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bp(GO:endocytosis)

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Entity

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

Appears in Networks 8

Perilous journey: a tour of the ubiquitin–proteasome system v1.0.0

Extracellular Monomeric and Aggregated Tau Efficiently Enter Human Neurons through Overlapping but Distinct Pathways v1.0.1

Tau Internalization is Regulated by 6-O Sulfation on Heparan Sulfate Proteoglycans (HSPGs) v1.0.1

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage from Shafiei et al., 2017

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

The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0

Autophagy and the ubiquitin-proteasome system: collaborators in neuroprotection v1.0.0

Protein aggregation can inhibit clathrin-mediated endocytosis by chaperone competition v1.0.0

In-Edges 25

a(MESH:Ubiquitin) regulates bp(GO:endocytosis) View Subject | View Object

For instance, ubiquitin can recruit other factors to mediate various cellular responses such as signaling, gene regulation, endocytosis, macro-autophagy, and DNA repair PubMed:24457024

Appears in Networks:

bp(GO:"mitotic G1 phase") positiveCorrelation bp(GO:endocytosis) View Subject | View Object

Endocytosis is known to increase during G1 phase25; therefore, it seemed logical that cell cycle regulators that can shorten the G1 phase could reduce the amount of tau uptake and vice versa. PubMed:29686391

Appears in Networks:

p(HGNC:BECN1) association bp(GO:endocytosis) View Subject | View Object

These results may be attributed to coincidental evidence of the involvement of Beclin 1 in VPS34-mediated trafficking pathways including macroautophagy and endocytosis [37], both of which are pronouncedly affected in AD pathology [38] PubMed:29758300

Appears in Networks:

p(HGNC:BIN1) increases bp(GO:endocytosis) View Subject | View Object

BIN1 is involved in the endocytosis and the endosomal sorting of membrane proteins PubMed:29758300

Appears in Networks:

path(MESH:"Alzheimer Disease") negativeCorrelation bp(GO:endocytosis) View Subject | View Object

These results may be attributed to coincidental evidence of the involvement of Beclin 1 in VPS34-mediated trafficking pathways including macroautophagy and endocytosis [37], both of which are pronouncedly affected in AD pathology [38] PubMed:29758300

Appears in Networks:

tloc(a(CHEBI:"amyloid-beta polypeptide 42"), fromLoc(GO:cytosol), toLoc(GO:lysosome)) positiveCorrelation bp(GO:endocytosis) View Subject | View Object

By up-regulating endocytosis, high dietary LDL-cholesterol and overexpression of its receptor ApoE (particularly ApoE 14) elevate bCTF levels and increase delivery of Ab1–42 to lysosomes in cellular model systems (Ji et al. 2006; Cossec et al. 2010). PubMed:22908190

Appears in Networks:

a(CHEBI:"amyloid-beta") positiveCorrelation bp(GO:endocytosis) View Subject | View Object

Endocytic pathway up-regulation in AD stemming in part from pathological rab 5 activation generates higher levels of Ab (Mathews et al. 2002; Grbovic et al. 2003) that must be cleared in part by lysosomes. PubMed:22908190

Appears in Networks:

a(CHEBI:"amyloid-beta") positiveCorrelation bp(GO:endocytosis) View Subject | View Object

Pathological rab5 activation, which in Down syndrome is dependent on bCTF generation (Jiang et al. 2010), can up-regulate endocytosis in a manner functionally equivalent to the elevated endocytosis associated with increased synaptic activity, which is considered a source of Ab generation (Cirrito et al. 2008). PubMed:22908190

Appears in Networks:
Annotations
MeSH
Down Syndrome

a(CHEBI:cholesterol) positiveCorrelation bp(GO:endocytosis) View Subject | View Object

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

Appears in Networks:

a(CHEBI:lipid) positiveCorrelation bp(GO:endocytosis) View Subject | View Object

Accelerated endocytosis also increases protein and lipid accumulation in endosomes and slows lysosomal degradation of endocytic cargoes (Cataldo et al. 2008), leading to lysosomal instability and neurodegeneration, as discussed below. PubMed:22908190

Appears in Networks:
Annotations
MeSH
Endosomes

act(a(GO:synapse)) positiveCorrelation bp(GO:endocytosis) View Subject | View Object

Pathological rab5 activation, which in Down syndrome is dependent on bCTF generation (Jiang et al. 2010), can up-regulate endocytosis in a manner functionally equivalent to the elevated endocytosis associated with increased synaptic activity, which is considered a source of Ab generation (Cirrito et al. 2008). PubMed:22908190

