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SYSTEMATIC NAME
IUBMB Comments
very-long-chain acyl-CoA:NADP+ oxidoreductase
This is the fourth component of the elongase, a microsomal protein complex responsible for extending palmitoyl-CoA and stearoyl-CoA (and modified forms thereof) to very-long-chain acyl CoAs. cf. EC 2.3.1.199, very-long-chain 3-oxoacyl-CoA synthase, EC 1.1.1.330, very-long-chain 3-oxoacyl-CoA reductase, and EC 4.2.1.134, very-long-chain (3R)-3-hydroxyacyl-[acyl-carrier protein] dehydratase.
in membrane fractions prepared from TER siRNA-treated HeLa cells, the conversion of trans-2-hexadecenoyl-CoA to palmitoyl-CoA is largely impaired, and only a small amount of palmitoyl-CoA is produced. Instead, trans-2-hexadecenoyl-CoA is the main product, and C14:0-CoA is also detected
ectopic expression of human trans-2-enoyl-CoA reductase TER in Saccharomyces cerevisiae TER homologue Tsc13-lowered cells causes recovery in the deficient sphingosine 1-phosphate metabolic pathway, lethality of VLCFA-deficient mutations
ectopic expression of human trans-2-enoyl-CoA reductase TER in Saccharomyces cerevisiae TER homologue Tsc13-lowered cells causes recovery in the deficient sphingosine 1-phosphate metabolic pathway, lethality of VLCFA-deficient mutations
enzyme Tsc13p is sequestered into nucleus-vacuole junctions from the peripheral endoplasmic reticulum through Vac8p-independent interactions with Nvj1p. During nutrient limitation, Tsc13p is incorporated into piecemeal microautophagy vesicles in an Nvj1p-dependent manner. The lumenal diameters of piecemeal microautophagy blebs and vesicles are significantly reduced in tsc13 and tsc13 elo3 mutant cells. Piecemeal microautophagy structures are also smaller in cells treated with cerulenin, an inhibitor of de novo fatty acid synthesis and elongation. The targeting of Tsc13p-green fluorescent protein into nucleus-vacuole junctions is perturbed by cerulenin
TER is involved sphingosine degradation within sphingolipids in the S1P metabolic pathway. trans-2-enoyl-CoA reductase TER catalyzes the saturation step of the sphingosine 1-phosphate (S1P) metabolic pathway. The pathways of sphingolipid degradation and synthesis, overview. Ectopic expression of human trans-2-enoyl-CoA reductase TER in Saccharomyces cerevisiae TER homologue Tsc13-lowered cells causes recovery in the deficient sphingosine 1-phosphate metabolic pathway
TER is involved sphingosine degradation within sphingolipids in the S1P metabolic pathway. trans-2-enoyl-CoA reductase TER catalyzes the saturation step of the sphingosine 1-phosphate (S1P) metabolic pathway. The pathways of sphingolipid degradation and synthesis, overview
TER is involved sphingosine degradation within sphingolipids in the S1P metabolic pathway. trans-2-enoyl-CoA reductase TER catalyzes the saturation step of the sphingosine 1-phosphate (S1P) metabolic pathway. The pathways of sphingolipid degradation and synthesis, overview
TER is involved sphingosine degradation within sphingolipids in the S1P metabolic pathway. trans-2-enoyl-CoA reductase TER catalyzes the saturation step of the sphingosine 1-phosphate (S1P) metabolic pathway. The pathways of sphingolipid degradation and synthesis, overview
heterologous expression functionally complements the temperature-sensitive phenotype of a yeast tsc13 mutant that is dfficient in enoyl reductase activity; heterologous expression functionally complements the temperature-sensitive phenotype of a yeast tsc13 mutant that is dfficient in enoyl reductase activity. Tsc13 cells expressing the reductase produce very long chain fatty acids, espcially C26:0
heterologous expression functionally complements the temperature-sensitive phenotype of a yeast tsc13 mutant that is dfficient in enoyl reductase activity. The heterologous protein interacts physically with the Elo2p and Elo3p components of the yeast elongase complex. Gene apparently encodes the sole enoyl reductase activity associated with microsomal fatty acid elongation in Arabidopsis thaliana
the tsc13 mutant accumulates high levels of long-chain bases as well as ceramides that harbor fatty acids with chain lengths shorter than 26 carbons. These phenotypes are exacerbated by the deletion of either the ELO2 or ELO3 gene, both of which are required for synthesis of very long chain fatty acids. Compromising the synthesis of malonyl coenzyme A by inactivating acetyl-CoA carboxylase in a tsc13 mutant is lethal
gene disruption results in a reduction of cuticular wax load and affects very long chain fatty acid composition of seed triacylglycerols and sphingolipids. Epidermal and seed-specific silencing of enzyme activity results in a reduction of cuticular wax load and the very long chaind fatty acid content of seed triacylglycerols, respectively, with no effects on plant morphogenesis. Cellular analysis reveals aberrant endocytic membrane traffic and defective cell expansion underlying the morphological defects of the disruption mutants
