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Appears in Networks 3

In-Edges 13

surf(p(HGNC:GRIK2)) negativeCorrelation act(p(HGNC:RAB5A)) View Subject | View Object

TTBK2 down-regulates GluK2 activity by decreasing the receptor protein abundance in the cell membrane via RAB5-dependent endocytosis, an effect that may protect against neuroexcitotoxicity. PubMed:27607061

Appears in Networks:

a(CHEBI:lipid) positiveCorrelation act(p(HGNC:RAB5A)) View Subject | View Object

It is this abnormal rab5 activation that causes protein and lipid accumulation in endosomes, slowed lysosomal degradation of endocytic cargoes,endosome swelling (Cataldo et al. 2008), and disrupted retrograde transport of endosomes (S Kim and RA Nixon, unpubl.). PubMed:22908190

a(MESH:Proteins) positiveCorrelation act(p(HGNC:RAB5A)) View Subject | View Object

It is this abnormal rab5 activation that causes protein and lipid accumulation in endosomes, slowed lysosomal degradation of endocytic cargoes,endosome swelling (Cataldo et al. 2008), and disrupted retrograde transport of endosomes (S Kim and RA Nixon, unpubl.). PubMed:22908190

bp(GO:"long-term synaptic depression") negativeCorrelation act(p(HGNC:RAB5A)) 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

bp(GO:"long-term synaptic potentiation") negativeCorrelation act(p(HGNC:RAB5A)) 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

bp(GO:"lysosomal protein catabolic process") negativeCorrelation act(p(HGNC:RAB5A)) View Subject | View Object

It is this abnormal rab5 activation that causes protein and lipid accumulation in endosomes, slowed lysosomal degradation of endocytic cargoes,endosome swelling (Cataldo et al. 2008), and disrupted retrograde transport of endosomes (S Kim and RA Nixon, unpubl.). PubMed:22908190

bp(GO:"neuron death") positiveCorrelation act(p(HGNC:RAB5A)) View Subject | View Object

Interactions between FAD-mutant forms of APP and APP binding protein (APP-BP1) on endosomes also initiate pathological rab5 activation, which was shown to promote a neuronal apoptosis cascade (Laifenfeld et al. 2007). PubMed:22908190

bp(GO:"regulation of endosome size") association p(HGNC:RAB5A) View Subject | View Object

Genes related to endocytosis, such as Rab5,Rab7, and Rab4, are among the earliest groups to showup-regulated transcription in AD(Ginsberg et al. 2010), and their corresponding proteins are abnormally recruited to endosomes, where they promote fusion and abnormal enlargement of early and late endosomes (Cataldo et al. 1997, 2008). PubMed:22908190

complex(a(GO:endosome), p(HGNC:APP, var("?")), p(HGNC:NAE1)) increases act(p(HGNC:RAB5A)) View Subject | View Object

Interactions between FAD-mutant forms of APP and APP binding protein (APP-BP1) on endosomes also initiate pathological rab5 activation, which was shown to promote a neuronal apoptosis cascade (Laifenfeld et al. 2007). PubMed:22908190

p(HBP:"APP C-terminally truncated carboxyl-terminal fragments") increases act(p(HGNC:RAB5A)) View Subject | View Object

Recently, these effects of increased App dosage were shown to be mediated specifically by the b-cleaved carboxy-terminal fragment of APP, bCTF (Jiang et al. 2010), which binds to a complex of signaling molecules on endosomes that pathologically activates rab5 (S Kim and RA Nixon, unpubl.). PubMed:22908190

p(HBP:"APP C-terminally truncated carboxyl-terminal fragments") increases act(p(HGNC:RAB5A)) 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

p(HGNC:RIN1) increases act(p(HGNC:RAB5A)) View Subject | View Object

Conversely, deletion of the neuronal rab5 GEF, rin1, reduces rab5 activation, increases LTP induction in the amygdala, and enhances fear learning and memory, most likely by increasing surface levels of AMPA receptors (Dhaka et al. 2003). PubMed:22908190

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:RAB5A) View Subject | View Object

