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  3. a(MESH:"Dendritic Cells")

a(MESH:"Dendritic Cells")

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
Dendritic Cells
Namespace
MeSH
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/01c9daa61012b37dd0a1bc962521ba51a15b38f1/external/mesh-names.belns

Appears in Networks 2

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

In-Edges 6

p(HGNC:TNFSF9) increases act(a(MESH:"Dendritic Cells")) View Subject | View Object

TNFSF9 (aka CD137L), induced 19-fold, can induce maturation of human immature monocyte-derived dendritic cells leading to an enhanced capacity of the dendritic cells to stimulate protective T cell responses, as compared to classical dendritic cells (Tang et al., 2011). PubMed:22020111

Appears in Networks:

act(complex(GO:"NF-kappaB complex")) increases a(MESH:"Dendritic Cells") View Subject | View Object

NF-κB is integrally involved in the orchestration of growth of dendritic arbors and critically regulates dendritic morphology because of its indispensable role in dendritic growth and branching PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:HES1) increases a(MESH:"Dendritic Cells") View Subject | View Object

NF-κB activation directly induces the transcription of Hes1 and Hes5 [206, 207], two key transcription factors involved in the regulation of expression of proteins involved in dendritic growth, morphology, and branching PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:HES5) increases a(MESH:"Dendritic Cells") View Subject | View Object

NF-κB activation directly induces the transcription of Hes1 and Hes5 [206, 207], two key transcription factors involved in the regulation of expression of proteins involved in dendritic growth, morphology, and branching PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:MAP1B) increases a(MESH:"Dendritic Cells") View Subject | View Object

NF-κB activates the expression of the two microtubule-associated proteins, microtubule-associated protein 1B (MAP1B) and microtubule-associated protein 2 (MAP2) [209], two major proteins known to play a pivotal role in the growth, elongation, and arborization of dendrites PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:MAP2) increases a(MESH:"Dendritic Cells") View Subject | View Object

NF-κB activates the expression of the two microtubule-associated proteins, microtubule-associated protein 1B (MAP1B) and microtubule-associated protein 2 (MAP2) [209], two major proteins known to play a pivotal role in the growth, elongation, and arborization of dendrites PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

Out-Edges 1

act(a(MESH:"Dendritic Cells")) increases bp(GO:"T cell activation") View Subject | View Object

TNFSF9 (aka CD137L), induced 19-fold, can induce maturation of human immature monocyte-derived dendritic cells leading to an enhanced capacity of the dendritic cells to stimulate protective T cell responses, as compared to classical dendritic cells (Tang et al., 2011). PubMed:22020111

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.