gene: EDAR
annotation_scope:
imported_annotations: 23
reviewed_annotations: 23
new_annotations: 0
retired_source_contexts: 0
This guide locates the evidence and distinguishes actual reading from cache availability. It is not an independent study. All 23 source identities and all existing cache bytes are preserved. A source-specific REMOVE is a curation judgment; the retracted source row has not been erased or marked as a retired export context.
| Source | Effective cache | Actual evidence and limits |
|---|---|---|
| PMID:10431241(https://pubmed.ncbi.nlm.nih.gov/10431241/) | Added, abstract only | Selected author-uploaded original cloning, genetics, predicted topology and Discussion. The EDAR–EDA ligand relationship was explicitly a hypothesis in this 1999 study; later experiments establish it. No figure pixels inspected. |
| PMID:11035039(https://pubmed.ncbi.nlm.nih.gov/11035039/) | Added, abstract only | Selected original Methods, ligand-binding Results/captions, NF-kappaB experiments and TRAF/NIK association examined separately. Secreted Myc-EDA-A1 and soluble EDAR-Fc were tested in conditioned media with controls, not as a homogeneous purified pair. Cell-based association does not establish direct contact with each signaling adaptor. |
| PMID:11039935(https://pubmed.ncbi.nlm.nih.gov/11039935/) | Added, abstract only | Complete positive abstract identifies EDA-A1 binding EDAR and EDA-A2 binding EDA2R. Full original recovery failed; unseen construct and organ-culture details are not asserted. |
| PMID:12270937(https://pubmed.ncbi.nlm.nih.gov/12270937/) | Existing, abstract only | Selected indexed original Introduction, Methods and Results. The Introduction explicitly states prior EDAR disease and ligand findings; new XEDAR assays are kept separate from the EDAR TAS annotation. |
| PMID:27144394(https://pubmed.ncbi.nlm.nih.gov/27144394/) | Added, full text; retracted | Relevant human constructs, co-IP Methods, binding Results and Fig. 1C caption examined. The later notice questions this same binding panel; the reference is invalidated and the source-specific assertion removed. Independent EDA–EDAR evidence remains positive. |
| PMID:32822567(https://pubmed.ncbi.nlm.nih.gov/32822567/) | Existing, full text | Human extracellular library, fusion-protein production and controlled retest Methods; actual Data S1, S4 and S5 workbooks. Both EDAR pairs appear in both orientations with triplicate data. No EDAR SPR record was found. Native signaling and physiological contact are not established by this screen. |
| PMID:42308199(https://pubmed.ncbi.nlm.nih.gov/42308199/) | Added, abstract only | Complete official notice independently recovered and read. It explicitly questions Fig. 1C of PMID:27144394 and retracts the results/conclusions after unresolved concerns. The abstract-only cache flag is unchanged. |
| PMID:12629675(https://pubmed.ncbi.nlm.nih.gov/12629675/) | Added, abstract only | Complete abstract describes mouse salivary-gland localization and developmental perturbations. Current MGI donor IDAs retain plasma-membrane and apical-part annotations. Detailed microscopy Methods/images were not recovered; positive curator evidence is not treated as a donor error. |
| PMID:19619491(https://pubmed.ncbi.nlm.nih.gov/19619491/) | Existing, flagged full text; content partial | The cache contains Introduction and Discussion. A separately recovered complete PMC2859042 original supplies the inspected mouse Methods and Results: early Wnt prepatterns persist in Edar-null/downless embryos, but placode borders and sustained focal Wnt activity are impaired. Constitutive EDAR does not bypass Wnt. Cache bytes remain unchanged; no human placode assay or figure-pixel inspection is claimed. |
| PMID:11780064(https://pubmed.ncbi.nlm.nih.gov/11780064/) | Added, abstract only | Complete normal-cache abstract: mouse Edaradd discovery, Edar death-domain association and linkage to downstream signaling; human EDARADD disease genetics. Full Methods/Results were not recovered, and human construct identity or purified binary binding is not inferred. |
The separately accessed PMID:10431241 original supplies the human cloning/genetic context and the explicit prospective ligand hypothesis. The PMID:11035039 original supplies the selected ligand and signaling experiments. Its original construct coordinates are not silently equated to the deposited IntAct feature ranges or both complete natural products.
The PMID:12270937 original distinguishes the EDAR background statements from new XEDAR experiments. The complete retraction notice identifies Fig. 1C concerns and the editorial decision; its machine-readable XML contains the same notice. No replacement identifier is substituted for PMID:27144394.