Appears in Networks:
Annotations
MeSH
Down Syndrome

a(MESH:Proteins) positiveCorrelation bp(GO:endocytosis) View Subject | View Object

Accelerated endocytosis also increases protein and lipid accumulation in endosomes and slows lysosomal degradation of endocytic cargoes (Cataldo et al. 2008), leading to lysosomal instability and neurodegeneration, as discussed below. PubMed:22908190

Appears in Networks:
Annotations
MeSH
Endosomes

bp(GO:"lysosomal protein catabolic process") negativeCorrelation bp(GO:endocytosis) View Subject | View Object

Accelerated endocytosis also increases protein and lipid accumulation in endosomes and slows lysosomal degradation of endocytic cargoes (Cataldo et al. 2008), leading to lysosomal instability and neurodegeneration, as discussed below. PubMed:22908190

Appears in Networks:
Annotations
MeSH
Endosomes

bp(GO:"regulation of synaptic plasticity") association bp(GO:endocytosis) View Subject | View Object

Although key to the survival of all cells, endocytosis supports unique neuronal functions, including aspects of synaptic transmission and plasticity underlying memory and learning. PubMed:22908190

Appears in Networks:

p(HGNC:APP, var("?")) increases bp(GO:endocytosis) View Subject | View Object

In DS, the extra copy of App causes endocytic up-regulation and endosome pathology similar to that seen at the earliest stages of sporadic AD, but beginning even earlier PubMed:22908190

Appears in Networks:
Annotations
MeSH
Down Syndrome

p(HGNC:APP) positiveCorrelation bp(GO:endocytosis) View Subject | View Object

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

Appears in Networks:

g(HBP:"APOE e4") positiveCorrelation bp(GO:endocytosis) View Subject | View Object

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

Appears in Networks:

p(HBP:"APP C-terminally truncated carboxyl-terminal fragments") positiveCorrelation bp(GO:endocytosis) View Subject | View Object

By up-regulating endocytosis, high dietary LDL-cholesterol and overexpression of its receptor ApoE (particularly ApoE 14) elevate bCTF levels and increase delivery of Ab1–42 to lysosomes in cellular model systems (Ji et al. 2006; Cossec et al. 2010). PubMed:22908190

Appears in Networks:

act(p(HGNC:RAB5A)) increases bp(GO:endocytosis) View Subject | View Object

Endocytic pathway up-regulation in AD stemming in part from pathological rab 5 activation generates higher levels of Ab (Mathews et al. 2002; Grbovic et al. 2003) that must be cleared in part by lysosomes. PubMed:22908190

Appears in Networks:

act(p(HGNC:RAB5A)) increases bp(GO:endocytosis) View Subject | View Object

Pathological rab5 activation, which in Down syndrome is dependent on bCTF generation (Jiang et al. 2010), can up-regulate endocytosis in a manner functionally equivalent to the elevated endocytosis associated with increased synaptic activity, which is considered a source of Ab generation (Cirrito et al. 2008). PubMed:22908190

Appears in Networks:
Annotations
MeSH
Down Syndrome

act(p(HGNC:RAB5A)) decreases bp(GO:endocytosis) View Subject | View Object

Pathological Rab5 activation driving endocytic dysfunction in AD may negatively impact longterm potentiation (LTP) and long-term depression (LTD) aspects of synaptic plasticity closely associated with learning and memory (Kessels et al. 2009) PubMed:22908190

Appears in Networks:

path(MESH:"Alzheimer Disease") negativeCorrelation bp(GO:endocytosis) View Subject | View Object

A continuum of pathological changes of the lysosomal network unfolds in neurons as Alzheimer disease progresses, including dysregulation of endocytosis, increased lysosome biogenesis and, later, progressive failure of lysosomal clearance mechanisms (Fig. 6; Nixon et al. 2006). PubMed:22908190

Appears in Networks:

path(MESH:"Alzheimer Disease") negativeCorrelation bp(GO:endocytosis) View Subject | View Object

Pathological Rab5 activation driving endocytic dysfunction in AD may negatively impact longterm potentiation (LTP) and long-term depression (LTD) aspects of synaptic plasticity closely associated with learning and memory (Kessels et al. 2009) PubMed:22908190

Appears in Networks:

bp(GO:"protein monoubiquitination") increases bp(GO:endocytosis) View Subject | View Object

