This is a manual assessment, not a provider-generated report. No exact OpenScientist query/report was found for ELOVL2/Q9NXB9 or ELOVL6/Q9H5J4 in the repository and global cache. An unrelated PGRPLC report mentioning elongases was not used.
The source/term JSON records the actual PTHR11157 target lineage, positive ancestral IBDs, absence of an on-lineage negative assertion, live term definitions and the exact IntAct query responses. Both targets descend from PTN000125390; donor count and target self-inclusion are not objections.
The publication cache remains abstract-only. Full author manuscript was read at HUSCAP, PDF, SHA256 bf4715a183e5631c78ec7d27ba3b8f270a99c0196aff7492b1c69f54f6df1f93. Figure 1B was visually inspected at PDF page 26 (zero-based 25), not inferred from the abstract. HEK293T membrane fractions expressing human proteins were assayed with 50 micromolar acyl-CoA and radiolabeled malonyl-CoA, 30 minutes at 37 C, three replicates. ELOVL6 signals for C18:2 and C18:3(n-3) are significantly above vector, although far below C16:0. ELOVL2 has no significant signal above vector on the tested saturated C16-C26 or C18:1 substrates; the finite panel cannot exclude every substrate or condition. Figure 1D maps ELOVL6's C16-to-C18 step upstream of longer-chain synthesis. Results describe ER localization for all seven proteins and CERS2 co-immunoprecipitation with all seven; indirect association remains possible. CERS2 functional regulation emphasized ELOVL1, not exclusive binding to ELOVL1.
GO:0042761 defines a very-long-chain fatty acid by an aliphatic tail containing more than 22 carbons; GO:0035338 and GO:0042759 use 13-22 tail carbons for long-chain species. Papers conventionally report total chain carbon numbers. C18 alone does not establish a VLCFA product; C24 clearly qualifies. An enzyme can perform an upstream synthesis step without catalyzing the terminal step. Reactome R-HSA-75876 includes the C16-to-C18 cycle in the route that continues to longer products; its own >20-carbon prose is not substituted for the GO boundary. GO:0036109 currently contains a chemical typo (omega-6/C18H32O2 for alpha-linolenic acid). The intended ALA route is omega-3, 18:3, as independently described in Reactome R-HSA-2046106. Source term ID and label are preserved.
PMID:25003994 full text and Figure 2D, image SHA256 90adb941576b4dbc3f7e8972206799c84e88992086a71f4e456ec6501b598b2d, show purified proteoliposome-reconstituted ELOVL6 overwhelmingly preferring C16:0. Other substrate bars are near baseline; the figure does not establish an all-conditions negative for the weak PUFA activities detected in the 2010 membrane assay. KAR co-reconstitution stimulates condensation even without KAR catalysis; active KAR plus NADPH gives additional stimulation. The authors discuss the lack of definitive physical-interaction evidence and possible detergent-micelle artifacts. Thus functional membership in the elongation machinery is supported without claiming a resolved binary interface or stoichiometry.
PMID:31529722 full manuscript was read from Tsukuba, SHA256 1a3f35d415d51660e710e96372f1235f24bae047b2f28cbeb3aa5f8efd95f46f. Figure 5 and its Results describe Elovl6-CerS4 colocalization and co-immunoprecipitation in HEK293 cells, alongside mouse liver lipidomics identifying the C18:0 ceramide pool. The study concerns mouse Elovl6 physiology and supports ortholog-conserved sphingolipid precursor synthesis; it does not show human ELOVL6 catalyzing CerS4's amide-bond reaction.
PMID:26214738 full text and Extended Data Figure 1 show human ELOVL6 rescue of fly dElovl6 lethality and establish the C16:0/C18:0 pathway. Fly mitochondrial-outer-membrane localization is not silently transferred to the human protein. PMID:26628376 studies mouse thermogenesis: ELOVL6-dependent lipid remodeling supports brown-adipose adaptation, with mitochondrial lipid composition and TFR1 signaling offered as mechanisms whose relative contributions remain unresolved. The tissue-specific process remains non-core, without treating lack of direct human assays as refutation.
IntAct HuRI records verify HMOX1, LCP2 and RTP2 pairings. The PMID:20937905 partner Q96G23 is CERS2, correcting the earlier CERS6 description. An empty current IntAct query for that paper does not negate the full-paper co-immunoprecipitation finding.