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p(HGNC:NGFR)

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Entity

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

Appears in Networks 3

Amyloid β oligomers (AβOs) in Alzheimer’s disease v1.0.0

Cholinergic system during the progression of Alzheimer’s disease: therapeutic implications v1.0.0

Tau Biochemistry v1.2.5

Tau Biochemistry Section of NESTOR

In-Edges 10

a(HBP:HBP00074) increases act(p(HGNC:NGFR)) View Subject | View Object

Synapse targeting of AβOs involves activation of p75NTR. PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Hippocampus

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:NGFR) View Subject | View Object

They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Plasma

path(MESH:"Cognitive Dysfunction") positiveCorrelation p(HGNC:NGFR) View Subject | View Object

They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Plasma

complex(a(MESHC:"pro-nerve growth factor, human"), p(HGNC:NGFR)) hasComponent p(HGNC:NGFR) View Subject | View Object

Appears in Networks:

bp(GO:"GO:0006665") association act(p(HGNC:NGFR)) View Subject | View Object

Recent evidence supports the notion that p75NTR has an intrinsic signaling capacity including: • Sphingolipid metabolism [98–100] • Activation of the JNK pathway [52,54,56,101–103] • Activation of the NF-kappaB pathway [104–109] • Activation of the Akt pathway [110] • Activation of the MAPK pathway [97,111] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

bp(GO:"GO:1901214") association p(HGNC:NGFR) View Subject | View Object

NGF is synthesized as a precursor (proNGF) molecule that is proteolytically cleaved to a mature biologically active neurotrophin peptide [49]. Mature NGF binds to the TrkA receptor, which stimulates signal transduction pathways mediating the majority of the survival and growth effects of NGF [50], and to the p75NTR receptor, which is a positive modulator of NGF/TrkA binding [50]. However, p75NTR has multiple functions, including apoptotic or cell death actions [51–56], which are dependent upon its interaction with various receptor chaperones [57–59]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

bp(MESH:D000375) increases p(HGNC:NGFR) View Subject | View Object

It is also important to note that TrkA reduces and p75NTR activates β-secretase strike (BACE) cleavage of the amyloid precursor protein (APP), which requires NGF binding and activation of the second messenger ceramide [66]. Aging may activate beta-amyloid (Ab) generation in the brain by ‘switching’ from TrkA to p75NTR, suggesting that NGF receptor balance is a molecular link between normal aging of the brain and AD in relation to amyloid processing. PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Cognitive Dysfunction

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

Appears in Networks:

complex(p(HGNC:NGFR), p(HGNC:SORT1)) hasComponent p(HGNC:NGFR) View Subject | View Object

Appears in Networks:

p(HBP:RAC1b) association p(HGNC:NGFR) View Subject | View Object

CBF tissues harvested from people who died with a clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment, or AD were immunolabeled for both p75NTR and Rac1b. Rac1b appeared as cytoplasmic diffuse granules, loosely aggregated filaments, or compact spheres in p75NTR-positive NB neurons. Although Rac1b colocalized with tau cytoskeletal markers, the percentage of p75NTR-immunoreactive neurons expressing Rac1b was significantly increased only in AD compared with both mild cognitive impairment and NCI. PubMed:22142809

Appears in Networks:
Annotations
Uberon
basal nucleus of telencephalon
Cell Ontology (CL)
cholinergic neuron
Disease Ontology (DO)
Alzheimer's disease

Out-Edges 11

p(HGNC:NGFR) positiveCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Plasma

p(HGNC:NGFR) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Plasma

p(HGNC:NGFR) association bp(GO:"GO:1901214") View Subject | View Object

NGF is synthesized as a precursor (proNGF) molecule that is proteolytically cleaved to a mature biologically active neurotrophin peptide [49]. Mature NGF binds to the TrkA receptor, which stimulates signal transduction pathways mediating the majority of the survival and growth effects of NGF [50], and to the p75NTR receptor, which is a positive modulator of NGF/TrkA binding [50]. However, p75NTR has multiple functions, including apoptotic or cell death actions [51–56], which are dependent upon its interaction with various receptor chaperones [57–59]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

