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p(HGNC:TREM2)

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Entity

Name
TREM2
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 3

Clearance systems in the brain-implications for Alzheimer disease. v1.0.1

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

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

In-Edges 6

path(MESH:"Alzheimer Disease") association p(HGNC:TREM2) View Subject | View Object

although genome-wide association studies have linked LOAD to several other genetic variants, such as TREM2 (triggering receptor expressed on myeloid cells 2),27 clusterin (CLU),28 and phosphatidylinositol-binding clathrin assembly protein (PICALM).28,29 PubMed:26195256

Appears in Networks:

a(CHEBI:"amyloid-beta polypeptide 42") increases p(HGNC:TREM2) 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) 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:

p(HGNC:MAPT) positiveCorrelation p(HGNC:TREM2) View Subject | View Object

In a more recent GWAS investigation, TREM2 (triggering receptor expressed on myeloid cells 2) was identified as one of the markers strongly associated with increased levels of tau and phosphorylated tau in cerebrospinal fluid from AD patients [91]. PubMed:29758300

Appears in Networks:
Annotations
MeSH
Cerebrospinal Fluid
MeSH
Alzheimer Disease

p(HGNC:VPS35) regulates act(p(HGNC:TREM2)) View Subject | View Object

VPS35, one of the retromer-related genes identified from GWAS datasets on AD [110], regulates TREM2’s function in microglia [111]. PubMed:29758300

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

p(HGNC:MAPT, pmod(Ph)) positiveCorrelation p(HGNC:TREM2) View Subject | View Object

In a more recent GWAS investigation, TREM2 (triggering receptor expressed on myeloid cells 2) was identified as one of the markers strongly associated with increased levels of tau and phosphorylated tau in cerebrospinal fluid from AD patients [91]. PubMed:29758300

Appears in Networks:
Annotations
MeSH
Cerebrospinal Fluid
MeSH
Alzheimer Disease

Out-Edges 12

p(HGNC:TREM2) hasVariant p(HGNC:TREM2, var("?")) View Subject | View Object

Appears in Networks:

p(HGNC:TREM2) association path(MESH:"Alzheimer Disease") View Subject | View Object

although genome-wide association studies have linked LOAD to several other genetic variants, such as TREM2 (triggering receptor expressed on myeloid cells 2),27 clusterin (CLU),28 and phosphatidylinositol-binding clathrin assembly protein (PICALM).28,29 PubMed:26195256

Appears in Networks:

p(HGNC:TREM2) hasVariant p(HGNC:TREM2, var("p.Arg47His")) View Subject | View Object

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:

act(p(HGNC:TREM2)) 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:

p(HGNC:TREM2) positiveCorrelation p(HGNC:MAPT) View Subject | View Object

In a more recent GWAS investigation, TREM2 (triggering receptor expressed on myeloid cells 2) was identified as one of the markers strongly associated with increased levels of tau and phosphorylated tau in cerebrospinal fluid from AD patients [91]. PubMed:29758300

Appears in Networks:
Annotations
MeSH
Cerebrospinal Fluid
MeSH
Alzheimer Disease

p(HGNC:TREM2) positiveCorrelation p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

In a more recent GWAS investigation, TREM2 (triggering receptor expressed on myeloid cells 2) was identified as one of the markers strongly associated with increased levels of tau and phosphorylated tau in cerebrospinal fluid from AD patients [91]. PubMed:29758300

Appears in Networks:
Annotations
MeSH
Cerebrospinal Fluid
MeSH
Alzheimer Disease

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

Recent work by Ulland et al. has also discovered an additional function of TREM2 in the maintenance of microglial macroautophagy and metabolism PubMed:29758300

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

p(HGNC:TREM2) increases bp(GO:"metabolic process") View Subject | View Object

Recent work by Ulland et al. has also discovered an additional function of TREM2 in the maintenance of microglial macroautophagy and metabolism PubMed:29758300

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

p(HGNC:TREM2) increases bp(GO:"metabolic process") View Subject | View Object

TREM2 deficiency in an AD mouse model results in suppressed metabolic function in microglia through the dampening of the mTOR signaling pathway, which subsequently elicits a compensatory autophagic response to address the metabolic defect [109]. PubMed:29758300

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

p(HGNC:TREM2) increases act(complex(GO:"TOR complex")) View Subject | View Object

TREM2 deficiency in an AD mouse model results in suppressed metabolic function in microglia through the dampening of the mTOR signaling pathway, which subsequently elicits a compensatory autophagic response to address the metabolic defect [109]. PubMed:29758300

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

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.