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p(HGNC:BECN1)

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Entity

Name
BECN1
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 5

Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0

Tau Biochemistry v1.2.5

Tau Biochemistry Section of NESTOR

Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation v1.0.0

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

mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0

In-Edges 21

a(CHEBI:"methylene blue") increases p(HGNC:BECN1) View Subject | View Object

Other compounds that act through AMPK acti- vation include the antiaggregant methylene blue (Supplementary Box 1), which elevated levels of beclin  1, p62 and LC3, induced autophagy and suppressed tau in organotypic neuronal cultures and a mouse model of FTD 101,102 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:Isorhynchophylline) increases p(HGNC:BECN1) View Subject | View Object

In addition, the plant-derived alkaloid isorhynchophylline upregulated beclin 1 independently of mTORC1 and promoted autophagic clearance of α-synuclein, although its precise mechanism of action remains to be clarified 175 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Machado-Joseph Disease

a(CHEBI:cilostazol) increases p(HGNC:BECN1) View Subject | View Object

Cilostazol (a phosphodiesterase 3 inhibitor) clears Aβ42 from neuronal cell lines by promoting autophagy, upregulating beclin 1, ATG5 and LC3, downregulating mTORC1 and inducing lysosomal cathepsin B; these actions of cilostazol involve activation of SIRT1 as well as upstream Tyr172 phosphorylation of AMPK 108,162,163 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
MeSH
Machado-Joseph Disease

a(CHEBI:spermidine) increases act(p(HGNC:BECN1)) View Subject | View Object

Spermidine inhibits the acetylation of ATG7 and histone H3, while induc- ing beclin 1 via blockade of its cleavage by caspase 3 (REF.168) . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Machado-Joseph Disease

complex(p(HGNC:BCL2), p(HGNC:BECN1)) hasComponent p(HGNC:BECN1) View Subject | View Object

Appears in Networks:

p(HGNC:BECN1, frag("?")) decreases act(p(HGNC:BECN1)) View Subject | View Object

Spermidine inhibits the acetylation of ATG7 and histone H3, while induc- ing beclin 1 via blockade of its cleavage by caspase 3 (REF.168) . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Machado-Joseph Disease

p(HGNC:BECN1, pmod(Ph)) increases act(p(HGNC:BECN1)) View Subject | View Object

Activation of ULK1 triggers autophagosome nucleation through activating phospho- rylation of AMBRA and beclin 1 within the autophagy- specific PIK3C3 complex 10 (FIG. 3) . PubMed:30116051

Appears in Networks:

p(HGNC:LRRK2, var("?")) decreases act(p(HGNC:BECN1)) View Subject | View Object

Some of these lead to an impairment of the ALN owing to reduced activation of beclin 1; another repercussion may be altered process- ing of APP, providing an unexpected link to AD 69,71–73 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Parkinson Disease

p(HGNC:PICALM) positiveCorrelation p(HGNC:BECN1) View Subject | View Object

A highly significant correlation was found between decreased levels of PICALM and increased levels of LC3-II (p=0.0032) or decreased levels of Beclin-1 (p=0.0295) in the total brain lysates from these diseases (Fig 6D,E). PubMed:27260836

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
Disease Ontology (DO)
Down syndrome
Disease Ontology (DO)
Pick's disease
Disease Ontology (DO)
progressive supranuclear palsy

a(PUBCHEM:135316034) decreases p(HGNC:BECN1) View Subject | View Object

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") decreases p(HGNC:BECN1) View Subject | View Object

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

Appears in Networks:

a(CHEBI:"methylene blue") increases p(HGNC:BECN1) View Subject | View Object

Methylene blue, a contrast agent that can reduce tau misfolding, has also been shown to induce macroautophagy, as indicated by elevated Beclin 1 and LC3-II levels and reduced tau and p62 levels in organotypic neuronal cultures and a mouse model of FTD [159] 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:macroautophagy) 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:

complex(GO:"phosphatidylinositol 3-kinase complex, class III") hasComponent p(HGNC:BECN1) View Subject | View Object

Appears in Networks:

path(MESH:"Alzheimer Disease") negativeCorrelation p(HGNC:BECN1) View Subject | View Object

