Search results for TST

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Protein (3 results from a total of 3)

TST

Identifier: R-HSA-1614531
Species: Homo sapiens
Compartment: mitochondrial matrix
Primary external reference: UniProt: TST: Q16762
Identifier: R-HSA-6787615
Species: Homo sapiens
Compartment: cytosol
Primary external reference: UniProt: GFUS: Q13630
Identifier: R-HSA-9014529
Species: Homo sapiens
Compartment: cytosol
Primary external reference: UniProt: TSTD1: Q8NFU3

Reaction (5 results from a total of 5)

Identifier: R-HSA-9013198
Species: Homo sapiens
Compartment: mitochondrial matrix
Cyanide is a potent metabolic poison, a major component of which is binding to and inhibition of cytochrome c oxidase (cytochrome a3), resulting in the rapid inhibition of oxidative phosphorylation (Hall & Rumack 1986). As a result, cells can't utilise oxygen, giving rise to central nervous system, cardiovascular and respiratory dysfunction that can result in permanent neurological defects and, in severe cases, death. At body's pH, cyanide exists mainly in the undissociated form hydrogen cyanide (HCN) which can cross cellular and subcellular membranes such as the blood brain barrier and mitochondrial membranes. Cyanide intoxication can occur after smoke inhalation, industrial exposure, ingestion of cyanogenic substances and cyanogenic food sources such as cassava. Antidotes for HCN poisoning cases include HCN binders, sulfur donors that convert HCN to the less toxic thiosulfate and competitors for HCN enzymatic binding sites such as NO (Petrikovics et al. 2015).

Two pathways in mammals are able to detoxify cyanide as thiocyanate via transfer of a sulfur atom: thiosulfate sulfurtransferase (TST aka rhodanese) in mitochondria and 3-mercaptopyruvate sulfurtransferase (MPST aka 3MST) in cytosol and mitochondria. TST can act to detoxify HCN by transsulfuration, that is mediating the transfer of a sulfur atom from thiosulfate (S2O3(2-)) to HCN to form the less toxic thiocyanic acid (HSCN) (Himwich & Saunders 1948, Aita et al. 1997, Zottola 2009). HSCN can be excreted in urine via the kidneys (Hamel 2011).
Identifier: R-HSA-6787623
Species: Homo sapiens
Compartment: cytosol
The de novo synthesis pathway for GDP-L-fucose is a two step pathway starting from GDP-mannose. In the second step, GDP-4-dehydro-6-deoxy-alpha-D-mannose (GDP-DHDMan) is epimerised and reduced to GDP-L-fucose (GDP-Fuc). The cytosolic enzyme GDP-L-fucose synthase (TSTA3, aka FX) appears to have both epimerase and reductase activities and functions as a homodimer (Tonetti et al. 1996, Zhou et al. 2013). In the first stage, the hydroxyl group at C-3 and the methyl group at C-5 of the mannose ring of GDP-DHDMan are epimerised to GDP-4-keto-6-deoxygalactose (GDP-KDGal).
Identifier: R-HSA-6787642
Species: Homo sapiens
Compartment: cytosol
The de novo synthesis pathway for GDP-L-fucose is a two step pathway starting from GDP-mannose. In the second step, GDP-4-dehydro-6-deoxy-alpha-D-mannose (GDP-DHDMan) is epimerised and reduced to GDP-L-fucose (GDP-Fuc). The cytosolic enzyme GDP-L-fucose synthase (TSTA3, aka FX) appears to have both epimerase and reductase activities and functions as a homodimer (Tonetti et al. 1996, Zhou et al. 2013). In the second stage, 4-reductase activity of TSTA3 dimer catalyses a hydride transfer from NADPH to the keto group at C-4 of GDP-4-keto-6-deoxygalactose (GDP-KDGal), yielding GDP-fucose (GDP-Fuc) and NADP+.
Identifier: R-HSA-9013533
Species: Homo sapiens
Compartment: mitochondrial matrix
Cyanide is a potent metabolic poison which binds to and inhibits cytochrome c oxidase (cytochrome a3), resulting in the rapid inhibition of oxidative phosphorylation (Hall & Rumack 1986). As a result, cells can't utilise oxygen, giving rise to central nervous system, cardiovascular and respiratory dysfunction that can result in permanent neurological defects and, in severe cases, death. At body's pH, cyanide exists mainly in the undissociated form hydrogen cyanide (HCN) which can cross cellular and subcellular membranes such as the blood brain barrier and mitochondrial membranes. Although humans are not typically exposed to cyanide, cyanide intoxication can occur after smoke inhalation, industrial exposure, ingestion of cyanogenic substances and cyanogenic food sources such as cassava. Antidotes for HCN poisoning cases include HCN binders, sulfur donors that convert HCN to the less toxic thiosulfate and competitors for HCN enzymatic binding sites such as NO (Petrikovics et al. 2015).

