1 suppression results in impaired microglial phagocytosis of Aβ and reduced recycling of TREM2 [108]. PubMed:29758300

Appears in Networks:
Annotations
Cell Ontology (CL)
microglial cell

p(MGI:Hmgb1) decreases bp(GO:phagocytosis) View Subject | View Object

In summary, these results indicate that heme from resuscitation with stored RBCs increases extracellular release of HMGB1, which inhibits macrophage phagocytosis of P. aeruginosa, leading to increased mortality. PubMed:29522519

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
Text Location
Results

Out-Edges 10

bp(GO:phagocytosis) regulates deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

By contrast, the parenchyma of the CNS is devoid of lymphatic vasculature2; in the brain, removal of cellular debris and toxic molecules, such as amyloid-β peptides, is mediated by a combination of transcellular transport mechanisms across the blood−brain and blood−cerebrospinal fluid (CSF) barriers7–9, phagocytosis and digestion by resident microglia and recruited monocytes and/or macrophages10,11, as well as CSF influx and ISF efflux through a paravascular (glymphatic) route12–14 PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain

bp(GO:phagocytosis) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Intracellular Aβ clearance can be achieved through UPS and ALS, and extracellular Aβ is degraded by glial phagocytosis, such as microglia, astrocytes, and proteases from neurons and astrocytes (Fig. 2) PubMed:29626319

Appears in Networks:
Annotations
MeSH
Extracellular Space

bp(GO:phagocytosis) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Microglial cells, the key immune cells of the brain, play an important part in the phagocytosis of Aβ PubMed:29626319

Appears in Networks:

bp(GO:phagocytosis) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Aβ is cleared by receptor-mediated microglial phagocytosis and degradation, such as scavenger receptors, chemokine-like receptor 1, toll-like receptors, and G protein-coupled receptors including formyl peptide receptor 2 (Yu and Ye 2015) PubMed:29626319

Appears in Networks:

bp(GO:phagocytosis) association p(HGNC:TREM2) View Subject | View Object

In addition, triggering receptor expressed on myeloid cells 2 (TREM2), ATP-binding cassette transporter A7, and CD33 also play key roles in microglial phagocytosis PubMed:29626319

Appears in Networks:

bp(GO:phagocytosis) association p(HGNC:ABCA7) View Subject | View Object

In addition, triggering receptor expressed on myeloid cells 2 (TREM2), ATP-binding cassette transporter A7, and CD33 also play key roles in microglial phagocytosis PubMed:29626319

Appears in Networks:

bp(GO:phagocytosis) association p(HGNC:CD33) View Subject | View Object

In addition, triggering receptor expressed on myeloid cells 2 (TREM2), ATP-binding cassette transporter A7, and CD33 also play key roles in microglial phagocytosis PubMed:29626319

Appears in Networks:

bp(GO:phagocytosis) increases deg(a(CHEBI:"amyloid-beta polypeptide 42")) View Subject | View Object

In addition, Aβ1–42 can increase the expression of TREM2, a surface signaling receptor in microglia, and the up-regulation of TRME2 can facilitate microglial phagocytosis of Aβ1–42 PubMed:29626319

Appears in Networks:

bp(GO:phagocytosis) decreases p(HGNC:MAPT) View Subject | View Object

There was direct evidence to show that microglial phagocytosis plays a pivotal role in clearance of tau in vitro and in vivo (Bolos et al. 2015) PubMed:29626319

Appears in Networks:
Annotations
Cell Ontology (CL)
microglial cell

bp(GO:phagocytosis) increases act(complex(GO:"NLRP3 inflammasome complex")) View Subject | View Object

Phagocytosis and subsequent lysosomal damage trigger by Aβ initiate the activation of the NLRP3 inflammasome in the microglia (Halle et al., 2008) PubMed:24561250

Appears in Networks:
Annotations
Cell Ontology (CL)
microglial cell
Confidence
High
NeuroMMSigDB
Amyloidogenic subgraph

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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.