| 2008 |
ELOVL5 is required in vivo for elongation of gamma-linolenic acid (C18:3 n-6) to dihomo-gamma-linolenic acid (C20:3 n-6) and stearidonic acid (C18:4 n-3) to omega3-arachidonic acid (C20:4 n-3); deletion of Elovl5 in mice reduces arachidonic acid and DHA levels, which activates SREBP-1c and its target genes, leading to hepatic steatosis reversible by dietary arachidonic acid and DHA supplementation. |
Elovl5 knockout mouse model, liver microsomal enzyme assay, dietary supplementation rescue |
Journal of lipid research |
High |
18838740
|
| 2012 |
Elovl5 controls gluconeogenesis through the mTORC2-Akt2-FoxO1 pathway: elevated Elovl5 activity increases cis-vaccenic acid (18:1 n-7) synthesis, induces rictor mRNA and protein, promotes rictor-mTOR interaction, and selectively phosphorylates Akt2-S473 (mTORC2 site) but not Akt2-T308, leading to FoxO1-S256 phosphorylation and reduced nuclear FoxO1; rictor knockdown blocks these effects. |
Adenoviral overexpression of Elovl5 in obese mice and HepG2 cells, Akt inhibitor treatment, rictor siRNA knockdown, fatty acid analysis, phospho-specific Western blotting |
Journal of lipid research |
High |
23099444
|
| 2014 |
Elovl5 activity regulates hepatic triglyceride catabolism in obese mice by producing fatty acid products (including cis-vaccenic acid) that activate PPARβ-dependent induction of ATGL (adipocyte triglyceride lipase) mRNA and protein, thereby promoting TG catabolism without affecting β-oxidation capacity; Elovl5 also reduces ER stress markers. |
Adenoviral Elovl5 overexpression in obese C57BL/6J mice, PPARβ agonist treatment, siRNA knockdown, fatty acyl carnitine profiling, Western blotting |
Journal of lipid research |
High |
24814977
|
| 2013 |
The differential ability of rat Elovl5 vs Elovl2 to elongate C22 omega-3 docosapentaenoic acid (DPA, 22:5n-3) to 24:5n-3 is determined by a single residue: cysteine at position 217 in Elovl2 (critical for DPA elongation) vs tryptophan at the equivalent position in Elovl5 (which cannot elongate DPA); this was established by chimeric protein and point mutation analysis in a yeast expression system. |
Yeast heterologous expression, Elovl2/Elovl5 chimeras, site-directed mutagenesis, fatty acid profiling |
Journal of lipid research |
High |
23873268
|
| 2014 |
ELOVL5 missense mutations (p.Gly230Val and p.Leu72Val) cause spinocerebellar ataxia type 38 (SCA38); mutant ELOVL5 shows aberrant perinuclear/Golgi accumulation rather than the normal widespread ER distribution, and affected individuals have reduced serum arachidonic acid and DHA. |
Linkage analysis, targeted resequencing, Sanger sequencing in families, transfection with subcellular localization imaging (immunofluorescence), serum fatty acid profiling |
American journal of human genetics |
High |
25065913
|
| 2017 |
Elovl5 knockout mice develop progressive motor deficits (beam balance test), hyposmia, and cerebellar atrophy with reduced molecular layer thickness and decreased distal Purkinje cell dendritic arborization (by Sholl analysis of biocytin-filled PCs), recapitulating SCA38 symptoms; dendritic spine density is preserved. |
Elovl5 knockout mouse model, behavioral testing, morphometric cerebellar analysis, biocytin filling with Sholl dendritic analysis |
Frontiers in cellular neuroscience |
High |
29163054
|
| 2021 |
ELOVL5 is directly transcriptionally induced by the androgen receptor (AR) in prostate cancer; ELOVL5 depletion alters mitochondrial morphology and function, increases reactive oxygen species, and suppresses prostate cancer cell proliferation, 3D growth, and in vivo tumor growth and metastasis; supplementation with cis-vaccenic acid (a direct ELOVL5 elongation product) reverses oxidative stress and proliferation/migration defects of ELOVL5 knockdown. |
Transcriptomics, ChIP, ELOVL5 siRNA/shRNA knockdown, mass spectrometry lipidomics, ROS assays, mitochondrial function assays, xenograft mouse models, cis-vaccenic acid supplementation rescue |
Cancer research |
High |
33547161
|
| 2015 |
Two SREBP binding sites in the human ELOVL5 gene (one ~10 kb upstream, one in exon 1) are identified as functional enhancer elements conserved among mammals; SREBP activates ELOVL5 transcription through these SRE motifs, establishing ELOVL5 as a direct SREBP-1 target gene within a negative feedback loop of de novo lipogenesis. |
