Literature summary for 3.1.3.1 extracted from

Lomashvili, K.A.; Garg, P.; Narisawa, S.; Millan, J.L.; ONeill, W.C.
Upregulation of alkaline phosphatase and pyrophosphate hydrolysis: potential mechanism for uremic vascular calcification (2008), Kidney Int., 73, 1024-1030.

Search for more literature for 3.1.3.1

Application

Application	Comment	Organism
medicine	a circulating factor causes pyrophosphate deficiency by regulating TNAP activity and vascular calcification in renal failure may result from the action of this factor	Mus musculus
medicine	a circulating factor causes pyrophosphate deficiency by regulating TNAP activity and vascular calcification in renal failure may result from the action of this factor	Rattus norvegicus

Protein Variants

Protein Variants	Comment	Organism
additional information	hydrolysis of pyrophosphate by rat aortic rings is reduced about half in aortas from mice lacking TNAP	Mus musculus
additional information	TNAP activity increases twofold in intact aortas and in aortic homogenates from rats made uremic by feeding adenine or by 5/6 nephrectomy. Immunoblotting showsS an increase in protein abundance but there is no increase in TNAP mRNA. An increase in TNAP activity and pyrophosphate hydrolysis also occurres when aortic rings from normal rats are incubated with uremic rat plasma	Rattus norvegicus

Inhibitors

Inhibitors	Comment	Organism	Structure
levamisole	hydrolysis of pyrophosphate by rat aortic rings is inhibited about half by the nonspecific alkaline phosphatase inhibitor levamisole. Hydrolysis is increased in aortic rings from uremic rats and all of this increase is inhibited by levamisole	Rattus norvegicus

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	-	-
Rattus norvegicus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
aorta	-	Mus musculus	-

Synonyms

Synonyms	Comment	Organism
tissue-nonspecific alkaline phosphatase	-	Mus musculus
tissue-nonspecific alkaline phosphatase	-	Rattus norvegicus
TNAP	-	Mus musculus
TNAP	-	Rattus norvegicus

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Release 2023.1 (January 2023)