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Literature summary for 3.4.22.57 extracted from

  • Valentin-Acevedo, A.; Sinquett, F.L.; Covey, L.R.
    c-Rel deficiency increases caspase-4 expression and leads to ER stress and necrosis in EBV-transformed cells (2011), PLoS ONE, 6, e25467.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.4.22.57

Localization

Localization Comment Organism GeneOntology No. Textmining
endoplasmic reticulum
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 Homo sapiens 5783
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Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Posttranslational Modification

Posttranslational Modification Comment Organism
proteolytic modification procaspase-4 is activated to mature caspase-4 Homo sapiens

Source Tissue

Source Tissue Comment Organism Textmining
B-lymphocyte primary, activated Homo sapiens
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lymphoblastoid cell line caspase-4 is upregulated in lymphoblastoid cells Homo sapiens
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Expression

Organism Comment Expression
Homo sapiens c-Rel is a negative regulator of caspase-4, e.g. in EBV lymphoblastoid cells down
Homo sapiens c-Rel as well as other endoplasmic reticulum stress genes directly modulate expression of caspase-4 additional information
Homo sapiens apoptosis-independent cell death is accompanied by increased expression of the inflammatory marker, caspase-4. Caspase-4 is upregulated in Pt1 cells and induced by interferons up

General Information

General Information Comment Organism
evolution caspase-4 is a member of the caspase family and a member of the interleukin-1beta coverting enzyme subfamily Homo sapiens
additional information elevated caspase activity in Pt1 cells is an outcome of increased caspase-4 activation Homo sapiens
physiological function caspase-4 is a member of the inflammatory family of caspases involved in the regulation of the endoplasmic reticulum stress response, autophagy and cell survival. Cell death is occurring through a caspase-independent mechanism Homo sapiens