For PMID:32822567, the original main article and publisher Data S1, Data S4 and Data S5 are the operative screen sources. The portable audit includes exact saved workbooks and checksums; future downloads must match before replay.
The source audit derives four EDAR incident screen records representing two pairs, three exact human library-sequence matches, five selected IntAct source records from 57 total, the three literal PTHR12120 IBDs, matching electronic-rule conditions and four Reactome paths to EDAR. A positive binding class does not transfer a partner's catalytic or signaling activity to EDAR.
EDA Q92838 is an independently established cytokine; LILRB1 Q8NHL6 is an independently established inhibitory signaling receptor. GO:0019955 and GO:0005102 describe binding to those partner classes. The latter term does not require receptor agonism. GO:0004896 captures EDAR's cytokine-receptor function; GO:0005031 specifically names tumor necrosis factor, so TNFR-family membership alone is insufficient.
The exact EDAR sequence and target path were checked in the 125-node PTHR12120 tree and MSA. The root IBDs for receptor activity and cytokine signaling, and the descendant IBD for plasma membrane, all lie on that path. The human target appearing among its own descendant sources is legitimate experimental grounding. Current mouse Edar Q9R187 and human EDA2R Q9HAV5 donor annotations were inspected separately; their distinct ligand specificity is preserved.
ARBA00027254, ARBA00028236 and ARBA00084990 have explicit condition sets matching the official EDAR FunFam. The epidermis rule also specifies Chordata. The current IPR047526 family mappings are distinguished from EDAR-specific experimental corroboration.
Reactome R-HSA-5669012 and R-HSA-5675656 both reach EDAR entity R-HSA-5669001, Q9UNE0 residues 27–448 at the plasma membrane. EDARADD's cytosolic location is not transferred to the receptor. These curated models do not establish equivalent activity of the two complete natural EDAR products.
The official EDAR record supplies two products, 448 and 480 residues. The longer product replaces Ala219 with a 33-residue cytoplasmic segment. The selected extracellular fragments are shared-region reagents; they do not establish equivalent full-product signaling. Signal-peptide cleavage is processing, not a third splice isoform.
The author-uploaded PMID:10431241 original linked above was inspected for cloning/genetic Results,
Discussion of the prospective ligand relationship, and the Methods section. The PMID:11035039
original was inspected for construct and ligand-binding Methods, ligand-binding and NF-kappaB
Results, TRAF/NIK association and corresponding captions. The PMID:12270937 original was inspected
for the Introduction's EDAR disease/ligand background, Methods and Results concerning XEDAR.
These are selected text and caption reads, not figure-pixel examination. The normal caches for
PMID:10431241, PMID:11035039 and PMID:12270937 remain abstract-only. Their optional reference-level
availability flags are omitted; the reference assessments and these original locators retain the
separate access account. All cache bytes and flags remain exact.
Ligand recognition and downstream signaling use reference-only support at the documented assay
scope. PMID:11035039 supplies the selected ligand-binding and NF-kappaB experiments, while
PMID:11039935 supplies the positive ligand-specificity abstract. The original URLs and section
locators above identify the evidence; no publication passage is asserted as a quotation.
The complete PMID:19619491 original provides
Results on early Wnt activity and placode borders in downless/Edar-null embryos, maintenance of focal
Wnt signaling at E15.5, and the Wnt dependence of constitutive LMP1–EDAR signaling. Its Methods
identify the mouse alleles, explant treatments and reporter/ChIP experiments. This supports a role
in primary hair placode refinement and maintenance, not Wnt-independent initiation or a directly
measured human placode phenotype. GO:0060789
is a current descendant of epidermis development, hair follicle development and ectodermal placode
development; the narrower process replaces the two broad epidermis-development assertions. Human
PMID:10431241 genetics supplies distinct corroborating disease evidence.
For EDAR–LILRB1, Data S4 spreadsheet rows 101 and 252 contain the two controlled bait/prey orientations;
Data S1 rows 69 and 376 locate the EDAR and LILRB1 library records. The portable extraction preserves
the measurements and sequence comparisons. Bidirectional triplicate positive binding plus LILRB1's
verified receptor identity supports signaling receptor binding. The lack of an EDAR Data S5 SPR row
leaves affinity and native contact unresolved; SPR and receptor agonism are not prerequisites for this
binding class. No second experimental platform is claimed. The retracted PMID:27144394 panel has its
own source-specific disposition and does not invalidate the independent controlled screen.
The PMID:11780064 abstract supports the Edaradd adaptor context at its stated mouse and human-genetics
scope. It is reference-only support for the existing receptor mechanism. No new publication excerpt
has been added. Article text remains separate from the 21 raw data inputs used by the portable audit.