Promoter/enhancer deletion analysis, luciferase reporter assays, electrophoretic mobility shift assay (EMSA) |
Biochemical and biophysical research communications |
Medium |
26321664
|
| 2021 |
ELOVL5-mediated fatty acid elongation in renal cell carcinoma promotes AKT Ser473 phosphorylation and AKT-mTOR-STAT3 signaling, supporting cell invasion via CCL2 upregulation; ELOVL5 knockout suppresses lipid droplet formation and induces apoptosis via ER stress; supplementation with arachidonic acid and EPA partially reverses proliferation and invasion defects. |
CRISPR/Cas9 ELOVL5 knockout, LC-MS lipidomics, Western blotting for AKT/mTOR/STAT3 signaling, fatty acid supplementation rescue, in vivo xenograft |
Cancer science |
Medium |
35670054
|
| 2021 |
ELOVL5-mediated PUFA elongation enhances lipid raft-associated AKT-mTOR signaling, contributing to enzalutamide resistance in neuroendocrine-like prostate cancer cells; ELOVL5 knockdown reduces neuroendocrine phenotype and resistance, while overexpression augments resistance in vitro and in vivo. |
shRNA knockdown, ELOVL5 overexpression, enzalutamide resistance assays, lipid raft isolation, AKT-mTOR signaling Western blotting, xenograft models |
Cancers |
Medium |
34439125
|
| 2022 |
Downregulation of ELOVL5 in breast cancer promotes EMT, cell invasion, and lung metastasis through lipid-droplet accumulation-dependent Smad2 acetylation, which upregulates TGF-β receptors; inhibition of TGF-β receptors or diacylglycerol acyltransferase (blocking lipid droplet formation) reverses invasion and metastasis caused by ELOVL5 loss. |
shRNA knockdown, lipid droplet imaging, TGF-β receptor inhibitor treatment, DGAT inhibitor treatment, Smad2 acetylation assay, murine breast cancer metastasis models |
Cell death & disease |
Medium |
36056008
|
| 2023 |
The SCA38-causing ELOVL5 p.G230V variant has normal enzymatic activity but is proteotoxic: it is mislocalized to the Golgi (instead of ER), undergoes increased proteasomal degradation, triggers unfolded protein response more strongly than wild-type, and decreases neuronal viability; homology modelling reveals p.G230V shifts Loop 6 and alters a conserved disulfide bond connecting Loop 2 and Loop 6 that is elongase-specific. |
Biochemical elongase activity assay in SCA38 fibroblasts, proteasome inhibitor treatment, UPR reporter assays in cortical neurons, immunofluorescence localization, homology structural modelling |
Human genetics |
High |
37199746
|
| 2018 |
ELOVL5 is the key elongase responsible for elongation of 18- and 20-carbon PUFAs in human T-cells; ELOVL5 expression is significantly upregulated upon T-cell activation/proliferation, and ELOVL5 knockdown markedly impairs elongation of these substrates and alters cellular PUFA profiles; no functional ELOVL2 was detected in these cells. |
siRNA knockdown of ELOVL5 in primary human T-cells and Jurkat cells, exogenous PUFA incorporation assays, RT-qPCR, fatty acid profiling |
Journal of lipid research |
Medium |
30293059
|
| 2021 |
ELOVL5 knockdown in bovine embryos reduces the content of specific phospholipid species (phosphatidylcholines, phosphatidylethanolamines) and triacylglycerol, while increasing cytoplasmic lipid droplet deposition, demonstrating that ELOVL5 participates in embryonic lipid composition of cellular membranes. |
Morpholino-mediated knockdown in bovine embryos, mass spectrometry-based lipid fingerprinting, lipid droplet imaging |
International journal of molecular sciences |
Medium |
33525659
|
| 2025 |
In Elovl5 knockout mouse cerebellum, deletion increases 18- and 20-carbon PUFAs, decreases long-chain PUFAs, and increases saturated/monounsaturated fatty acids in synaptosomes; loss of Elovl5 impairs replenishment of the readily releasable pool of synaptic vesicles at climbing fiber and parallel fiber synapses, and shortens endocannabinoid-mediated suppression of excitation (SSE) in Purkinje cells, linking ELOVL5-dependent lipid composition to synaptic transmission and plasticity. |
Elovl5 knockout mice, electrophysiological recordings in Purkinje cells (paired-pulse and high-frequency stimulation protocols), synaptosome lipid analysis, SSE assays |
The Journal of neuroscience |
High |
40789653
|
| 2021 |
