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p(HGNC:BCL2)

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Entity

Name
BCL2
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 7

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

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

Tau degradation: the ubiquitin-proteasome system versus the autophagy-lysosome system. v1.0.0

Amyloid-Binding Alcohol Dehydrogenase (ABAD) Inhibitors for the Treatment of Alzheimer’s Disease v1.0.0

Phosphatase: PP2A structural importance, regulation and its aberrant expression in cancer v1.0.0

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0

In-Edges 10

a(CHEBI:"amyloid-beta") decreases p(HGNC:BCL2) View Subject | View Object

Whatever the mechanism of uptake, it is interesting to note that the signaling pathways evoked by the accumulation of intracellular Abeta resemble those evoked by extracellularly applied Abeta: transgenic rats overexpressing Abeta intraneuronally display elevated levels of phosphorylated ERK2 (Echeverria et al., 2004), as do rat hippocampal slices in response to bath-applied Abeta (Dineley et al., 2001). Again, bath-applied Abeta causes an increase in BAX and a decrease in BCL2 expression in neurons or neuronlike cell lines (Koriyama et al., 2003; Clementi et al., 2006). PubMed:19293145

Appears in Networks:

a(CHEBI:"amyloid-beta") decreases act(p(HGNC:BCL2)) View Subject | View Object

AKT interacts with BAD to regulate apoptosis and, interestingly, also has many interacting partners in the insulin signaling pathway. Abeta increased activity of BAD, lowered the activity of the antiapoptotic protein BCL2, in rat hippocampal neurons in primary culture (Koriyama et al., 2003) and has been shown to be toxic to human neuroblastoma cells by increasing BAX activity and decreasing BCl-2 activity (Clementi et al., 2006). PubMed:19293145

Appears in Networks:

a(CHEBI:donepezil) increases p(HGNC:BCL2) View Subject | View Object

The AD therapeutic AChE inhibitors donepezil, galantamine, and tacrine increase BCL2 expression when applied to cultured neuronal cells (Arias et al., 2004; Takada-Takatori et al., 2006). In these cells, nicotine promotes cell survival and causes the phosphorylation of the proapoptotic protein Bcl2-associated X protein (BAX), through the PI3K/AKT pathway, reducing the movement of BAX from the cytosol to the mitochondria and inhibiting its apoptotic activity (Xin and Deng, 2005). PubMed:19293145

Appears in Networks:
Annotations
MeSH
Neurons

a(CHEBI:galanthamine) increases p(HGNC:BCL2) View Subject | View Object

The AD therapeutic AChE inhibitors donepezil, galantamine, and tacrine increase BCL2 expression when applied to cultured neuronal cells (Arias et al., 2004; Takada-Takatori et al., 2006). In these cells, nicotine promotes cell survival and causes the phosphorylation of the proapoptotic protein Bcl2-associated X protein (BAX), through the PI3K/AKT pathway, reducing the movement of BAX from the cytosol to the mitochondria and inhibiting its apoptotic activity (Xin and Deng, 2005). PubMed:19293145

Appears in Networks:
Annotations
MeSH
Neurons

act(a(CHEBI:nicotine)) increases p(HGNC:BCL2) View Subject | View Object

The neuroprotective effects of nicotine are blocked by inhibitors of either PI3K or SRC family kinases, and nicotine evokes an increase in levels of phosphorylated AKT, B-cell chronic lymphocytic leukemia/lymphoma (BCL2), and BCL-2-like protein (Shimohama and Kihara, 2001), which are further downstream in the PI3K/AKT pathway (Fig. 3). PubMed:19293145

Appears in Networks:

a(CHEBI:tacrine) increases p(HGNC:BCL2) View Subject | View Object

The AD therapeutic AChE inhibitors donepezil, galantamine, and tacrine increase BCL2 expression when applied to cultured neuronal cells (Arias et al., 2004; Takada-Takatori et al., 2006). In these cells, nicotine promotes cell survival and causes the phosphorylation of the proapoptotic protein Bcl2-associated X protein (BAX), through the PI3K/AKT pathway, reducing the movement of BAX from the cytosol to the mitochondria and inhibiting its apoptotic activity (Xin and Deng, 2005). PubMed:19293145

Appears in Networks:
Annotations
MeSH
Neurons

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

Appears in Networks:

a(PUBCHEM:5757) increases p(HGNC:BCL2) View Subject | View Object

It enhances the expression of anti- apoptotic proteins, such as Bcl-2 and Bcl-xL, and down-regulates the expression of Bim, a pro-apoptotic factor, preventing programmed cell death. 90, 100 Estradiol also activates antioxidant systems to protect neuronal cells from apoptosis by upregulating the expression of manganese superoxide dismutase and glutathione peroxidase. 101 PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

complex(GO:"NF-kappaB complex") increases p(HGNC:BCL2) View Subject | View Object

The anti-apoptotic effects of NF-κB have been ascribed to its ability to trans-activate the expression of a multitude of anti-apoptotic genes such as Bcl-2, Bcl-XL, and Bfl-1/A1 in the neurons of the amygdala, olfactory bulb, and the CA1/CA3 region of the hippocampus PubMed:28745240

Appears in Networks:
Annotations
MeSH
Amygdala
MeSH
CA1 Region, Hippocampal
MeSH
CA3 Region, Hippocampal
MeSH
Olfactory Bulb
MeSH
Alzheimer Disease

p(HGNC:TNF) increases p(HGNC:BCL2) View Subject | View Object

Stimulation of neuronal cells by TNF-α has been shown to upregulate transactivation of anti-apoptotic gene products and neurotrophins such as Bcl-2 and NGF respectively PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Alzheimer Disease

Out-Edges 4

p(HGNC:BCL2) decreases bp(GO:autophagy) View Subject | View Object

For instance, c-Jun NH 2-terminal kinase 1 (JNK1) may induce autophagy by phosphorylating Bcl-2 or Bim and abolishing their inhibitory effects on autophagy (Luo et al., 2012; Wei et al., 2008). PubMed:23528736

Appears in Networks:

p(HGNC:BCL2) hasVariant p(HGNC:BCL2, pmod(Ph)) View Subject | View Object

Appears in Networks:

p(HGNC:BCL2) decreases bp(GO:"apoptotic process") View Subject | View Object

It enhances the expression of anti- apoptotic proteins, such as Bcl-2 and Bcl-xL, and down-regulates the expression of Bim, a pro-apoptotic factor, preventing programmed cell death. 90, 100 Estradiol also activates antioxidant systems to protect neuronal cells from apoptosis by upregulating the expression of manganese superoxide dismutase and glutathione peroxidase. 101 PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

p(HGNC:BCL2) decreases bp(GO:"apoptotic process") View Subject | View Object

The anti-apoptotic effects of NF-κB have been ascribed to its ability to trans-activate the expression of a multitude of anti-apoptotic genes such as Bcl-2, Bcl-XL, and Bfl-1/A1 in the neurons of the amygdala, olfactory bulb, and the CA1/CA3 region of the hippocampus PubMed:28745240

Appears in Networks:
Annotations
MeSH
Amygdala
MeSH
CA1 Region, Hippocampal
MeSH
CA3 Region, Hippocampal
MeSH
Olfactory Bulb
MeSH
Alzheimer 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.