General Information:

Id: 1,914
Diseases: Alzheimer disease - [OMIM]
Homo sapiens
article
Reference: Lee M et al.(2010) Depletion of GSH in glial cells induces neurotoxicity: relevance to aging and degenerative neurological diseases. FASEB J. 24: 2533-2545 [PMID: 20228251]

Interaction Information:

Comment Decreasing intracellular levels of GSH by inhibiting gamma-glutamylcysteine synthetase with BSO induced a neuroinflammatory response in microglia, astrocytes, and the surrogate THP-1 and U373 cell lines, which involved induction of phospho-NF-kappaB, phospho-p38, phospho-JNK and phospho- p42/p44-ERK.
Formal Description
Interaction-ID: 14683

drug/chemical compound

Glutathione

affects_activity of

in glia cells; Decreasing intracellular levels of GSH induce a neuroinflammatory response in microglia and astrocytes.
Drugbank entries Show/Hide entries for Glutathione
Comment Decreasing intracellular levels of GSH by inhibiting gamma-glutamylcysteine synthetase with BSO induced a neuroinflammatory response in microglia, astrocytes, and the surrogate THP-1 and U373 cell lines, which involved induction of phospho-NF-kappaB, phospho-p38, phospho-JNK and phospho- p42/p44-ERK.
Formal Description
Interaction-ID: 14783

gene/protein

GCLC

affects_quantity of

drug/chemical compound

Glutathione

Drugbank entries Show/Hide entries for GCLC or Glutathione
Comment Decreasing intracellular levels of GSH by inhibiting gamma-glutamylcysteine synthetase with BSO induced a neuroinflammatory response in microglia, astrocytes, and the surrogate THP-1 and U373 cell lines, which involved induction of phospho-NF-kappaB, phospho-p38, phospho-JNK and phospho- p42/p44-ERK.
Formal Description
Interaction-ID: 14784

affects_quantity of

drug/chemical compound

Glutathione

Drugbank entries Show/Hide entries for
Comment Decreasing intracellular levels of GSH by inhibiting gamma-glutamylcysteine synthetase with BSO induced a neuroinflammatory response in microglia, astrocytes, and the surrogate THP-1 and U373 cell lines, which involved induction of phospho-NF-kappaB, phospho-p38, phospho-JNK and phospho- p42/p44-ERK.
Formal Description
Interaction-ID: 14786

affects_activity of

gene/protein

GCLC

Drugbank entries Show/Hide entries for GCLC
Comment Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis with BSO causes human microglia, human astrocytes, THP-1 cells, and U373 cells to secrete materials toxic to human neuroblastoma SH-SY5Y cells and stimulates them to release TNF-alpha, IL-6, and nitrite ions.
Formal Description
Interaction-ID: 14800

affects_quantity of

drug/chemical compound

Glutathione

Drugbank entries Show/Hide entries for
Comment Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis with BSO causes human microglia, human astrocytes, THP-1 cells, and U373 cells to secrete materials toxic to human neuroblastoma SH-SY5Y cells and stimulates them to release TNF-alpha, IL-6, and nitrite ions.
Formal Description
Interaction-ID: 14803

affects_activity of

Oxidative stress is induced by inhibition of glutathione biosynthesis.
Comment Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis with BSO causes human microglia, human astrocytes, THP-1 cells, and U373 cells to secrete materials toxic to human neuroblastoma SH-SY5Y cells and stimulates them to release TNF-alpha, IL-6, and nitrite ions.
Formal Description
Interaction-ID: 14804

decreases_activity of

Comment Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis with BSO causes human microglia, human astrocytes, THP-1 cells, and U373 cells to secrete materials toxic to human neuroblastoma SH-SY5Y cells and stimulates them to release TNF-alpha, IL-6, and nitrite ions.
Formal Description
Interaction-ID: 14819

