TECR

Trans-2,3-enoyl-CoA reductase is an enzyme that in humans is encoded by the TECR gene.[5]

TECR
Available structures PDB Ortholog search: PDBe RCSB List of PDB id codes 2DZJ
Identifiers
Aliases	TECR, GPSN2, MRT14, SC2, TER, trans-2,3-enoyl-CoA reductase
External IDs	OMIM: 610057 MGI: 1915408 HomoloGene: 36231 GeneCards: TECR
Gene location (Human) Chr. Chromosome 19 (human)[1] Band 19p13.12 Start 14,517,085 bp[1] End 14,565,980 bp[1]
Gene location (Mouse) Chr. Chromosome 8 (mouse)[2] Band 8 C2|8 40.22 cM Start 83,571,698 bp[2] End 83,607,971 bp[2]
Gene ontology Molecular function • oxidoreductase activity, acting on the CH-CH group of donors • GO:0001948 protein binding • very-long-chain-acyl-CoA dehydrogenase activity • oxidoreductase activity • very-long-chain enoyl-CoA reductase activity Cellular component • cytoplasm • integral component of membrane • integral component of endoplasmic reticulum membrane • endoplasmic reticulum membrane • endoplasmic reticulum • cell nucleus • membrane Biological process • fatty acid elongation • fatty acid biosynthetic process • long-chain fatty-acyl-CoA biosynthetic process • very long-chain fatty acid biosynthetic process • oxidation-reduction process • fatty acid metabolic process • lipid metabolism • sphingolipid metabolic process Sources:Amigo / QuickGO
Orthologs
Species	Human	Mouse
Entrez	9524	106529
Ensembl	ENSG00000099797	ENSMUSG00000031708
UniProt	Q9NZ01	Q9CY27
RefSeq (mRNA)	NM_004868 NM_138501 NM_001321170	NM_027179 NM_134118
RefSeq (protein)	NP_001308099 NP_612510	NP_081455 NP_598879
Location (UCSC)	Chr 19: 14.52 – 14.57 Mb	Chr 8: 83.57 – 83.61 Mb
PubMed search	[3]	[4]
Wikidata
View/Edit Human View/Edit Mouse

This gene encodes a multi-pass membrane protein that resides in the endoplasmic reticulum, and belongs to the steroid 5-alpha reductase family. The elongation of microsomal long and very long chain fatty acid consists of 4 sequential reactions. This protein catalyzes the final step, reducing trans-2,3-enoyl-CoA to saturated acyl-CoA. Alternatively spliced transcript variants have been found for this gene.[5]

Clinical relevance

Mutations in this gene have been shown to cause non-syndromic mental retardation.[6]

References

1. GRCh38: Ensembl release 89: ENSG00000099797 - Ensembl, May 2017
2. GRCm38: Ensembl release 89: ENSMUSG00000031708 - Ensembl, May 2017
3. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
4. "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
5. "Entrez Gene: Trans-2,3-enoyl-CoA reductase". Retrieved 2011-12-30.
6. Çalışkan M, Chong JX, Uricchio L, Anderson R, Chen P, Sougnez C, Garimella K, Gabriel SB, dePristo MA, Shakir K, Matern D, Das S, Waggoner D, Nicolae DL, Ober C (April 2011). "Exome sequencing reveals a novel mutation for autosomal recessive non-syndromic mental retardation in the TECR gene on chromosome 19p13". Hum. Mol. Genet. 20 (7): 1285–9. doi:10.1093/hmg/ddq569. PMC 3115579. PMID 21212097.

Further reading

• Moon, Y. -A.; Horton, J. D. (2002). "Identification of Two Mammalian Reductases Involved in the Two-carbon Fatty Acyl Elongation Cascade". Journal of Biological Chemistry. 278 (9): 7335–7343. doi:10.1074/jbc.M211684200. PMID 12482854.
• Hashmi, G.; Shariff, T.; Seul, M.; Vissavajjhala, P.; Hue-Roye, K.; Charles-Pierre, D.; Lomas-Francis, C.; Chaudhuri, A.; Reid, M. E. (2005). "A flexible array format for large-scale, rapid blood group DNA typing". Transfusion. 45 (5): 680–688. doi:10.1111/j.1537-2995.2005.04362.x. PMID 15847654.
• Lehner, R.; Kuksis, A. (1996). "Biosynthesis of triacylglycerols". Progress in Lipid Research. 35 (2): 169–201. doi:10.1016/0163-7827(96)00005-7. PMID 8944226.
• Mao, M.; Fu, G.; Wu, J. S.; Zhang, Q. H.; Zhou, J.; Kan, L. X.; Huang, Q. H.; He, K. L.; Gu, B. W.; Han, Z. -G.; Shen, Y.; Gu, J.; Yu, Y. -P.; Xu, S. -H.; Wang, Y. -X.; Chen, S. -J.; Chen, Z. (1998). "Identification of genes expressed in human CD34+ hematopoietic stem/progenitor cells by expressed sequence tags and efficient full-length cDNA cloning". Proceedings of the National Academy of Sciences of the United States of America. 95 (14): 8175–8180. doi:10.1073/pnas.95.14.8175. PMC 20949. PMID 9653160.

This article incorporates text from the United States National Library of Medicine, which is in the public domain.