EC Number   |
General Information |
Reference |
|---|
   3.5.1.92 | malfunction |
enzyme vanin-1 mutation N131S is associated with high blood pressure or hypertension via vanin-1 misfolding and degradation as the underlying molecular mechanism |
734998 |
| 3.5.1.92 | 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 |
-, 757352 |
| 3.5.1.92 | malfunction |
mutant mice with a reduced serum pantetheinase activity are anemic and prone to phenylhydrazine-induced anemia. A cytofluorometric and spectroscopic analysis documents an increased frequency of erythrocytes with an autofluorescent aging phenotype. This is associated with an enhanced oxidative stress and shear stress-induced hemolysis. Red blood cell transfer and bone marrow chimera experiments show that the aging phenotype is not cell intrinsic but conferred by the environment, leading to a shortening of red blood cell half-life. Phenotype analysis, detailed overview |
-, 755763 |
| 3.5.1.92 | malfunction |
PPAR-alpha KO mice show a negligible liver vnn1 expression, even after stimulation with various agonists. Vanin 1 overexpression increases glucose output by specifically increasing the hepatic transcription levels of gluconeogenic genes, while vnn1 knockdown decreases the glucose output of murine hepatocytes |
757002 |
| 3.5.1.92 | malfunction |
vanin 1 knockout mice display an enhanced resistance to oxidative stress and show down-regulated tissue inflammation in response to oxidative stress. Vanin knockout mice exhibit a loss of cysteamine-mediated inhibition of peroxisome proliferator-activated receptor gamma. Vanin 1 deficient islets are twice as susceptible to cell death as wild type cells |
718754 |
| 3.5.1.92 | malfunction |
Vnn1 deficiency favors soft tissue sarcoma development in p16/p19-/- mice |
757538 |
| 3.5.1.92 | metabolism |
enzyme Vnn1 is a valid biomarker for aggressive soft tissue sarcomas (STS) prognosis. Analysis of a route to regulate tumor growth rates through the modulation of CoA and cysteamine levels |
757538 |
| 3.5.1.92 | metabolism |
formation of pantothenic acid allows for a continuous production of CoA, as pantothenic acid is a structural component of this cofactor. In addition, pantothenic acid appears to have profibrotic effects, being involved in the promotion of proliferation and migration of dermal fibroblasts. Moreover, pantothenic acid contributes to restoring CoA levels in the mitochondria, resulting in enhanced mitochondrial activity. Vanin 1 also plays a role in the regulation of a number of metabolic pathways |
756998, 757002 |
| 3.5.1.92 | metabolism |
formation of pantothenic acid allows for a continuous production of CoA, as pantothenic acid is a structural component of this cofactor. In addition, pantothenic acid appears to have profibrotic effects, being involved in the promotion of proliferation and migration of dermal fibroblasts. Moreover, pantothenic acid contributes to restoring CoA levels in the mitochondria, resulting in enhanced mitochondrial activity. Vanin 1 also plays a role in the regulation of a number of metabolic pathways. In fact, the vnn1 gene is one of the positive targets of the peroxisome proliferator-activated receptor alpha (PPAR-alpha) in mouse liver. PPAR-alpha is a key regulator of the liver's response to fasting |
757002 |
| 3.5.1.92 | metabolism |
inactivation of vnn1 on the development of fibrosis, endothelial alterations, and immunological activation in mice with HOCl- and bleomycin-induced systemic sclerosis (SSc) |
-, 757352 |