affects_activity of

tissue/cell line

microglia

in human
Comment Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis with BSO causes human microglia, human astrocytes, THP-1 cells, and U373 cells to secrete materials toxic to human neuroblastoma SH-SY5Y cells and stimulates them to release TNF-alpha, IL-6, and nitrite ions.
Formal Description
Interaction-ID: 14821

affects_activity of

tissue/cell line

astrocyte

in human
Comment Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis with BSO causes human microglia, human astrocytes, THP-1 cells, and U373 cells to secrete materials toxic to human neuroblastoma SH-SY5Y cells and stimulates them to release TNF-alpha, IL-6, and nitrite ions.
Formal Description
Interaction-ID: 14823

affects_activity of

tissue/cell line

THP-1 cell

in human
Comment Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis is correlated with activation of the inflammatory pathways P38 MAP-kinase, Jun-N-terminal kinase, and NF-kappaB.
Formal Description
Interaction-ID: 14850

affects_activity of

Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis is correlated with activation of the inflammatory pathways.
Comment Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis is correlated with activation of the inflammatory pathways P38 MAP-kinase, Jun-N-terminal kinase, and NF-kappaB.
Formal Description
Interaction-ID: 14852

affects_activity of

gene/protein

p38 MAPK

Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis is correlated with activation of the inflammatory pathways.
Comment Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis is correlated with activation of the inflammatory pathways P38 MAP-kinase, Jun-N-terminal kinase, and NF-kappaB.
Formal Description
Interaction-ID: 14854

affects_activity of

gene/protein

JUN kinase kinase

Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis is correlated with activation of the inflammatory pathways.
Comment Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis is correlated with activation of the inflammatory pathways P38 MAP-kinase, Jun-N-terminal kinase, and NF-kappaB.
Formal Description
Interaction-ID: 14856

affects_activity of

complex/PPI

NF-kappaB complex

Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis is correlated with activation of the inflammatory pathways.
Comment BSO in the culture medium causes an almost 3-fold increase in [Ca2+]i in microglia and astrocytes over a 24-h period, which is reduced to half by the addition of CTM.
Formal Description
Interaction-ID: 14857

increases_quantity of

drug/chemical compound

Ca2+

in microglia and astrocytes
Comment Clotrimazole (CTM) is an inhibitor of Ca2+-influx through TRPM2 channels.
Formal Description
Interaction-ID: 14858

drug/chemical compound

Clotrimazole

decreases_activity of

complex/PPI

Calcium channel

Drugbank entries Show/Hide entries for Clotrimazole
Comment Clotrimazole (CTM) is an inhibitor of Ca2+-influx through TRPM2 channels.
Formal Description
Interaction-ID: 14859

drug/chemical compound

Clotrimazole

decreases_quantity of

drug/chemical compound

Ca2+

Drugbank entries Show/Hide entries for Clotrimazole
Comment TRPM2 mRNA is expressed by glial cells.
Formal Description
Interaction-ID: 14861

gene/protein

TRPM2

is_expressed_in

tissue/cell line

glial cell

Comment Clotrimazole (CTM) is an inhibitor of Ca2+-influx through TRPM2 channels.
Formal Description
Interaction-ID: 14862

gene/protein

TRPM2

is_part_of

complex/PPI

Calcium channel

Comment Clotrimazole (CTM) is an inhibitor of Ca2+-influx through TRPM2 channels.
Formal Description
Interaction-ID: 14864

gene/protein

TRPM2

affects_activity of

complex/PPI

Calcium channel

Comment Clotrimazole (CTM) is an inhibitor of Ca2+-influx through TRPM2 channels.
Formal Description
Interaction-ID: 14865

gene/protein

TRPM2

affects_activity of

complex/PPI

Calcium channel

Comment Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis is correlated with activation of the inflammatory pathways P38 MAP-kinase, Jun-N-terminal kinase, and NF-kappaB.
Formal Description
Interaction-ID: 106879

affects_activity of

Oxidative stress is correlated with activation of the inflammatory pathway NF-kappaB.