For example, levels of Beclin 1, a key component of the class III type phosphoinositide 3-kinase/VPS34 complex essential to the pre-autophagosomal structure (PAS), has been suggested to be reduced in AD brains [16,17], with Rohn et al. demonstrating the cleavage of Beclin 1 by caspase-3 in the AD brain and colocalization of the cleaved product with NFTs [16]. PubMed:29758300

Appears in Networks:
Annotations
MeSH
Brain

path(MESH:"Alzheimer Disease") decreases p(HGNC:BECN1) View Subject | View Object

In line with this, reduced Beclin 1 levels, as seen in AD models [16], increase the levels of intracellular and extracellular Aβ peptides, supporting the role of macroautophagy in the generation and degradation of Aβ [33,35]. PubMed:29758300

Appears in Networks:

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

In particular, at BA 22, the vast majority of abnormally expressed genes referred to key autophagy genes (i.e., BECN1, ULK2, ATG3), which were significantly down-regulated compared with controls PubMed:30061532

Appears in Networks:

path(MESH:Schizophrenia) decreases p(HGNC:BECN1) View Subject | View Object

In particular, at BA 22, the vast majority of abnormally expressed genes referred to key autophagy genes (i.e., BECN1, ULK2, ATG3), which were significantly down-regulated compared with controls PubMed:30061532

Appears in Networks:

path(MESH:Schizophrenia) decreases p(HGNC:BECN1) View Subject | View Object

In detail, the analysis of mRNA expression of a key protein for autophagy initiation, namely beclin1, revealed a significant region-specific reduction in hippocampal samples from 12 schizophrenic patients compared with 12 age-matched healthy controls. PubMed:30061532

Appears in Networks:
Annotations
MeSH
Hippocampus

path(MESH:Schizophrenia) decreases p(HGNC:BECN1) View Subject | View Object

Immuno-histochemical analysis showed a three-fold decrease in the number of beclin1-positive cells in Map6+/- mice PubMed:30061532

Appears in Networks:

Out-Edges 10

p(HGNC:BECN1) hasVariant p(HGNC:BECN1, frag("?")) View Subject | View Object

Appears in Networks:

p(HGNC:BECN1) hasVariant p(HGNC:BECN1, pmod(Ph)) View Subject | View Object

Appears in Networks:

act(p(HGNC:BECN1)) increases bp(GO:"autophagosome assembly") View Subject | View Object

Activation of ULK1 triggers autophagosome nucleation through activating phospho- rylation of AMBRA and beclin 1 within the autophagy- specific PIK3C3 complex 10 (FIG. 3) . PubMed:30116051

Appears in Networks:

p(HGNC:BECN1) positiveCorrelation p(HGNC:PICALM) View Subject | View Object

A highly significant correlation was found between decreased levels of PICALM and increased levels of LC3-II (p=0.0032) or decreased levels of Beclin-1 (p=0.0295) in the total brain lysates from these diseases (Fig 6D,E). PubMed:27260836

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
Disease Ontology (DO)
Down syndrome
Disease Ontology (DO)
Pick's disease
Disease Ontology (DO)
progressive supranuclear palsy

p(HGNC:BECN1) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

For example, levels of Beclin 1, a key component of the class III type phosphoinositide 3-kinase/VPS34 complex essential to the pre-autophagosomal structure (PAS), has been suggested to be reduced in AD brains [16,17], with Rohn et al. demonstrating the cleavage of Beclin 1 by caspase-3 in the AD brain and colocalization of the cleaved product with NFTs [16]. PubMed:29758300

Appears in Networks:
Annotations
MeSH
Brain

p(HGNC:BECN1) decreases a(MESH:"Amyloid beta-Peptides") View Subject | View Object

In line with this, reduced Beclin 1 levels, as seen in AD models [16], increase the levels of intracellular and extracellular Aβ peptides, supporting the role of macroautophagy in the generation and degradation of Aβ [33,35]. PubMed:29758300

Appears in Networks:

p(HGNC:BECN1) association bp(GO:macroautophagy) 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: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:BECN1) increases bp(GO:phagocytosis) View Subject | View Object

For example, Beclin 1 suppression results in impaired microglial phagocytosis of Aβ and reduced recycling of TREM2 [108]. PubMed:29758300

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

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

In particular, at BA 22, the vast majority of abnormally expressed genes referred to key autophagy genes (i.e., BECN1, ULK2, ATG3), which were significantly down-regulated compared with controls PubMed:30061532

Appears in Networks:

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.