Literature summary for 1.11.1.9 extracted from

Westphal, K.; Stangl, V.; Faehling, M.; Dreger, H.; Weller, A.; Baumann, G.; Stangl, K.; Meiners, S.
Human-specific induction of glutathione peroxidase-3 by proteasome inhibition in cardiovascular cells (2009), Free Radic. Biol. Med., 47, 1652-1660.

Search for more literature for 1.11.1.9

Natural Substrates/ Products (Substrates)

Natural Substrates	Organism	Comment (Nat. Sub.)	Natural Products	Comment (Nat. Pro.)	Rev.	Reac.
glutathione + ROOH	Homo sapiens	-	glutathione disulfide + ROH + H2O	-	?

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	P22352	-	-
no activity in Bos taurus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
aortic smooth muscle cell	GPx-3 is detected at very low levels under basal conditions	Homo sapiens	-
HAEC cell	GPx-3 is detected at very low levels under basal conditions	Homo sapiens	-
HUVEC cell	GPx-3 is detected at very low levels under basal conditions	Homo sapiens	-
plasma	GPx-3 is secreted into the plasma	Homo sapiens	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
glutathione + ROOH	-	Homo sapiens	glutathione disulfide + ROH + H2O	-	?

Synonyms

Synonyms	Comment	Organism
glutathione peroxidase-3	-	Homo sapiens
GPx-3	-	Homo sapiens

Expression

Organism	Comment	Expression
Homo sapiens	GPx-3 is induced by MG132 in HUVEC cells with an exponential increase in GPx-3 mRNA up to 120fold of control levels within 48 h. GPx-3 is still upregulated by a factor of 3-4 even after 72 and 96 h of proteasome inhibition. HAEC cells upregulate GPx-3 by more than 40fold in response to MG132. Proteasome inhibition clearly induces GPx-3 in HAoSMCs by a factor of 18	up

General Information

General Information	Comment	Organism
physiological function	glutathione peroxidase-3 is a key antioxidant enzyme in the plasma. Endothelial cell-derived GPx-3 protects the vasculature from oxidative stress	Homo sapiens

Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.

Release 2023.1 (January 2023)