This guide records the selected primary-source readings, biological scope and source-specific review. The genuine import contains 42 original QuickGO contexts, 42 exported rows and 42 distinct stored annotations. The source evidence preserves the complete original objects and their exact joins to the untouched seed. Scoped validation outcomes are recorded in the notes and structured source evidence.
HGNC FOXE3 and reviewed UniProt Q13461 establish human FOXE3, also named FKHL12/FREAC8. The displayed protein has 319 residues and no current alternative-products comment. Historical mouse constructs and disease variants are not extra human natural products.
All 42 original QuickGO objects, qualifiers, references, evidence codes and WITH/FROM groups are embedded in the source evidence. The genuine export and seed both retain 42 distinct contexts, with zero source collisions, NOT assertions or extensions. Indices below are zero-based original raw indices; the evidence supplies their actual stored-index joins. The review totals are 15 ACCEPT, 12 KEEP_AS_NON_CORE, 2 UNDECIDED, 11 TOO_GENERAL and 2 MODIFY.
| Original study | Raw contexts | Reference assessment | Actual access |
|---|---|---|---|
| Original study 10652278 | 0, 6, 41 | UNVERIFIED | Selected original text/captions |
| Original study 11980846 | 10 | VERIFIED | Selected original text/captions |
| Original study 16199865 | 33, 35 | VERIFIED | Selected original text/captions |
| Original study 17064680 | 13, 16, 27, 29, 31 | VERIFIED | Selected original text/captions |
| Original study 22527307 | 22, 25, 36 | UNVERIFIED | Abstract/preview or supplement listing only |
| Original study 25504734 | 4, 7, 40 | UNVERIFIED | Abstract/preview or supplement listing only |
| Original study 27218149 | 11, 14, 21 | VERIFIED | Selected original text/captions |
| Original study 8825632 | 8 | UNVERIFIED | Abstract/preview or supplement listing only |
Reference assessments distinguish correct identity from whether the source supports the particular assertion. In particular, the original mouse text of 10652278 was inspected, but the exact link to the imported human IDA contexts remains UNVERIFIED. No paper is called misattributed from a title or incomplete abstract. No figure pixels or actual supplements were inspected for these readings.
Inspected scope: Results: browser lines 114–228; Discussion: 229–252; Methods: 253–278; human_scope: 116–117, 140–141, 252, 257
Identifier and selected original mouse Methods/Results/Discussion were verified. Mouse lens genetics supports developmental biology, but the exact supporting link for the three original human IDA transcription/complex assertions remains unresolved. Human cloning-probe use and an unpublished cDNA comparison are not human functional assays. This UNVERIFIED judgment is specific to the annotated human assay attribution, not doubt about the paper identity or a declaration of misattribution.
Inspected scope: Original journal pp1351–1354; browser lines148–177,188–203,279–300,352–360,379–404.
Selected original Methods/Results were read through the browser’s extraction of the linked journal PDF, including journal pages 1351–1354. Mouse forkhead fragments in reticulocyte lysate bind a FOXC1 consensus probe; the corresponding human R90L fragment is reported to bind in data not shown. Human 319-aa lens cDNA, mouse fragment versus full-length scope and uncertain R90L disease causality remain distinct. The separate direct binary PDF download failed; original text extraction succeeded. Figure pixels and supplements were not read.
Inspected scope: Methods: browser lines 116–138; Results: 139–182; Discussion: 183–203
Selected original mouse knockout Methods/Results/Discussion and captions establish lens epithelial proliferation/differentiation defects, with mixed B6 × 129 background and targeted coding-region loss. Human rows are explicit ISS transfers. Direct DLAD binding and universal tissue autonomy are not established. The proposed hypomorphic-dyl explanation is interpretation challenged by the later congenic 17064680 comparison.
Inspected scope: Materials and methods: Targeting Foxe3; Histology/in situ/immunohistochemistry; Volume measurements. Results: Targeted deletion phenocopies dyl; anterior segment mesenchyme. Figure2–4 captions. Discussion: dyl is a null allele; anterior segment; Pax6 dosage.