Genes related to endocytosis, such as Rab5,Rab7, and Rab4, are among the earliest groups to showup-regulated transcription in AD(Ginsberg et al. 2010), and their corresponding proteins are abnormally recruited to endosomes, where they promote fusion and abnormal enlargement of early and late endosomes (Cataldo et al. 1997, 2008). PubMed:22908190

Out-Edges 16

act(p(HGNC:RAB5A)) decreases bp(HP:Neurodegeneration) View Subject | View Object

Interestingly, genetic or pharmacological activation of RAB5 countered neurodegeneration in mouse C9ORF72 models of ALS and FTD 187 . PubMed:30116051

act(p(HGNC:RAB5A)) negativeCorrelation surf(p(HGNC:GRIK2)) View Subject | View Object

TTBK2 down-regulates GluK2 activity by decreasing the receptor protein abundance in the cell membrane via RAB5-dependent endocytosis, an effect that may protect against neuroexcitotoxicity. PubMed:27607061

Appears in Networks:

p(HGNC:RAB5A) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Genes related to endocytosis, such as Rab5,Rab7, and Rab4, are among the earliest groups to showup-regulated transcription in AD(Ginsberg et al. 2010), and their corresponding proteins are abnormally recruited to endosomes, where they promote fusion and abnormal enlargement of early and late endosomes (Cataldo et al. 1997, 2008). PubMed:22908190

p(HGNC:RAB5A) increases complex(a(GO:"early endosome"), a(GO:"late endosome")) View Subject | View Object

Genes related to endocytosis, such as Rab5,Rab7, and Rab4, are among the earliest groups to showup-regulated transcription in AD(Ginsberg et al. 2010), and their corresponding proteins are abnormally recruited to endosomes, where they promote fusion and abnormal enlargement of early and late endosomes (Cataldo et al. 1997, 2008). PubMed:22908190

p(HGNC:RAB5A) association bp(GO:"regulation of endosome size") View Subject | View Object

Genes related to endocytosis, such as Rab5,Rab7, and Rab4, are among the earliest groups to showup-regulated transcription in AD(Ginsberg et al. 2010), and their corresponding proteins are abnormally recruited to endosomes, where they promote fusion and abnormal enlargement of early and late endosomes (Cataldo et al. 1997, 2008). PubMed:22908190

act(p(HGNC:RAB5A)) positiveCorrelation a(MESH:Proteins) View Subject | View Object

It is this abnormal rab5 activation that causes protein and lipid accumulation in endosomes, slowed lysosomal degradation of endocytic cargoes,endosome swelling (Cataldo et al. 2008), and disrupted retrograde transport of endosomes (S Kim and RA Nixon, unpubl.). PubMed:22908190

act(p(HGNC:RAB5A)) positiveCorrelation a(CHEBI:lipid) View Subject | View Object

It is this abnormal rab5 activation that causes protein and lipid accumulation in endosomes, slowed lysosomal degradation of endocytic cargoes,endosome swelling (Cataldo et al. 2008), and disrupted retrograde transport of endosomes (S Kim and RA Nixon, unpubl.). PubMed:22908190

act(p(HGNC:RAB5A)) negativeCorrelation bp(GO:"lysosomal protein catabolic process") View Subject | View Object

It is this abnormal rab5 activation that causes protein and lipid accumulation in endosomes, slowed lysosomal degradation of endocytic cargoes,endosome swelling (Cataldo et al. 2008), and disrupted retrograde transport of endosomes (S Kim and RA Nixon, unpubl.). PubMed:22908190

act(p(HGNC:RAB5A)) positiveCorrelation bp(GO:"neuron death") View Subject | View Object

Interactions between FAD-mutant forms of APP and APP binding protein (APP-BP1) on endosomes also initiate pathological rab5 activation, which was shown to promote a neuronal apoptosis cascade (Laifenfeld et al. 2007). PubMed:22908190

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

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

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

act(p(HGNC:RAB5A)) increases 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

act(p(HGNC:RAB5A)) negativeCorrelation bp(GO:"long-term synaptic potentiation") 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

act(p(HGNC:RAB5A)) negativeCorrelation bp(GO:"long-term synaptic depression") 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

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.