This guide distinguishes the material actually inspected from the scientific inference drawn from it. Article access below describes selected original material and is separate from the actual normal-cache availability listed below. Under the user’s explicit instruction for this ClinGen campaign, no new supporting-text quotations are added. Reference-only support and the original source locators remain available for manual verification; the substring validator does not independently verify paraphrased scientific claims. The accompanying evidence record retains the original source objects, reviewed judgments and input identities.
PubMed and the original article DOI identify the JBC study. Selected original text was read from an author-uploaded article replica.
Locators: article pages 20507–20512; Experimental Procedures sections on constructs, yeast two-hybrid, co-immunoprecipitation and repression assays; Results on the VP motif, interaction and BF-1/PLU-1 repression; Figures 3–7 captions. Figure pixels were not independently inspected.
Human fetal-brain BF-1 NM_005249 and sequence-checked constructs were used. Yeast two-hybrid and reciprocal tagged co-immunoprecipitation support PLU-1 association. HEK293 assays tether GAL4DBD–BF-1 to five GAL4 sites and an adenovirus major late promoter. PLU-1 enhances repression; VP-motif mutants retain basal repression but lose the added effect. The HT1080 BF-1 co-immunoprecipitation is transfected/tagged; the endogenous PAX9 experiment concerns PAX9. GAL4 tethering does not test native FOXG1 recognition, and these assays do not measure purified affinity. PLU-1's corepressor or demethylase activity is not assigned to FOXG1.
The original PMC article is also available as original full XML. Full XML was recovered; selected Results, Methods and Figures 6–8 captions were read. Figure pixels and supplementary data were not independently audited.
Locators: Results describing FOXG1/TLE association, TLE silencing and GRG6 antagonism; Figures 6e–g, 7 and 8; Methods on cell culture, co-immunoprecipitation, lentiviral knockdown and ChIP. The retained zero-based body-paragraph extraction locates these at Results 11–16 and Methods 29, 36, 38 and 39.
Human patient-derived BT048 cells provide reciprocal endogenous FOXG1/TLE1 co-immunoprecipitation and sequential ChIP at the p21 promoter. FOXG1/TLE perturbations and GRG6 antagonism supply functional context. Cross-linked chromatin fragments were 300–500 bp, so co-occupancy is not base-resolution contact. Complex recovery is not purified binary affinity or stoichiometry. Tagged GRG6/FOXG1 assays in U87MG cells are separate. Human tumor-cell experiments and mouse xenografts remain distinct, and tumor propagation is not converted into a new general developmental annotation. The selected Results sections on BTIC proliferation and astroglial gene expression (retained paragraphs 6–9; Figures 3–4) additionally show reduced sphere formation/proliferation after FOXG1 silencing, increased CDKN1A and astroglial markers, and reduced SOX2/BMI1 expression. These human tumor-derived progenitor findings supply the context-specific propagation synthesis; they are not normal-human neural stem-cell assays.
Use the original paper and its original sequence/PWM supplementary workbook. In the original workbook, worksheet S1 sequence information, row 266, identifies FOXG1B, ENSG00000176165 and a 135-amino-acid eDBD; the S2 motif entries for FOXG1 are rows 5118 and 5123. The retained workbook SHA256 is 4994eb7b3e33eb301541cf7d53d8be0936d5bdb6b504f5d63719e133f40004a6.
The best ungapped alignment is current P55316 residues 163–297, with R281P and R291A. Both match documented historical reference-sequence conflicts outside the annotated 181–275 forkhead domain. Authentic target-specific motif selection supports sequence-specific double-stranded DNA binding with these construct limits. It does not establish an exact wild-type fragment, natural alternative product, the effects of either difference, full-length cellular affinity or endogenous promoter specificity.
The original publisher PDF was accessed through a text reader. Selected Methods, Results and Figures 3–4 captions were read. Direct local PDF download returned 403; no local PDF or figure-pixel inspection is claimed.
Locators: Methods E2028–E2030, PDF pages 2–4, covering cloning/mutagenesis, microscopy and the CDKN1A assay; functional Results E2032–E2033, PDF pages 6–7, and Figures 3–4 captions. The human clinical Results are at retained text lines 194–215, before the functional localization section; they provide independent clinical developmental evidence, distinct from expression and construct assays. The retained Methods and functional Results excerpts are lines 108–187 and 225–264 respectively.
Human BC035020/IMAGE4823883 was expressed as an N-terminal EGFP fusion. A reported Pro-to-Arg codon 82 difference was repaired before generating R244C, and constructs were sequence-checked. This does not independently map every residue to current P55316 or establish a natural product. HeLa and DAOY cells show dispersed nuclear WT signal excluding nucleoli; R244C forms foci partly overlapping SC35. Retinoic-acid-treated SH-SY5Y cells were transfected, GFP-sorted and assessed for CDKN1A mRNA by qRT-PCR normalized to HPRT. The WT decrease is reported as data not shown, while Figure 4 compares mutant and WT. These are localization and expression endpoints, not a direct DNA-binding assay or proof of altered splicing. The codon 82 repair does not imply repair of the unrelated HT-SELEX construct.
