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p(HGNC:GLRX2)

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Entity

Name
GLRX2
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 1

Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation v1.0.0

In-Edges 4

a(PUBCHEM:135316034) increases p(HGNC:GLRX2) View Subject | View Object

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

Appears in Networks:
Annotations
MeSH
Colorectal Neoplasms

a(PUBCHEM:135316034) increases p(HGNC:GLRX2) View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

Appears in Networks:
Annotations
MeSH
Colorectal Neoplasms

path(MESH:"Colorectal Neoplasms") increases p(HGNC:GLRX2) View Subject | View Object

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

Appears in Networks:

path(MESH:"Colorectal Neoplasms") positiveCorrelation p(HGNC:GLRX2) View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

Appears in Networks:

Out-Edges 1

p(HGNC:GLRX2) positiveCorrelation path(MESH:"Colorectal Neoplasms") View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. 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.