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Literature summary for 1.3.1.124 extracted from

  • Blomme, A.; Ford, C.; Mui, E.; Patel, R.; Ntala, C.; Jamieson, L.; Planque, M.; McGregor, G.; Peixoto, P.; Hervouet, E.; Nixon, C.; Salji, M.; Gaughan, L.; Markert, E.; Repiscak, P.; Sumpton, D.; Blanco, G.; Lilla, S.; Kamphorst, J.; Graham, D.; Faulds, K
    2,4-dienoyl-CoA reductase regulates lipid homeostasis in treatment-resistant prostate cancer (2020), Nat. Commun., 11, 2508 .
    View publication on PubMedView publication on EuropePMC
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Application

Application Comment Organism
diagnostics the enzyme is a clinically relevant biomarker for castration-resistant prostate cancer (CRPC) Homo sapiens
medicine mitochondrial 2,4-dienoyl-CoA reductase is a clinically relevant biomarker for castration-resistant prostate cancer. DECR1 participates in redox homeostasis by controlling the balance between saturated and unsaturated phospholipids. DECR1 knockout induces ER stress and sensitizes castration-resistant prostate cancer cells to ferroptosis. In vivo, DECR1 deletion impairs lipid metabolism and reduces castration-resistant prostate cancer tumor growth Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrion
-
 Homo sapiens 5739
-

Organism

Organism UniProt Comment Textmining
Homo sapiens Q16698
-
-

Source Tissue

Source Tissue Comment Organism Textmining
LNCaP cell
-
 Homo sapiens
-
prostate gland
-
 Homo sapiens
-
prostate gland cancer cell castration-resistant prostate cancer Homo sapiens
-

Synonyms

Synonyms Comment Organism
2,4-dienoyl-CoA reductase
-
 Homo sapiens
DECR1
-
 Homo sapiens

General Information

General Information Comment Organism
malfunction enzyme (DECR1) knockout induces ER stress and sensitises castration-resistant prostate cancer cells to ferroptosis. In vivo, DECR1 deletion impairs lipid metabolism and reduces tumour growth of castration-resistant prostate cancer, emphasizing the importance of DECR1 in the development of treatment resistance Homo sapiens
physiological function DECR1 participates in redox homeostasis by controlling the balance between saturated and unsaturated phospholipids. DECR1 knockout induces ER stress and sensitizes castration-resistant prostate cancer cells to ferroptosis. In vivo, DECR1 deletion impairs lipid metabolism and reduces castration-resistant prostate cancer tumor growth Homo sapiens
physiological function the enzyme regulates lipid homeostasis in treatment-resistant prostate cancer Homo sapiens