the enoyl reductase Tsc13 is responsible for the accumulation of phloretic acid via reduction of p-coumaroyl-CoA. Tsc13 is an essential enzyme involved in fatty acid synthesis and cannot be deleted
the trans-2-enoyl-CoA reductase, TER, functions in very long-chain fatty acid (VLCFA) synthesis and is involved in the fatty acid elongation cycle, where palmitic acid synthesized by fatty acid synthase or fatty acids taken from foods are elongated to very long-chain fatty acids (VLCFAs) with carbon chain lengths greater than 20
the trans-2-enoyl-CoA reductase, TER, functions in very long-chain fatty acid (VLCFA) synthesis and is involved in the fatty acid elongation cycle, where palmitic acid synthesized by fatty acid synthase or fatty acids taken from foods are elongated to very long-chain fatty acids (VLCFAs) with carbon chain lengths greater than 20
the trans-2-enoyl-CoA reductase, TER, functions in very long-chain fatty acid (VLCFA) synthesis and is involved in the fatty acid elongation cycle, where palmitic acid synthesized by fatty acid synthase or fatty acids taken from foods are elongated to very long-chain fatty acids (VLCFAs) with carbon chain lengths greater than 20
the trans-2-enoyl-CoA reductase, TER, functions in very long-chain fatty acid (VLCFA) synthesis and is involved in the fatty acid elongation cycle, where palmitic acid synthesized by fatty acid synthase or fatty acids taken from foods are elongated to very long-chain fatty acids (VLCFAs) with carbon chain lengths greater than 20
the N and C termini of the enzyme reside in the cytoplasm, and six putative membrane-spanning domains have been identified. The N-terminal domain including the first membrane-spanning segment contains sufficient information for targeting to the endoplasmic reticulum membrane
Tsc13p coimmunoprecipitates with Elo2p and Elo3p, which are required for veryl long chain fatty acid synthesis, suggesting that the elongating proteins are organized in a complex
gene TECR, cloning from liver cDNA, Ectopic expression of human trans-2-enoyl-CoA reductase TER in Saccharomyces cerevisiae TER homologue Tsc13-lowered cells
HeLa cells are transfected with control siRNA or TER si RNA, siRNA-generated enzyme knockout mutant. Knockdown of TER in HeLa cells causes decreased sphingosine 1-phosphate metabolism in vitro and a reduction in the dihydrosphingosine metabolism
with the aim of commercially interesting production of phenylpropanoids, such as flavonoids and stilbenoids, site saturation mutagenesis is used for modification of the enzyme to reduce the side activity without disrupting the natural function, identification of a number of amino acid changes which slightly increase flavonoid production but without reducing the formation of side product. The complementation of TSC13 by the gene homologue from plants essentially eliminates the unwanted side reaction, while retaining the productivity of phenylpropanoids in a simulated fed batch fermentation. The native open reading frame (ORF) of TSC13 is replaced by gene homologues from Arabidospis thaliana (AtECR), Gossypium hirsutum (GhECR2) and Malus domestica (MdECR), using a split URA3 cassette under the control of the native TSC13 promoter
YRF50 cells (BY4741,pTSC13::KanMX4-tTA-ptetO7) are constructed by replacing the promoter of the TSC13 gene (pTSC13) with tetO7 promoter (ptetO7) using the KanMX4-tTA-ptetO7 cassette from the pCM225 plasmid. Strains ABY83 and ABY80 cells are constructed by deletion of the TSC13 gene in BY4741 cells bearing the pTW6 or pAB119 plasmid, respectively, using a tsc13DELTA::LEU2 fragment by homologous recombination. Generation of Saccharomyces cerevisiae Tsc13-lowered cells
YRF50 cells (BY4741,pTSC13::KanMX4-tTA-ptetO7) are constructed by replacing the promoter of the TSC13 gene (pTSC13) with tetO7 promoter (ptetO7) using the KanMX4-tTA-ptetO7 cassette from the pCM225 plasmid. Strains ABY83 and ABY80 cells are constructed by deletion of the TSC13 gene in BY4741 cells bearing the pTW6 or pAB119 plasmid, respectively, using a tsc13DELTA::LEU2 fragment by homologous recombination. Generation of Saccharomyces cerevisiae Tsc13-lowered cells
Disruptions of the Arabidopsis enoyl-CoA reductase gene reveal an essential role for very-long-chain fatty acid synthesis in cell expansion during plant morphogenesis
Lehka, B.J.; Eichenberger, M.; Bjoern-Yoshimoto, W.E.; Vanegas, K.G.; Buijs, N.; Jensen, N.B.; Dyekjaer, J.D.; Jenssen, H.; Simon, E.; Naesby, M.
Improving heterologous production of phenylpropanoids in Saccharomyces cerevisiae by tackling an unwanted side reaction of Tsc13, an endogenous double-bond reductase