1.3.1.124: 2,4-dienoyl-CoA reductase [(3E)-enoyl-CoA-producing]
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For detailed information about 2,4-dienoyl-CoA reductase [(3E)-enoyl-CoA-producing], go to the full flat file.
Reaction
Synonyms
2,4-dienoyl coenzyme A reductase, 2,4-dienoyl-CoA reductase, 4-enoyl-CoA reductase, DCR, DECR, DECR1, DECR2, DELTA2,DELTA4-dienoyl-CoA reductase, More, pDCR, SPS19
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General Information
General Information on EC 1.3.1.124 - 2,4-dienoyl-CoA reductase [(3E)-enoyl-CoA-producing]
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malfunction
metabolism
key enzyme required for beta-oxidation of polyunsaturated fatty acids
physiological function
cold intolerance of Decr-/- mice is due to failure in maintaining appropriate heat production at least partly due to failure of brown adipose tissue (BAT) thermogenesis
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
an SPS19 deleted strain is unable to utilize petroselineate (cis-C18:1(6)) as the sole carbon source, but remains viable on oleate (cis-C18:1(9)). SPS19 is dispensable for growth and sporulation on solid acetate and oleate media, but is essential for these processes to occur on petroselineate
physiological function
cold intolerance of Decr?/? mice is due to failure in maintaining appropriate heat production at least partly due to failure of brown adipose tissue thermogenesis. Activation of lipolysis is attenuated despite of functional norepinephrine-signaling and inappropriate expression of genes contributing to thermogenesis in interscapular brown adipose rissue when the Decr?/? mice are exposed to cold
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
physiological function
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dienoyl-CoA and NADPH bind to the 2,4-dienoyl-CoA reductase via a sequential kinetic mechanism with a random order of nucleotide and dienoyl-CoA addition. A proton transfer step is rate limiting for (2E,4E)-hexa-2,4-dienoyl-CoA substrate, addition of a phenyl ring to the diene in 5-phenyl-(2E,4E)-2,4-pentadienoyl-CoA results in the reversal of the rate-determining step. The chemical mechanism is stepwise where hydride transfer from NADPH occurs followed by protonation of the dienolate intermediate
physiological function
human mitochondrial 2,4-reductase functions in the beta-oxidation of unsaturated fatty acids. A yeast sps19D mutant expressing human 2,4-reductase ending with the native C-terminus cannot grow on petroselinic acid medium but can grow when the protein is extended with a peroxisomal targeting tripeptide, Ser-Lys-Leu
physiological function
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in vitro, 4-cis-decenoyl-CoA is only degraded when the 2,4-dienoyl-CoA reductase step in linoleic acid degradation is not blocked by lack of NADPH
physiological function
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metabolism of unsaturated fatty acids occurs mainly in the mitochondria and the peroxisomes of the proximal tubule in the kidney
physiological function
SPS19 is induced during sporulation in diploids. Under oleate induction conditions, SPS19 is transcribed via an oleate response element (ORE) independently of ploidy or sporulation.The SPS19 ORE is the binding target of the Pip2p and Oaf1p transcription factors
physiological function
the reductase does not seem to constitute a rate limiting step in the peroxisomal degradation of docosahexaenoic acid. The reduction of docosaheptaenoyl-CoA is severely decreased in the presence of albumin
physiological function
the removal of double bonds from odd-numbered carbons in arachidonic acid requires both NADPH-dependent 2,4-dienoyl-CoA reductase and delta 3,5,delta 2,4-dienoyl-CoA isomerase. One complete cycle of 5,8-14:2 and 5,8,11,14-20:4 beta-oxidation yields, respectively, 6-dodecenoic and 6,9,12-octadecatrienoic acids
physiological function
the enzyme regulates lipid homeostasis in treatment-resistant prostate cancer