Selected original publisher-indexed Methods/Results/captions were read; direct publisher access failed. Targeted-null and dyl comparisons after five Balb/c backcrosses support lens and anterior-segment developmental outcomes and mouse nuclear immunostaining. Distinguish positive anatomy from hypothetical lens-derived signals and unresolved tissue autonomy. No figure pixels or supplementary data were read.
Inspected scope: Publisher abstract Methods/Results; browser lines38–53; subscription preview explicitly identified.
Authentic publisher abstract/preview was inspected. Human HLEB-3 FOXE3 shRNA reduces RNA/protein and growth and causes G1 arrest. Full original Methods/Results, perturbation-specificity/rescue details and the exact apoptosis endpoint were unavailable. Positive abstract observations are retained without claiming full experimental verification or refuting the curator from an omitted abstract detail.
Inspected scope: Authentic publisher abstract and supporting-information description; actual SI and original body inaccessible.
Authentic abstract and publisher supplement descriptions were recovered; original Methods/Results, actual supplement and images remain inaccessible. The abstract reports variant band-shift/transactivation differences and intermediate modeled heterozygotes without dominant-negative evidence in that experiment. No host, exact construct sequence, purified assay or localization result is inferred from the listing.
Inspected scope: Human family/segregation evidence: clinical evaluation, linkage and Sanger/exome sequencing; WT/C240* nuclear localization; DNAJB1 promoter occupancy and variant effects on DNAJB1 expression. Methods: ChIP, reporter assay, target RNA, and the separate DNAJB1 knockdown and zebrafish dnajb1 experiments. Selected original text and captions were read, including the human family/segregation material; the exact private paragraph ledger is retained separately.
Selected original XML Methods/Results/captions were inspected. Human familial FOXE3 variants, HLE anti-FOXE3 ChIP and ectopic HEK293FT DNAJB1 reporter/RNA assays support developmental/transcriptional evidence; ChIP Methods do not state FOXE3 overexpression. The discovery-screen direction sentence conflicts with surrounding results, so independent reporter/qPCR findings govern the direction assessment. DNAJB1 knockdown and zebrafish dnajb1 rescue remain downstream-gene tests, not FOXE3 perturbations. No figure pixels or actual supplements were read.
Inspected scope: Original publisher abstract; authenticated PubMed metadata.
Identifier and authentic abstract verify human FREAC8/FKHL12 cloning/mapping within a forkhead-gene study. The original body and exact target-specific TF experiment were not recovered. The original TAS citation is retained without a wrong-reference or wrong-gene inference.
The human ISS/IEA contexts preserve Q9QY14 and the separate Ensembl alternatives. The complete current mouse query contains 56 original objects; 17 human contexts have explicit same-term joins. These joins do not rewrite human evidence codes or imply that every historic mouse source was inspected. Auxiliary donor references retained only as provenance, including 10890982, do not become newly verified primary assays or automatically expand the normal-source plan.
The original 11980846 binding study tests reticulocyte-lysate translated mouse forkhead residues 60–175 with a FOXC1 consensus probe. The human R90L result is reported as data not shown. Human 319-aa identity, mouse 288-aa sequence, domain fragments and disease constructs remain distinct. The rare R90L observation was not established as causal disease evidence.
The 27218149 study includes human family segregation, antibody ChIP in HLE cells and separate ectopic HEK293FT reporter/RNA experiments. The ChIP Methods do not state FOXE3 overexpression for that assay. Formaldehyde-crosslinked chromatin enrichment is not purified binary DNA binding. The positive reporter effect is not a universal activation claim for every target or allele, and steady-state RNA is not a direct nascent-transcription measurement. DNAJB1 knockdown and zebrafish dnajb1 rescue are not human FOXE3 perturbations.
The authentic PTHR11829 tree and alignment each contain 1,182 nodes with identical node sets. The human Q13461 target sequence exactly reproduces 319 residues. All six incoming IBA contexts descend from the corresponding positive PTN000930906 assertion and match literal original IBD provenance. The two fungal negative records are off the target path. Current versus retained historical source-list differences remain explicit, and Q13461 as a nuclear self-donor is legitimate descendant evidence.
The three existing PTHR11829 family files were reused byte-for-byte from main after source ownership and identity checks. The independent tree/MSA/IBD analysis remains distinct from those normal family caches.
