Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniPathway vocabulary mapping
Electronic Gene Ontology annotations created by transferring manual GO annotations between related proteins based on shared sequence features
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Automatic assignment of GO terms using logical inference, based on on inter-ontology links
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
A 5-bp deletion in ELOVL4 is associated with two related forms of autosomal dominant macular dystrophy.
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The familial 5-bp ELOVL4 deletion, retinal expression and homology to yeast elongation proteins linked very-long-chain lipid biology to inherited macular degeneration; the study did not establish photoreceptor GPCR activity.
"Bioinformatic analysis of ELOVL4 revealed that it has homology to a group of yeast proteins that function in the biosynthesis of very long chain fatty acids."
Dominant negative mechanism underlies autosomal dominant Stargardt-like macular dystrophy linked to mutations in ELOVL4.
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Tagged wild-type human ELOVL4 localized to the ER and copurified with coexpressed ELOVL4, including a C-terminally truncated disease mutant. Heterogeneous detergent complexes and possible aggregation leave oligomeric stoichiometry and catalytic competence unresolved.
"Wild type ELOVL4 containing an endoplasmic reticulum retention sequence was localized to the endoplasmic reticulum as expected."
ELOVL1 production of C24 acyl-CoAs is linked to C24 sphingolipid synthesis.
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The comparative membrane assay included human ELOVL4 and detected weak but significant saturated C24:0/C26:0-CoA elongation-associated output. It assigns ELOVL4 to the condensing step without resolving the complete chain-length distribution or purified intermediate kinetics.
"Elongases catalyze the first of four steps in the VLCFA elongation cycle; mammals have seven elongases (ELOVL1-7). In the present study, we determined the precise substrate specificities of all the ELOVLs by in vitro analyses."
A reference map of the human binary protein interactome.
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Large-scale systematic yeast two-hybrid map (HuRI) of human binary protein-protein interactions; the source of many ELOVL4 GO:0005515 IPI annotations.
"Here we present a human 'all-by-all' reference interactome map of human binary protein interactions, or 'HuRI'."
The 3-hydroxyacyl-CoA dehydratase 1/2 form complex with trans-2-enoyl-CoA reductase involved in substrates transfer in very long chain fatty acid elongation.
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The abstract describes the four-component ER elongation machinery and HACD-TECR complex. It provides pathway context but does not by itself authenticate the imported ELOVL4-TECR pair; operative source-specific evidence remains unavailable.
"the VLCFAs elongation machinery is located in ER membrane and consists of four components, FA elongase (ELOVL), 3-ketoacyl-CoA reductase (KAR), 3-hydroxyacyl-CoA dehydratase (HACD), and trans-2-enoyl-CoA reductase (TECR)"
UniProt entry Q9GZR5 (ELOV4_HUMAN)
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ELOVL4 catalyzes the first and rate-limiting reaction of the four-reaction long/very-long-chain fatty acid elongation cycle in the ER, adding two carbons per cycle and producing very-long-chain saturated and polyunsaturated fatty acids.
"Catalyzes the first and rate-limiting reaction of the four"
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ELOVL4 is an endoplasmic reticulum membrane multi-pass membrane protein.
"Endoplasmic reticulum membrane"
Role of ELOVL4 and very long-chain polyunsaturated fatty acids in mouse models of Stargardt type 3 retinal degeneration.
The role of ELOVL1 in very long-chain fatty acid homeostasis and X-linked adrenoleukodystrophy.
Changes in the daily rhythm of lipid metabolism in the diabetic retina.
The Elovl4 Spinocerebellar Ataxia-34 Mutation 736T>G (p.W246G) Impairs Retinal Function in the Absence of Photoreceptor Degeneration.
Synapse-Specific Defects in Synaptic Transmission in the Cerebellum of W246G Mutant ELOVL4 Rats-a Model of Human SCA34.
ELOVL4 source evidence and access guide
ELOVL4 reproducible source, PAINT, interaction and rule analysis