Two pathways in mammals are able to detoxify cyanide as thiocyanate via transfer of a sulfur atom: thiosulfate sulfurtransferase (TST aka rhodanese) in mitochondria and 3-mercaptopyruvate sulfurtransferase (MPST aka 3MST) in cytosol and mitochondria. 3MPYR has been investigated for the potential treatment of HCN poisoning but its half life is very short, being rapidly metabolised when given intravenously (Nagahara & Sawada 2003). Also, it is a metabolite of cysteine metabolism but cysteine is present in low amounts in the brain and heart, limiting the ability of MPST to be effective in acute HCN poisoning. The pro-drug sulfanegen is the hemithioacetal cyclic dimer of 3MPYR and has been demonstrated to be effective against HCN poisoning in animal studies (Brenner et al. 2010, Belani et al. 2012). Sulfanegen provides the sulfur atom for the transsulfuration of HCN by MPST (Belani et al. 2012). HSCN can be excreted in urine via the kidneys (Hamel 2011). In a mass exposure scenario (such as terrorism or industrial accident), a rapidly-acting antidote that can be administered quickly to a large number of people is essential; sulfanegen can be rapidly administered by intramuscular injection (Patterson et al. 2016).
Identifier: R-HSA-9013471
Species: Homo sapiens
Compartment: mitochondrial matrix
Cyanide is a potent metabolic poison which binds to and inhibits cytochrome c oxidase (cytochrome a3), resulting in the rapid inhibition of oxidative phosphorylation (Hall & Rumack 1986). As a result, cells can't utilise oxygen, giving rise to central nervous system, cardiovascular and respiratory dysfunction that can result in permanent neurological defects and, in severe cases, death. At body's pH, cyanide exists mainly in the undissociated form hydrogen cyanide (HCN) which can cross cellular and subcellular membranes such as the blood brain barrier and mitochondrial membranes. Although humans aren't typically exposed to toxic levels of cyanide, cyanide intoxication can occur after smoke inhalation, industrial exposure, ingestion of cyanogenic substances and cyanogenic food sources such as cassava. Antidotes for HCN poisoning cases include HCN binders, sulfur donors that convert HCN to the less toxic thiosulfate and competitors for HCN enzymatic binding sites such as NO (Nagahara et al. 1999, Petrikovics et al. 2015).

Two pathways in mammals are able to detoxify cyanide as thiocyanate via transfer of a sulfur atom: thiosulfate sulfurtransferase (TST aka rhodanese) in mitochondria and 3-mercaptopyruvate sulfurtransferase (MPST aka 3MST) in cytosol and mitochondria. MPST mediates the transfer of a sulfur atom from 3-methylpryuvate (3MPYR) to HCN to form the less toxic thiocyanic acid (HSCN) (Himwich & Saunders 1948, Zottola 2009, Moeller et al. 2017). HSCN can be excreted in urine via the kidneys (Hamel 2011). Although the primary role of MPST is not cyanide detoxification, a large body of animal data has demonstrated cyanide is rapidly converted to thiocyanate in vivo when 3MPYR is administered, even in species with low MPST activity (Brenner et al. 2010, Belani et al. 2012).

Interactor (1 results from a total of 1)

Identifier: Q5T7W7
Species: Homo sapiens
Primary external reference: UniProt: Q5T7W7

Complex (1 results from a total of 1)

Identifier: R-HSA-6787635
Species: Homo sapiens
Compartment: cytosol
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