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Literature summary for 5.3.4.1 extracted from

  • Hahm, E.; Li, J.; Kim, K.; Huh, S.; Rogelj, S.; Cho, J.
    Extracellular protein disulfide isomerase regulates ligand-binding activity of alphaMbeta2 integrin and neutrophil recruitment during vascular inflammation (2013), Blood, 121; 3789-800, S1-15.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 5.3.4.1

Application

Application Comment Organism
medicine the enzyme is a therapeutic target for preventing and treating inappropriate neutrophil sequestration Mus musculus
medicine the enzyme is a therapeutic target for preventing and treating inappropriate neutrophil sequestration Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
extracellular
-
 Mus musculus
-
-
extracellular
-
 Homo sapiens
-
-

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
blood platelet
-
 Mus musculus
-
blood platelet
-
 Homo sapiens
-
lymphocyte
-
 Mus musculus
-
lymphocyte
-
 Homo sapiens
-
monocyte
-
 Mus musculus
-
monocyte
-
 Homo sapiens
-
neutrophil
-
 Mus musculus
-
neutrophil
-
 Homo sapiens
-

Synonyms

Synonyms Comment Organism
PDI
-
 Mus musculus
PDI
-
 Homo sapiens
protein disulfide isomerase
-
 Mus musculus
protein disulfide isomerase
-
 Homo sapiens

General Information

General Information Comment Organism
physiological function extracellular protein disulfide isomerase (PDI) regulates ligand-binding activity of alphaMbeta2 integrin and neutrophil recruitment during vascular inflammation. Neutrophil PDI is required for neutrophil adhesion and crawling during tumor necrosis factor-alpha-induced vascular inflammation in vivo Mus musculus
physiological function extracellular protein disulfide isomerase (PDI) regulates ligand-binding activity of alphaMbeta2 integrin and neutrophil recruitment during vascular inflammation. Neutrophil PDI is required for neutrophil adhesion and crawling during tumor necrosis factor-alpha-induced vascular inflammation in vivo Homo sapiens