This view was initially challenged by the observation that monoubiquitination operates as a key signal in endocytosis, a process important for numerous cell functions including lysosomal biogenesis [62] PubMed:18930136

Appears in Networks:

a(HBP:"polyQ aggregates") decreases bp(GO:endocytosis) View Subject | View Object

Previous studies have shown that ag- gregation of expanded polyQ negatively affects endocytosis in yeast and in human HEK 293 cells (34). PubMed:24706768

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
HEK293

Out-Edges 27

bp(GO:endocytosis) increases tloc(p(HGNC:MAPT, var("p.Pro301Ser")), fromLoc(GO:"extracellular region"), toLoc(MESH:Neurons)) View Subject | View Object

Thus, monomeric and aggregated tau both efficiently enter neurons via the endosome/lysosome system, and they are actively trafficked within vesicles over long distances within neurons over several hours PubMed:29590627

Appears in Networks:

bp(GO:endocytosis) increases tloc(a(HBP:"Tau aggregates"), fromLoc(GO:"extracellular region"), toLoc(MESH:Neurons)) View Subject | View Object

Thus, monomeric and aggregated tau both efficiently enter neurons via the endosome/lysosome system, and they are actively trafficked within vesicles over long distances within neurons over several hours PubMed:29590627

Appears in Networks:

bp(GO:endocytosis) increases tloc(a(HBP:"Tau aggregates"), fromLoc(GO:"extracellular region"), toLoc(MESH:Neurons)) View Subject | View Object

These data indicate that, at the concentrations studied, aggregated tau enters neurons almost entirely via endocytosis PubMed:29590627

Appears in Networks:

bp(GO:endocytosis) positiveCorrelation bp(GO:"mitotic G1 phase") View Subject | View Object

Endocytosis is known to increase during G1 phase25; therefore, it seemed logical that cell cycle regulators that can shorten the G1 phase could reduce the amount of tau uptake and vice versa. PubMed:29686391

Appears in Networks:

bp(GO:endocytosis) increases tloc(a(HBP:"Tau aggregates"), fromLoc(GO:endosome), toLoc(GO:lysosome)) View Subject | View Object

Evidence shows that tau aggregates colocalize with dextran and HeLa cells, hinting that internalized aggregates are transported in endosomal vesicles and passed through the endosomal pathway to lysosomes (Wu et al., 2013) PubMed:28420982

Appears in Networks:
Annotations
MeSH
Extracellular Space
Confidence
High
MeSH
Exosomes
MeSH
Alzheimer Disease

bp(GO:endocytosis) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

These results may be attributed to coincidental evidence of the involvement of Beclin 1 in VPS34-mediated trafficking pathways including macroautophagy and endocytosis [37], both of which are pronouncedly affected in AD pathology [38] PubMed:29758300

Appears in Networks:

bp(GO:endocytosis) association p(HGNC:BECN1) View Subject | View Object

These results may be attributed to coincidental evidence of the involvement of Beclin 1 in VPS34-mediated trafficking pathways including macroautophagy and endocytosis [37], both of which are pronouncedly affected in AD pathology [38] PubMed:29758300

Appears in Networks:

bp(GO:endocytosis) increases bp(GO:learning) View Subject | View Object

Although key to the survival of all cells, endocytosis supports unique neuronal functions, including aspects of synaptic transmission and plasticity underlying memory and learning. PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) increases tloc(a(GO:"intrinsic component of plasma membrane"), fromLoc(GO:"plasma membrane"), toLoc(GO:lysosome)) View Subject | View Object

A second route to lysosomes, the endocytic pathway, delivers extracellular material and plasma membrane constituents to lysosomes under the direction of specific targeting signals (Nixon 2004). PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) increases act(a(MESH:Neurons)) View Subject | View Object

Although key to the survival of all cells, endocytosis supports unique neuronal functions, including aspects of synaptic transmission and plasticity underlying memory and learning. PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) association bp(GO:"regulation of synaptic plasticity") View Subject | View Object

Although key to the survival of all cells, endocytosis supports unique neuronal functions, including aspects of synaptic transmission and plasticity underlying memory and learning. PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) increases bp(GO:memory) View Subject | View Object

Although key to the survival of all cells, endocytosis supports unique neuronal functions, including aspects of synaptic transmission and plasticity underlying memory and learning. PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) increases bp(MESH:"Synaptic Transmission") View Subject | View Object

