EC Number   |
General Information |
Reference |
|---|
   5.3.4.1 | malfunction |
deletion of the ncgl2478 gene increases the size of growth inhibition zones. Site-directed mutagenesis confirms Cys24 as the resolving Cys residue, while Cys21 is the nucleophilic cysteine that is oxidized to a sulfenic acid and then forms an intramolecular disulfide bond with Cys24 or a mixed disulfide with MSH under oxidative stress |
-, 763778 |
| 5.3.4.1 | malfunction |
enzyme inhibition results ina 25% loss of vessel caliber post-injury. This is accompanied by decreased hydrogen peroxide formation and changes in collagen organization, resulting in increased arterial stiffness |
747923 |
| 5.3.4.1 | malfunction |
enzyme silencing decreases Nox1 expression and reactive oxygen species production as well as platelet-derived growth factor-induced Rac1 and RhoA activities |
727921 |
| 5.3.4.1 | malfunction |
enzyme silencing prevents Nox responses to angiotensin II and inhibits Akt phosphorylation in vascular cells and parasite phagocytosis in macrophages |
727573 |
| 5.3.4.1 | malfunction |
functional inhibition of protein disulfide isomerase by S-nitrosylation may contribute to pathophysiology in both mutant superoxide dismutase 1-linked disease and sporadic amyotrophic lateral sclerosis |
702970 |
| 5.3.4.1 | malfunction |
inhibition of cell surface PDI induces a marked increase in tissue factor procoagulant function |
714598 |
| 5.3.4.1 | malfunction |
mice lacking AGR2 are viable but are highly susceptible to colitis, indicating a critical role for AGR2 in protection from disease |
706539 |
| 5.3.4.1 | malfunction |
PDI inhibition or silencing increases apoptosis and inhibits migration and adhesion of endothelial cells, overview |
701629 |
| 5.3.4.1 | malfunction |
PDIA6-deficient cells hyperrespond to endoplasmic reticulum stress with sustained autophosphorylation of inositol-requiring enzyme 1alpha and splicing of XBP1 mRNA, resulting in exaggerated upregulation of UPR target genes and increased apoptosis. In vivo, PDIA6-deficient Caenorhabditis elegans exhibits constitutive unfolded protein response and fails to complete larval development |
728306 |
| 5.3.4.1 | malfunction |
PDIL2-3 knockdown causes aberrant accumulation of prolamins in endoplasmic reticulum-derived type-I protein bodies whereas the oxidative folding of vacuole-targeted proteins, such as proglutelins and alpha-globulin, is hardly affected. PDIL2-3 knockdown inhibits the accumulation of Cys-rich 10-kD prolamin in the core of type-I protein bodies |
716521 |
