Application | Comment | Organism |
---|---|---|
diagnostics | potential use of vanin-1 as a marker of severity and therapeutic target in systemic sclerosis (SSc) | Mus musculus |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
membrane | vanin-1 is a ubiquitous membrane-bound enzyme | Mus musculus | 16020 | - |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
(R)-pantetheine + H2O | Mus musculus | - |
(R)-pantothenate + 2-aminoethanethiol | - |
? | |
(R)-pantetheine + H2O | Mus musculus BALB/c | - |
(R)-pantothenate + 2-aminoethanethiol | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | Q9Z0K8 | - |
- |
Mus musculus BALB/c | Q9Z0K8 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
fibroblast | primary | Mus musculus | - |
skin | - |
Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
(R)-pantetheine + H2O | - |
Mus musculus | (R)-pantothenate + 2-aminoethanethiol | - |
? | |
(R)-pantetheine + H2O | - |
Mus musculus BALB/c | (R)-pantothenate + 2-aminoethanethiol | - |
? |
Synonyms | Comment | Organism |
---|---|---|
pantetheinase | - |
Mus musculus |
vanin-1 | - |
Mus musculus |
VNN1 | - |
Mus musculus |
pH Optimum Minimum | pH Optimum Maximum | Comment | Organism |
---|---|---|---|
8 | - |
assay at | Mus musculus |
Organism | Comment | Expression |
---|---|---|
Mus musculus | inactivation of vnn1 on the development of fibrosis, endothelial alterations, and immunological activation in mice with HOCl- and bleomycin-induced systemic sclerosis (SSc) | additional information |
General Information | Comment | Organism |
---|---|---|
malfunction | evaluation of the effects of the inactivation of vnn1 on the development of fibrosis, endothelial alterations, and immunological activation in mice with HOCl- and bleomycin-induced systemic sclerosis (SSc). The vanin-1/pantetheinase pathway is activated in wild-type BALB/c mice through hypochlorous acid (HOCl)-induced SSc. Hyperactivity of the vanin-1/pantetheinase pathway may reduce the vasculoprotective effects of pantethine, while genetic inactivation of vanin-1 has a protective effect | Mus musculus |
metabolism | inactivation of vnn1 on the development of fibrosis, endothelial alterations, and immunological activation in mice with HOCl- and bleomycin-induced systemic sclerosis (SSc) | Mus musculus |
physiological function | the vanin-1 gene (vnn1) encodes an enzyme with pantetheinase activity that converts vasculoprotective pantethine into profibrotic pantothenic acid and pro-oxidant cystamine. By hydrolyzation of pantethine, vanin-1 delivers cysteamine and pantothenic acid to tissues. Cysteamine is rapidly converted into cystamine that can regulate the function of other target proteins by a disulfide reaction. In particular, cystamine abrogates glutathione (GSH) production by inhibiting gamma-glutamyl synthase, the rate-limiting enzyme of GSH synthesis, thus strongly reducing reactive oxygen species (ROS) scavenging. In contrast, pantothenic acid, the other by-product of vanin-1, exerts profibrotic effects by promoting the proliferation and migration of dermal fibroblasts, as well as collagen synthesis | Mus musculus |