The 53 imported contexts have been reviewed, with 17 ACCEPT, 17 MODIFY, 12 KEEP_AS_NON_CORE and 7 UNDECIDED decisions after the explicit localization refinement. Source objects, all 17 original reference identities and existing biological fields, and the three ordered natural products are unchanged. Thirteen unique references are added from genuine normal caches; PMID:16332939 was already in the intake, while twelve were fetched additively. No new publication quotation, annotation, core function or status change is introduced. The standalone description remains for the subsequent synthesis phase.
The initial accepted lane merge is retained privately as an immutable baseline (18 ACCEPT and 16 MODIFY). The sole annotation adjudication at integration refines the endometrial nucleus assertion to nucleoplasm using independent human HPA and Reactome evidence. PMID:18775884 itself remains nuclear-only and uses a shared long/short antibody. The refinement does not identify every product or extend it to every tissue. The source guide records the separate access scopes and public original links.
Shared assessments of PMID:28473536 and PMID:36646760 retain both accepted source-access accounts. Human extended DNA-binding-domain SELEX, the historical L/S transcription constructs and the natural 433/508/500-residue records are not equated. The 2023 chromatin experiment includes trace HeLa extract; its naked-DNA reactions are distinguished. Printed supplementary Table S4 gives the cDNA accessions and printed Table S5 the vector/tag record; the main-text table numbering differs. Current sequence correspondence does not verify every historical plasmid base.
The imported NOT embryonic-placenta-development claim remains negated and unresolved. Steroid-specific assertions remain unresolved despite the positive marine-sterol pharmacology lead. The morula study was actually read and supplies mouse Esrrb transcriptional evidence, but does not settle that particular developmental transfer; the inner-ear claim retains its original-access limitation. These are claim-specific uncertainties, not evidence of biological absence.
The following entry preserves the database-lane journal and its stage-specific counts. Its statement about six pending direct reviews describes that earlier stage; all 53 reviews are now combined.
Reviewed 47 database-origin contexts using the actual PAINT tree/MSA/IBD, target-matching ARBA conditions, InterPro mappings, HPA antibody/cell data and Reactome participant chains. Five PAINT placements are valid, both human and mouse alignments are exact, and self-WITH is retained as legitimate descendant evidence. Both Reactome location routes explicitly reach human ESRRB residues 1–433 in nucleoplasm.
Human ERRβ-L/S assays in PMID:36646760 provide direct sequence-dependent DNA binding and polymerase-II transcription evidence. Supplementary Figure S5b includes trace HeLa extract; naked-DNA assays are distinguished. Current construct accessions map to 508/433-aa products, without verification of historical plasmid sequences or a claim for the 500-aa product. The three natural product records remain separate.
The database recommendations are 16 ACCEPT, 12 KEEP_AS_NON_CORE, 14 MODIFY and 5 UNDECIDED. The unresolved claims are steroid-specific receptor activity, steroid binding, steroid-initiated signaling, precise inner-ear development where operative original experiments remain inaccessible, and the specific morula-formation role. Marine sterol antagonism is a positive published lead; orphan classification does not refute ligand responsiveness. The morula study actually assays mouse Esrrb and shows an earlier transcriptional contribution, but it does not resolve the specific transferred process. Neither uncertainty rests on a title-based attribution claim.
Contextual stem-cell, retinal, Integrator and polymerase-complex roles are retained with their actual organism, preparation and mechanistic limits. This phase adds no annotations, core functions or publication quotations. All source objects, six other pending reviews, three products and normal cache bytes are unchanged. The source guide records direct original links, operative sections and access limits.
Thirteen annotation reasons replace a duplicated human ERRβ-L/S assay-and-product paragraph with the relevant positive assay and a pointer to its complete reference review and source-guide account. Decisions, support objects, source fields and product boundaries are unchanged. The full historical-construct/current-sequence distinction and the trace HeLa-extract condition remain explicit in the reference review, guide and combined assessment above.