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

It is also important to note that TrkA reduces and p75NTR activates β-secretase strike (BACE) cleavage of the amyloid precursor protein (APP), which requires NGF binding and activation of the second messenger ceramide [66]. Aging may activate beta-amyloid (Ab) generation in the brain by ‘switching’ from TrkA to p75NTR, suggesting that NGF receptor balance is a molecular link between normal aging of the brain and AD in relation to amyloid processing. PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Cognitive Dysfunction

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

It is also important to note that TrkA reduces and p75NTR activates β-secretase strike (BACE) cleavage of the amyloid precursor protein (APP), which requires NGF binding and activation of the second messenger ceramide [66]. Aging may activate beta-amyloid (Ab) generation in the brain by ‘switching’ from TrkA to p75NTR, suggesting that NGF receptor balance is a molecular link between normal aging of the brain and AD in relation to amyloid processing. PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Cognitive Dysfunction

act(p(HGNC:NGFR)) association bp(GO:"GO:0006665") View Subject | View Object

Recent evidence supports the notion that p75NTR has an intrinsic signaling capacity including: • Sphingolipid metabolism [98–100] • Activation of the JNK pathway [52,54,56,101–103] • Activation of the NF-kappaB pathway [104–109] • Activation of the Akt pathway [110] • Activation of the MAPK pathway [97,111] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

act(p(HGNC:NGFR)) increases bp(GO:"GO:0007254") View Subject | View Object

Recent evidence supports the notion that p75NTR has an intrinsic signaling capacity including: • Sphingolipid metabolism [98–100] • Activation of the JNK pathway [52,54,56,101–103] • Activation of the NF-kappaB pathway [104–109] • Activation of the Akt pathway [110] • Activation of the MAPK pathway [97,111] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

act(p(HGNC:NGFR)) increases bp(GO:"GO:0038061") View Subject | View Object

Recent evidence supports the notion that p75NTR has an intrinsic signaling capacity including: • Sphingolipid metabolism [98–100] • Activation of the JNK pathway [52,54,56,101–103] • Activation of the NF-kappaB pathway [104–109] • Activation of the Akt pathway [110] • Activation of the MAPK pathway [97,111] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

act(p(HGNC:NGFR)) increases bp(GO:"GO:0043491") View Subject | View Object

Recent evidence supports the notion that p75NTR has an intrinsic signaling capacity including: • Sphingolipid metabolism [98–100] • Activation of the JNK pathway [52,54,56,101–103] • Activation of the NF-kappaB pathway [104–109] • Activation of the Akt pathway [110] • Activation of the MAPK pathway [97,111] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

act(p(HGNC:NGFR)) increases bp(GO:"GO:0000165") View Subject | View Object

Recent evidence supports the notion that p75NTR has an intrinsic signaling capacity including: • Sphingolipid metabolism [98–100] • Activation of the JNK pathway [52,54,56,101–103] • Activation of the NF-kappaB pathway [104–109] • Activation of the Akt pathway [110] • Activation of the MAPK pathway [97,111] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

p(HGNC:NGFR) association p(HBP:RAC1b) View Subject | View Object

CBF tissues harvested from people who died with a clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment, or AD were immunolabeled for both p75NTR and Rac1b. Rac1b appeared as cytoplasmic diffuse granules, loosely aggregated filaments, or compact spheres in p75NTR-positive NB neurons. Although Rac1b colocalized with tau cytoskeletal markers, the percentage of p75NTR-immunoreactive neurons expressing Rac1b was significantly increased only in AD compared with both mild cognitive impairment and NCI. PubMed:22142809

Appears in Networks:
Annotations
Uberon
basal nucleus of telencephalon
Cell Ontology (CL)
cholinergic neuron
Disease Ontology (DO)
Alzheimer's 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.