An authentic abstract and selected original Methods/Results were accessed through the PMC record and an author-uploaded original article. Locators: pages 5002–5012, Bacterial expression, Selection of binding sites and Figure 1 caption; retained text lines 4080–4185 and 14645–15070. The selected assays explicitly describe FREAC2/3/4/7 forkhead-domain GST constructs. Family-alignment figure pixels were not inspected. Exact FOXG1-specific support for the historical TAS assertion was not recovered; this does not establish wrong-gene attribution or contradict independently supported FOXG1 DNA binding. Original PMC XML/PDF access failures are retained as access diagnostics.
The publisher record and authentic indexed abstract describe human fetal-brain/testis clones and human/mouse expression. Original full Methods/Results were not recovered in bounded attempts. Precise DNA-binding and developmental perturbation support therefore remains source-specific uncertainty. Historical HFK1/HFK2/HFK3 interpretations are qualified by current official sequence information and PMID:17260156; no current natural products are inferred from these clone names.
The authentic PubMed abstract reports human fetal-brain expression and historical HBF1/HBF2 sequence/gene interpretations. Original full Methods/Results were not recovered. Expression alone is not developmental participation, and unseen perturbation assays are not certified. The original TAS identifier remains preserved while the gene-level developmental assertion is refined to telencephalon development using independent clinical and developmental evidence; the older paper is not presented as a newly verified perturbation assay.
Only the authentic indexed and publisher abstract was read; the publisher provides a subscription preview. The comparative study reports no human FOXG1 duplication and a likely FOXG1A artifact. Predicted microRNA recognition sites in the accessed material are not experimentally measured regulation. This source helps qualify historical identity claims; it does not create alternative products.
The official Reactome R-HSA-9618021 event includes human FOXG1 entity R-HSA-9022629, explicitly mapped to P55316 chain 1–489 in nucleoplasm. This supports the retained curated location and FOXO–SMAD complex context.
The model bibliography, PMID:15084259(https://pubmed.ncbi.nlm.nih.gov/15084259/) (original DOI), was subsequently inspected through publisher-indexed original Results, Figures 5–6 captions and Discussion. Locators are “FoxG1 Is a FoxO Antagonist that Suppresses p21Cip1 Induction” and “FoxG1 and PI3K Mediate Glioblastoma Resistance to TGF-β Cytostasis,” especially Figure 6C–F. Endogenous U87MG FOXG1–FOXO3 complex recovery and conditional p21/cytostasis responses support the mechanism. Human HaCaT/DU145 expression assays, COS-1 tagged co-immunoprecipitation and mouse telencephalon experiments remain distinct. The deposited Addgene 14935 human insert does not establish every assay construct. Direct publisher/PDF requests returned 403; complete Experimental Procedures, supplementary material and figure pixels were not inspected. This is a selected bibliography consultation, not a newly acquired normal publication cache or a purified-binding claim.
The actual PTHR46617 tree and MSA contain 65 matching nodes. Human leaf PTN002483625 matches all 489 residues of official P55316 and descends from PTN000216104. All three incoming IBAs—GO:1990837, GO:0006357 and GO:0005634—join literal positive IBDs on that lineage, with original donors unchanged and no family negative records. The DNA-binding IBD explicitly includes P55316 experimental evidence. This is valid descendant grounding, not circularity; phylogenetic grounding and the biological action judgment remain separate.
The official GO:0001222 definition supports corepressor-binding specificity without transferring the partner's own activity. Official is_a paths support the broader-term judgments: GO:1990837 → GO:0043565 → GO:0003677; GO:0000981 → GO:0003700; GO:0006357 → GO:0006355; and GO:0000122 → GO:0045892. These are ontology relations, not an assertion that every source used the same assay.
The unresolved source tasks are recovery of the precise historical TAS assay passages and exact comparison of older full-length constructs to current P55316. They are distinct from the biological questions about partner recruitment, dosage and neural cell state. The genuine 19-row seed mapping and normal-cache availability have been verified. Ordinary authored-review validation and strict GOA matching passed; no provider-generated report is claimed.
All 12 planned source files are present. Existing PMID:28473536, PMID:7957066 and Reactome:R-HSA-9618021 bytes were preserved. The publication caches contain full text for PMID:24356439 and PMID:28473536; the other six publication caches are abstract-only. Separately inspected original passages remain documented above. Cache flags do not upgrade any source-specific correctness assessment.
The normal PANTHER fetch reports 66 resolved nodes and preserves nine annotation rows. Three rows at PTN000216104 exactly match the incoming FOXG1 IBD assertions. Six additional rows at PTN000930906 remain in the normal slice; their placement is not inferred from the separately retained 65-node tree/MSA proof. Both source versions are retained without rewriting either.
The three original brain-development rows are refined to GO:0021537 telencephalon development. The typed path is part_of GO:0030900 forebrain development, then part_of GO:0007420 brain development. Human clinical Results and the Figure 1 caption in PMID:21280142 describe frontal cortical abnormalities and a thin corpus callosum. Combined with developmental context, these support the gene-level refinement while the older TAS assay-access limits remain explicit.
The five TOO_GENERAL rows represent four checked parent/child redundancies, with DNA binding present twice; all retain their source fields. The normal PAINT union also contains PTN000930906, which is absent from the retained 65-node topology. The fetcher collects ancestral references across family members, so presence in that union does not establish ancestry of the human target. GO:0000978 requires sequence-specific cis-regulatory DNA binding; atomic base-contact resolution is unnecessary, but regional occupancy alone does not establish sequence specificity. As the term is an is_a descendant of retained GO:1990837, no redundant NEW assertion is added. Target placement and any evidence-backed refinement remain explicit source follow-up questions.