Although key to the survival of all cells, endocytosis supports unique neuronal functions, including aspects of synaptic transmission and plasticity underlying memory and learning. PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

A continuum of pathological changes of the lysosomal network unfolds in neurons as Alzheimer disease progresses, including dysregulation of endocytosis, increased lysosome biogenesis and, later, progressive failure of lysosomal clearance mechanisms (Fig. 6; Nixon et al. 2006). PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Pathological Rab5 activation driving endocytic dysfunction in AD may negatively impact longterm potentiation (LTP) and long-term depression (LTD) aspects of synaptic plasticity closely associated with learning and memory (Kessels et al. 2009) PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) positiveCorrelation p(HGNC:APP) View Subject | View Object

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) positiveCorrelation g(HBP:"APOE e4") View Subject | View Object

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) positiveCorrelation a(CHEBI:cholesterol) View Subject | View Object

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) positiveCorrelation a(MESH:Proteins) View Subject | View Object

Accelerated endocytosis also increases protein and lipid accumulation in endosomes and slows lysosomal degradation of endocytic cargoes (Cataldo et al. 2008), leading to lysosomal instability and neurodegeneration, as discussed below. PubMed:22908190

Appears in Networks:
Annotations
MeSH
Endosomes

bp(GO:endocytosis) positiveCorrelation a(CHEBI:lipid) View Subject | View Object

Accelerated endocytosis also increases protein and lipid accumulation in endosomes and slows lysosomal degradation of endocytic cargoes (Cataldo et al. 2008), leading to lysosomal instability and neurodegeneration, as discussed below. PubMed:22908190

Appears in Networks:
Annotations
MeSH
Endosomes

bp(GO:endocytosis) negativeCorrelation bp(GO:"lysosomal protein catabolic process") View Subject | View Object

Accelerated endocytosis also increases protein and lipid accumulation in endosomes and slows lysosomal degradation of endocytic cargoes (Cataldo et al. 2008), leading to lysosomal instability and neurodegeneration, as discussed below. PubMed:22908190

Appears in Networks:
Annotations
MeSH
Endosomes

bp(GO:endocytosis) positiveCorrelation a(CHEBI:"amyloid-beta") View Subject | View Object

Endocytic pathway up-regulation in AD stemming in part from pathological rab 5 activation generates higher levels of Ab (Mathews et al. 2002; Grbovic et al. 2003) that must be cleared in part by lysosomes. PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) positiveCorrelation a(CHEBI:"amyloid-beta") View Subject | View Object

Pathological rab5 activation, which in Down syndrome is dependent on bCTF generation (Jiang et al. 2010), can up-regulate endocytosis in a manner functionally equivalent to the elevated endocytosis associated with increased synaptic activity, which is considered a source of Ab generation (Cirrito et al. 2008). PubMed:22908190

Appears in Networks:
Annotations
MeSH
Down Syndrome

bp(GO:endocytosis) positiveCorrelation act(a(GO:synapse)) View Subject | View Object

Pathological rab5 activation, which in Down syndrome is dependent on bCTF generation (Jiang et al. 2010), can up-regulate endocytosis in a manner functionally equivalent to the elevated endocytosis associated with increased synaptic activity, which is considered a source of Ab generation (Cirrito et al. 2008). PubMed:22908190

Appears in Networks:
Annotations
MeSH
Down Syndrome

bp(GO:endocytosis) positiveCorrelation p(HBP:"APP C-terminally truncated carboxyl-terminal fragments") View Subject | View Object

By up-regulating endocytosis, high dietary LDL-cholesterol and overexpression of its receptor ApoE (particularly ApoE 14) elevate bCTF levels and increase delivery of Ab1–42 to lysosomes in cellular model systems (Ji et al. 2006; Cossec et al. 2010). PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) positiveCorrelation tloc(a(CHEBI:"amyloid-beta polypeptide 42"), fromLoc(GO:cytosol), toLoc(GO:lysosome)) View Subject | View Object

By up-regulating endocytosis, high dietary LDL-cholesterol and overexpression of its receptor ApoE (particularly ApoE 14) elevate bCTF levels and increase delivery of Ab1–42 to lysosomes in cellular model systems (Ji et al. 2006; Cossec et al. 2010). PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) increases a(GO:lysosome) View Subject | View Object

This view was initially challenged by the observation that monoubiquitination operates as a key signal in endocytosis, a process important for numerous cell functions including lysosomal biogenesis [62] PubMed:18930136

Appears in Networks:

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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.