Elovl5 expression in the adult mouse CNS is region- and cell-type-specific: highest in cerebellar Purkinje cells, mitral cells of olfactory regions, brainstem, and motor-related telencephalic regions; Elovl5 is expressed in oligodendroglial cells at various maturation stages and in microglia, with heterogeneous expression in astrocytes. |
Elovl5-reporter mouse line, immunofluorescence on CNS sections, primary glial cell cultures |
Frontiers in neuroanatomy |
Medium |
33994961
|
| 2007 |
ELOVL5 mRNA is specifically localized to the basal layer of sebaceous gland cells in the pheromone-producing head skin of male goats but absent in non-pheromone-producing rump skin and orchidectomized goat head skin, implicating ELOVL5 in pheromone fatty acid synthesis in sebaceous glands. |
In situ hybridization on goat skin sections |
The Journal of reproduction and development |
Medium |
17827874
|
| 2017 |
Estrogen promotes hepatic LCPUFA synthesis by downregulating miR-218-5p, which directly targets and represses ELOVL5; miR-218-5p binds the 3'UTR of ELOVL5 (validated by luciferase reporter assay) and negatively regulates ELOVL5 mRNA and protein levels, thereby modulating PUFA biosynthesis at the post-transcriptional level. |
Luciferase 3'UTR reporter assay, miRNA mimic/inhibitor transfection, Western blotting, qPCR in chicken hepatocytes |
International journal of molecular sciences |
Medium |
28665359
|
| 2019 |
miR-21-3p directly targets the 3'UTR of Elovl5 in bovine mammary epithelial cells (validated by luciferase reporter assay) and negatively regulates Elovl5 mRNA and protein; miR-21-3p mimics promote triglyceride production, an effect attributed to Elovl5 suppression. |
Luciferase 3'UTR reporter assay, miRNA mimic/inhibitor transfection, qPCR, Western blotting |
DNA and cell biology |
Medium |
30707627
|
| 2024 |
miR-218-5p directly targets and suppresses Elovl5 expression in mouse hepatocytes (validated by dual luciferase reporter assay); miR-218-5p inhibition upregulates Elovl5 and suppresses SREBP1-mediated lipogenesis signaling, reducing lipid accumulation in a palmitic acid-induced NAFLD model; the pro-lipogenic effect of miR-218-5p is blocked by si-Elovl5, confirming Elovl5 as the functional target. |
Dual luciferase reporter assay, gain/loss-of-function miRNA experiments in AML12 cells and HFD mouse model, SREBP1 pathway Western blotting |
Biochemical pharmacology |
Medium |
38972428
|
| 2023 |
Deletion of Elovl5 in LDLR-deficient mice activates SREBP-1, increases hepatic triglyceride and cholesterol, elevates VLDL/IDL/LDL plasma lipids, and results in marked aortic atherosclerotic plaques; Elovl5-deficient macrophages show slightly elevated PGE2 secretion (likely due to Cox-2) but no major differences in M1/M2 polarization markers. |
Elovl5-/-;Ldlr-/- double knockout mice, lipoprotein profiling, hepatic lipid analysis, aortic plaque quantification, bone marrow-derived macrophage polarization assays |
Biochemical and biophysical research communications |
Medium |
38000296
|
| 2025 |
ELOVL5 physically binds to STING and inhibits TBK1 interaction with STING and its translocation to the Golgi, thereby reducing STING-mediated inflammatory signaling in lung epithelial cells; Elovl5 deficiency impairs lung inflammation resolution after influenza infection and reduces AKT1-mediated tissue repair; ELOVL5 also decreases eicosanoid levels in alveolar epithelial cells. |
In vivo CRISPR screen (AAV9-Sleeping Beauty), Elovl5 conditional knockout in lung epithelial cells, co-immunoprecipitation of ELOVL5 with STING, STING-TBK1 interaction assay, Golgi trafficking assay, eicosanoid profiling |
bioRxivpreprint |
Medium |
|
| 2025 |
ELOVL5 promotes VLC-PUFA production in HCMV-infected cells and aids removal of erucic acid (C22:1, an endogenous antiviral fatty acid) by elongation; ELOVL5 activity is stimulated by HCMV infection and reduces C22:1 levels, thereby mollifying the antiviral effect of erucic acid on virus replication. |
Lipidomics, erucic acid supplementation, ELOVL5 functional assay in HCMV-infected cells |
bioRxivpreprint |
Low |
|
| 2025 |
ELOVL5 is a super-enhancer-driven oncogene in T-ALL; ELOVL5 knockdown suppresses T-ALL cell proliferation and induces apoptosis in vitro and reduces tumor burden in xenograft models; RNA-seq shows ELOVL5 promotes T-ALL progression by activating MYC signaling and upregulating SERBP1. |
H3K27ac ChIP-seq, shRNA knockdown, RNA-seq, xenograft mouse models, SERBP1 silencing |
Genomics |
Medium |
41016515
|