The specific Pol II TF, regulatory DNA-recognition and Pol II regulation terms are supported by is_a-only ancestry checks. Lens development reaches organ and system development through mixed part_of/is_a paths: the first step is part_of camera-type eye development, and the route to system development additionally passes through visual/sensory-system development. The broad electronic rows are treated as general developmental coverage; lens development is not called their pure subclass.
One core describes GO:0000981 Pol II DNA-binding transcription-factor activity in nucleus/chromatin, with the experimentally supported positive DNAJB1 regulatory response and the lens epithelial proliferation and early fiber-differentiation restraint program. Broad lens development remains accepted in the original rows but is not repeated among the more specific structured core processes. The general molecular-function class remains direction-neutral; the positive process claim is bounded to the tested target response. Two contexts remain UNDECIDED: apoptosis and transcription regulator complex. No stable isolated transcription complex, autophagy or cochaperone chemistry is assigned to FOXE3. Source-assay uncertainty also remains explicit in gene-level positive or TOO_GENERAL judgments; independent evidence does not authenticate inaccessible original experiments. There are no NEW annotations or added quotations.
The unmodified gene fetcher acquired eight publication caches and reused three existing PTHR11829 family files unchanged. The caches for PMID:10652278, PMID:16199865 and PMID:27218149 carry full text; the other five contain abstracts. Cached availability and the selected-original reading scope above are separate observations: selected originals for PMID:11980846 and PMID:17064680 were inspected beyond their abstract-only caches. A full-text cache flag does not upgrade any uninspected assay or supplement.
No FOXE3 provider job was attempted because the shared Falcon/perplexity credential failure remained unresolved. This review uses the accepted manual primary-source research; no provider report was manufactured. Default validation, strict GOA matching, computed status, history, conservation and private rendering are complete; their actual outcomes are recorded in the notes and evidence.
Notes · Structured source evidence
The original broad DNA-binding/TF contexts remain TOO_GENERAL relative to retained specific functions. The nuclear-location claim remains accepted with the inaccessible original localization assay explicitly unverified. The revised transcription, lens and cell-cycle decisions below preserve all original sources and qualifiers. Apoptosis and transcription regulator complex remain UNDECIDED because their relevant source assertions are unresolved.
The two original transcription-process rows at stored indices 21 and 24 are refined to GO:0045944, based on the selected human DNAJB1 ChIP, reporter and target-RNA Results/Methods in PMID:27218149 (sections 10–11 and 27–29, Figure 3 caption). A transcription factor can contribute work to transcription; this refinement does not rely on restricting the process to catalytic polymerase subunits. GO:0045944 positively_regulates GO:0006366, so that relation is not used as an is_a subsumption argument. The original qualifiers, citations and evidence codes remain intact. GO:0006357 is TOO_GENERAL relative to its actual is_a child GO:0045944; the positive direction comes from the human experiment, not a revised PAINT ancestor claim.
The five original GO:2001111/GO:1902747 rows now represent the developmental core consistently. The mouse loss-of-function observations support lens epithelial maintenance and restraint of premature fiber differentiation, not uniform inhibition of every maturation step. Human growth evidence and congenital phenotypes remain distinct from the mouse perturbations and do not identify a complete set of direct human targets. The cultured human G1-arrest observation in the authentic PMID:22527307 abstract is retained as non-core cell-cycle regulation. Its original full Methods/Results and rescue controls remain uninspected; neither independent proliferation evidence nor a retained annotation upgrades that access status. An exclusively downstream mechanism has not been established and is not used to label the row over-annotated.
The campaign’s explicit reference-only evidence policy requires no new publication quotations and preserves immutable caches. The absence of supporting_text is therefore intentional and does not claim that the verbatim-quote validator checked excerpts. Reference correctness records source-to-claim verification, not whether the normal cache has full text: selected original browser-extracted Methods/Results/captions support PMID:11980846 and PMID:17064680, whereas the exact imported human assay link for the inspected mouse paper PMID:10652278 remains unresolved. The selected original URLs and locators above allow those scopes to be checked. No provider retry was made under the unresolved credentials.
For PMID:8825632, retained official PubMed metadata gives DOI 10.1006/geno.1995.1266 and PII S0888-7543(85)71266-9. The existing publisher URL retains that identifier; it is not replaced by a guessed year-based PII.