Literature summary for 3.4.11.22 extracted from

Aldhamen, Y.; Pepelyayeva, Y.; Rastall, D.; Seregin, S.; Zervoudi, E.; Koumantou, D.; Aylsworth, C.; Quiroga, D.; Godbehere, S.; Georgiadis, D.; Stratikos, E.; Amalfitano, A.
Autoimmune disease-associated variants of extracellular endoplasmic reticulum aminopeptidase 1 induce altered innate immune responses by human immune cells (2015), J. Innate Immun., 7, 275-289.

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Application

Application	Comment	Organism
medicine	exposure of human peripheral blood mononuclear cells to isoform ERAP1 polymorphic variant proteins as well as ERAP1 overexpression increases inflammatory cytokine and chemokine production, and enhances immune cell activation. ERAP1 is able to activate innate immunity via multiple pathways, including the NOD-like receptor NLRP3 inflammasome. These responses vary if autoimmune disease-associated variants of ERAP1 are examined in the assay systems. Blocking ERAP1 cellular internalization augments IL-1beta production	Homo sapiens

Localization

Localization	Comment	Organism	GeneOntology No.	Textmining

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	Q9NZ08	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining

General Information

General Information	Comment	Organism
physiological function	exposure of human peripheral blood mononuclear cells to isoform ERAP1 polymorphic variant proteins as well as ERAP1 overexpression increases inflammatory cytokine and chemokine production, and enhances immune cell activation. ERAP1 is able to activate innate immunity via multiple pathways, including the NOD-like receptor NLRP3 inflammasome. These responses vary if autoimmune disease-associated variants of ERAP1 are examined in the assay systems. Blocking ERAP1 cellular internalization augments IL-1beta production	Homo sapiens

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Release 2023.1 (January 2023)