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p(HGNC:CDKN2A)

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Entity

Name
CDKN2A
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 3

Tau protein aggregation is associated with cellular senescence in the brain v1.0.0

Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation 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(GO:"neurofibrillary tangle") association p(HGNC:CDKN2A) View Subject | View Object

Similarly, elevated expression of the cyclin dependent kinase inhibitor 2a, Cdkn2a, is one of the most robust markers of cellular senescence, and its protein product, p16INK4A, co-localizes with NFTs in human AD (Arendt et al., 1996) PubMed:30126037

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons
MeSH
Alzheimer Disease

a(GO:"neurofibrillary tangle") positiveCorrelation p(HGNC:CDKN2A) View Subject | View Object

Consistent with the results from transgenic mice, CDKN2A was upregulated in PSP brains (P = 0.0415, Figure 4g) and expression correlated with NFT deposition, specifically in the parietal lobe (ANOVA, P = 0.0008; Kendall’s Tau rank correlation P = 0.059, Figure 4h) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Parietal Lobe
MeSH
Supranuclear Palsy, Progressive

a(GO:"neurofibrillary tangle") increases p(HGNC:CDKN2A) View Subject | View Object

Collectively, these findings led us to conclude that NFTs were directly linked to senescence-associated Cdkn2a upregulation, which in turn was a strong predictor of neurodegeneration and cognitive decline PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Parietal Lobe
MeSH
Supranuclear Palsy, Progressive

bp(GO:"cellular senescence") increases p(HGNC:CDKN2A) View Subject | View Object

Similarly, elevated expression of the cyclin dependent kinase inhibitor 2a, Cdkn2a, is one of the most robust markers of cellular senescence, and its protein product, p16INK4A, co-localizes with NFTs in human AD (Arendt et al., 1996) PubMed:30126037

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons
MeSH
Alzheimer Disease

bp(HP:Neurodegeneration) association p(HGNC:CDKN2A) View Subject | View Object

Collectively, these findings led us to conclude that NFTs were directly linked to senescence-associated Cdkn2a upregulation, which in turn was a strong predictor of neurodegeneration and cognitive decline PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Parietal Lobe
MeSH
Supranuclear Palsy, Progressive

path(MESH:"Cognitive Dysfunction") association p(HGNC:CDKN2A) View Subject | View Object

Collectively, these findings led us to conclude that NFTs were directly linked to senescence-associated Cdkn2a upregulation, which in turn was a strong predictor of neurodegeneration and cognitive decline PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Parietal Lobe
MeSH
Supranuclear Palsy, Progressive

path(MESH:"Supranuclear Palsy, Progressive") positiveCorrelation p(HGNC:CDKN2A) View Subject | View Object

Consistent with the results from transgenic mice, CDKN2A was upregulated in PSP brains (P = 0.0415, Figure 4g) and expression correlated with NFT deposition, specifically in the parietal lobe (ANOVA, P = 0.0008; Kendall’s Tau rank correlation P = 0.059, Figure 4h) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Supranuclear Palsy, Progressive

a(PUBCHEM:135316034) decreases p(HGNC:CDKN2A) 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") increases p(HGNC:CDKN2A) 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:

m(HGNC:MIR125B1) positiveCorrelation p(HGNC:CDKN2A) View Subject | View Object

In AD brains, miRNA-125b is observed as the most abundant exhibiting strong positive correlation with glial fibrillary acidic protein and vimentin and negative correlation with reduced cyclin dependent kinase 2A PubMed:25652642

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease

Out-Edges 6

p(HGNC:CDKN2A) association a(GO:"neurofibrillary tangle") View Subject | View Object

Similarly, elevated expression of the cyclin dependent kinase inhibitor 2a, Cdkn2a, is one of the most robust markers of cellular senescence, and its protein product, p16INK4A, co-localizes with NFTs in human AD (Arendt et al., 1996) PubMed:30126037

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons
MeSH
Alzheimer Disease

p(HGNC:CDKN2A) positiveCorrelation a(GO:"neurofibrillary tangle") View Subject | View Object

Consistent with the results from transgenic mice, CDKN2A was upregulated in PSP brains (P = 0.0415, Figure 4g) and expression correlated with NFT deposition, specifically in the parietal lobe (ANOVA, P = 0.0008; Kendall’s Tau rank correlation P = 0.059, Figure 4h) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Parietal Lobe
MeSH
Supranuclear Palsy, Progressive

p(HGNC:CDKN2A) positiveCorrelation path(MESH:"Supranuclear Palsy, Progressive") View Subject | View Object

Consistent with the results from transgenic mice, CDKN2A was upregulated in PSP brains (P = 0.0415, Figure 4g) and expression correlated with NFT deposition, specifically in the parietal lobe (ANOVA, P = 0.0008; Kendall’s Tau rank correlation P = 0.059, Figure 4h) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Supranuclear Palsy, Progressive

p(HGNC:CDKN2A) association bp(HP:Neurodegeneration) View Subject | View Object

Collectively, these findings led us to conclude that NFTs were directly linked to senescence-associated Cdkn2a upregulation, which in turn was a strong predictor of neurodegeneration and cognitive decline PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Parietal Lobe
MeSH
Supranuclear Palsy, Progressive

p(HGNC:CDKN2A) association path(MESH:"Cognitive Dysfunction") View Subject | View Object

Collectively, these findings led us to conclude that NFTs were directly linked to senescence-associated Cdkn2a upregulation, which in turn was a strong predictor of neurodegeneration and cognitive decline PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Parietal Lobe
MeSH
Supranuclear Palsy, Progressive

p(HGNC:CDKN2A) positiveCorrelation m(HGNC:MIR125B1) View Subject | View Object

In AD brains, miRNA-125b is observed as the most abundant exhibiting strong positive correlation with glial fibrillary acidic protein and vimentin and negative correlation with reduced cyclin dependent kinase 2A PubMed:25652642

Appears in Networks:
Annotations
MeSH
Brain
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.