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Appears in Networks 2

In-Edges 7

bp(GO:autophagy) decreases a(CHEBI:lipid) View Subject | View Object

Decreased autophagy in the diseased brain may contribute to aberrant lipid accumulation that occurs along with an increased incidence of the metabolic syndrome in aged humans [76] PubMed:29758300

bp(GO:autophagy) increases deg(a(CHEBI:lipid)) View Subject | View Object

While autophagic-lysosomal degradation is more commonly associated with protein degradation, it serves to degrade all cellular material including carbohydrates and lipids. PubMed:29758300

bp(GO:autophagy) negativeCorrelation a(CHEBI:lipid) View Subject | View Object

In addition to the direct modulation of protein generation, lipids can also influence the levels of proteins through autophagic clearance; for instance, increasing lipid contents has been shown to impair autophagy [72]. PubMed:29758300

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

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

Out-Edges 7

a(CHEBI:lipid) regulates bp(GO:"energy homeostasis") View Subject | View Object

In addition to their structural role in membranes, lipids are essential in the maintenance of cellular energy homeostasis as well as regulation of intracellular signaling pathways PubMed:29758300

a(CHEBI:lipid) regulates bp(GO:"intracellular signal transduction") View Subject | View Object

In addition to their structural role in membranes, lipids are essential in the maintenance of cellular energy homeostasis as well as regulation of intracellular signaling pathways PubMed:29758300

a(CHEBI:lipid) regulates bp(GO:macroautophagy) View Subject | View Object

Decreased triglyceride breakdown upon macroautophagy inhibition and impairment in macroautophagy by lipid supplementation demonstrates reciprocally interrelated regulation of autophagy and lipids [72] PubMed:29758300

a(CHEBI:lipid) regulates bp(GO:"amyloid-beta metabolic process") View Subject | View Object

Lipid biology can also impact proteinopathy, with strong evidence that Aβ metabolism is modulated by lipids PubMed:29758300

a(CHEBI:lipid) negativeCorrelation bp(GO:autophagy) View Subject | View Object

In addition to the direct modulation of protein generation, lipids can also influence the levels of proteins through autophagic clearance; for instance, increasing lipid contents has been shown to impair autophagy [72]. PubMed:29758300

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(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

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.