BCL2L1

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Entity

Name: BCL2L1
Namespace: hgnc
Namespace Version: 20180906
Namespace URL: https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 4

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

Amyloid-Binding Alcohol Dehydrogenase (ABAD) Inhibitors for the Treatment of Alzheimer’s Disease 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 8

act(a(CHEBI:nicotine)) increases p(HGNC:BCL2L1) 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:

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

a(PUBCHEM:5757) increases p(HGNC:BCL2L1) 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:

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

Annotations

MeSH: Neurons

a(CHEBI:"amyloid-beta") decreases p(HGNC:BCL2L1) View Subject | View Object

Recent evidence has cogently shown that Amyloid-β induces apoptosis in rat primary neurons and human post-mitotic neuronal cells by reducing Bcl-XL expression level and evoking the release of cytochrome c from the mitochondria in a NF-κB – dependent manner PubMed:28745240

Appears in Networks:

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

Annotations

MeSH: Alzheimer Disease

complex(GO:"NF-kappaB complex") decreases p(HGNC:BCL2L1) View Subject | View Object

Appears in Networks:

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

Annotations

MeSH: Alzheimer Disease

complex(GO:"NF-kappaB complex") increases p(HGNC:BCL2L1) View Subject | View Object

This is counter-intuitive as it is established that NF-κB positively regulates the expression of Bcl-XL and other members of the Bcl2 family PubMed:28745240

Appears in Networks:

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

Annotations

MeSH: Alzheimer Disease

complex(GO:"NF-kappaB complex") increases p(HGNC:BCL2L1) 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:

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

Annotations

MeSH: Amygdala
MeSH: CA1 Region, Hippocampal
MeSH: CA3 Region, Hippocampal
MeSH: Olfactory Bulb
MeSH: Alzheimer Disease

a(CHEBI:"amyloid-beta") decreases p(HGNC:BCL2L1) View Subject | View Object

Mechanistically, the Aβ induced neuronal apoptosis has been attributed to the increase in the ratio of proapoptotic gene (BAX) transcription to that of the anti-apoptotic gene Bcl-Xl, and/or to the reduction in constitutively activated NF-κB with consequent increase in the cytoplasmic IκB proteins PubMed:25652642

Appears in Networks:

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

Annotations

MeSH: Alzheimer Disease

p(HGNC:GRM5) increases act(p(HGNC:BCL2L1)) View Subject | View Object

In metabotrophic glutamate receptor-5 (mGlu5) agonist pretreated primary cortical neurons or neuroblastoma cells, Aβ induced toxicity was suppressed by selective activation of c-rel containing NF-κB dimers and transactivation of anti-apoptotic genes, Mn-SOD and Bcl-Xl [26] (Figs 1B, 2A) PubMed:25652642