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  3. g(HGNC:"MIR101-1")

g(HGNC:"MIR101-1")

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

Entity

Name
MIR101-1
Namespace
hgnc
Namespace Version
20190224
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/efc856fb009a39e4d284269a6801f79ed3d3cf56/external/hgnc-names.belns

Appears in Networks 1

New insights into the role of microRNAs and long noncoding RNAs in most common neurodegenerative diseases v1.0.0

In-Edges 1

path(MESH:"Alzheimer Disease") association g(HGNC:"MIR101-1") View Subject | View Object

Besides, by directly affecting APP, miR‐101 can cause its downregulation, which ultimately provides the basis for AD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

Out-Edges 5

g(HGNC:"MIR101-1") decreases p(HGNC:APP) View Subject | View Object

On the other hand, miR‐101, by downregulating RanBP9, can indirectly reduce the production of APP PubMed:30663117

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

g(HGNC:"MIR101-1") decreases act(p(HGNC:APP)) View Subject | View Object

Besides, by directly affecting APP, miR‐101 can cause its downregulation, which ultimately provides the basis for AD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

g(HGNC:"MIR101-1") decreases act(p(HGNC:RANBP9)) View Subject | View Object

On the other hand, miR‐101, by downregulating RanBP9, can indirectly reduce the production of APP PubMed:30663117

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

g(HGNC:"MIR101-1") association path(MESH:"Alzheimer Disease") View Subject | View Object

Besides, by directly affecting APP, miR‐101 can cause its downregulation, which ultimately provides the basis for AD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

g(HGNC:"MIR101-1") decreases path(MESH:"Alzheimer Disease") View Subject | View Object

Given the important role of miR‐101 in preventing AD, miR‐101 reduction can play a role in AD development PubMed:30663117

Appears in Networks:
Annotations
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.