One DNA-binding transcription activator core captures the experimentally coupled recognition of regulatory DNA and positive RNA-polymerase-II transcription. Human ERRβ-L/S DNA binding and transcript production in PMID:36646760 are the principal evidence; the exact human eDBD in PMID:28473536 independently supports sequence recognition. Chromatin is the activity location. The core uses neither a separate generic binding activity nor a second ancestral transcription-factor activity, and it does not assign RNA polymerase catalysis to ESRRB.
The human chromatin reaction includes PGC-1α/p300 and trace HeLa nuclear extract, whereas the naked-DNA experiment directly measures transcript output with general factors and polymerase. Current accession correspondence to 508/433 residues does not verify every base of the historical L/S plasmids or demonstrate the 500-residue product. These boundaries are preserved in the reference reviews and the source guide. Mouse stem-cell and developmental findings remain contextual assessments rather than extra human core processes. Steroid-specific uncertainties are unchanged; positive receptor pharmacology is retained without an assertion about a native ligand.
All 53 accepted review/source objects, 30 references, three product records and 33 normal files remain unchanged. No NEW annotation, quotation, status change or extra reference is introduced. The 26 selected dependency roles and seven retained private intake-context caches are carried forward exactly from the accepted integration.
Final canonical validation records COMPLETE with 0 advisories. All 53 imported contexts, 30 reference records and three natural products remain as assessed. All 108 authored narratives appear in the private rendering. No NEW annotation or publication quotation was introduced.
Biallelic ESRRB variants cause DFNB35, an autosomal recessive nonsyndromic hearing disorder. The original study identifies segregating variants in five families and severe-to-profound hearing loss; its cochlear transcript assay uses human fetuses, while developmental in situ and postnatal localization use mouse and rat, respectively. The missense structural effects are modeled. These findings establish auditory relevance without specifying whether each pathogenic allele disrupts developmental differentiation, mature ion homeostasis or both (PMID:18179891, Methods; Figures 1–7 and Table 2). The inner-ear-development transfer remains unresolved at that mechanistic/stage level; this does not discount the human disease association.
Stem-cell population maintenance is retained as a contextual transcriptional contribution. The original mouse-cell rescue is positive, and independent mouse studies link Esrrb occupancy and transcription to self-renewing populations with culture dependence and Nr5a2 redundancy (PMID:25522312, Figures 3–4; PMID:34397088, Figures 1–3; PMID:23040478, Figures 3–4). The historical rescue insert is not sequence-mapped, and the human iPSC arm perturbs nucleostemin. Human ESRRB transcription assays support conserved molecular capability, not universal human stem-cell dependence.
For human transcription, Supplementary Figure S5b measures chromatin activation with trace HeLa extract; S5j measures DNA binding; S5k compares WT and DNA-binding mutants in transcription; S5l tests competitive inhibition by added TFIIHp52. The human and mouse panels are distinguished (PMID:36646760, Methods and Supplementary Figure S5). The independently read retinal original, rather than its abstract-only normal cache, supplies the DY131/4-hydroxytamoxifen and promoter-mutant evidence (PMID:20534447, Results and Figure 1K). The reporter insert remains unmapped to a particular human product. The UniProt ESRRB FUNCTION record also records ERRE recognition; the specific human activity is grounded in the primary binding/transcription experiments already cited.
The campaign curation instructions explicitly require no new publication quotations and preservation of normal cache bytes. Accordingly this revision supplies public original URLs, experiment locators and bare reference support without claiming that an absent quotation passed a verbatim-substring check. Genuine Falcon and perplexity-lite research attempts failed (403 and quota/authentication responses); no provider output was fabricated. Earlier entries above retain the counts and validation status of their own phases. This revision changes one action, from UNDECIDED to KEEP_AS_NON_CORE, leaving six unresolved contexts and the single transcription-activator core unchanged. Canonical validation of this revision is still to be performed.
Revised canonical validation passes all six checks, with all 112 authored narratives present in the private rendering. Computed COMPLETE has zero validation advisories; the six explicitly UNDECIDED assertions remain unresolved. All 53 source objects, three products and the single core remain unchanged. Thirty-one references include the genuine newly cited DFNB35 cache. All 27 selected normal sources and eight unrelated baseline files/modes remain unchanged; no publication quotation was added.