This evidence map distinguishes a cached full-text flag from the original sections actually consulted. Selected original-source readings were shared among independent reviewers; their scope is stated per paper. No publication quotations or new annotations were added.
Original-source locator for the selected reading. Selected Methods and Results on GST forkhead-domain production, binding-site selection, footprinting and circular-permutation DNA bending; no figure-pixel inspection.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 9, 20, 46, 47, 50, 141.
Selected original author-uploaded Methods and Results identify human FREAC3 and assay bacterially expressed GST forkhead-domain constructs by site selection, footprinting and circular permutation. The DNA-bending evidence is genuine but fragment-bounded. Full-length localization was not assayed, and transcriptional activation was cited as work in preparation.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 92.
Selected original cloning, expression and Discussion sections identify the historical 5-3/L12143 sequence associated with current FOXC1. Activation was inferred and future assays were proposed, consistent with the inherited NAS evidence. Historical translated fragments are not silently treated as the current full-length protein or additional natural products. Relevance assessment: The historical cloning and expression study establishes target identity and expression context; transcriptional activation was inferred and left for future assays.
Mutations of the forkhead/winged-helix gene, FKHL7, in patients with Axenfeld-Rieger anomaly.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: 0.
The authentic original abstract supports human FKHL7/FOXC1 variation associated with anterior-segment disease. The full original was inaccessible in this consultation, so detailed developmental assays and clinical subgroup claims were not replayed. Relevance assessment: Human disease-associated variation supports developmental relevance, rather than directly establishing the molecular transcriptional mechanism.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: 1.
Original abstract and indexed first-page material describe mouse Mf1 expression in developing hearts and human congenital-heart associations. Full Methods were not recovered; retain developmental context without claiming a human autonomous assay. Relevance assessment: Expression in developing mouse heart and human disease association support developmental context, rather than directly testing the molecular transcriptional mechanism.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: auxiliary donor support.
The authentic abstract directly describes mouse Foxc1 renal/ureteric phenotypes and compound Foxc1/Foxc2 dosage effects. Q61850 is mouse Foxc2, but the same paper also studies Foxc1; this is not a wrong-paralog conclusion. Full experimental detail remains unverified.
Original-source locator for the selected reading. Selected original Methods and Results, as described below.
Normal cache full-text flag: true. Reference assessment: VERIFIED. Original raw contexts: 18, 22, 125.
Selected original Methods and Results assay human WT and patient-variant FOXC1 constructs in COS-7 localization and cell-extract DNA-binding experiments, with a six-site HeLa reporter. These establish WT capability without assigning mutant behavior to every natural product.
DSCAM, a highly conserved gene in mammals, expressed in differentiating mouse brain.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: 2.
The authentic identifier resolves to a DSCAM mouse-brain paper. The full text was inaccessible, so the existing FOXC1 experimental activation assertion remains unresolved. The abstract alone does not establish a wrong-gene attribution or an identifier replacement. Relevance assessment: Provisional to the inspected content: the authentic DSCAM abstract supplies no checkable FOXC1 functional result. The inaccessible full text and original FOXC1 annotation remain unresolved; this is not a finding of irrelevance, misattribution or a wrong identifier.
Original-source locator for the selected reading. Original PMC indexed full text, Results113–114 and Fig1G-H caption, Methods249–260 and selected Discussion. No image pixels or supplement inspected.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 126.
Selected original Results and Methods directly describe nuclear Foxc1 immunostaining in cultured human aortic smooth-muscle cells. Mouse compound-mutant cardiovascular and somite experiments are separate. Antibody-generation controls cited to another paper were not independently replayed.
Original-source locator for the selected reading. Plasmids, Cell Culture, Indirect Immunofluorescence, Transactivation Assays; Nuclear-localization Results; Transcription Activation by FOXC1 Is Mediated by N- and C-terminal Activation Domains
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 23, 65, 127.
Selected original human FOXC1 deletion and WT reporter experiments identify activation regions flanking the forkhead domain, a phosphorylated inhibitory region, and nuclear-localization determinants. HeLa and COS-7 assays do not establish every endogenous promoter or physiological product.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: 93.
The authentic abstract reports TGF-beta1-responsive FOXC1 expression and growth inhibition after re-expression in HeLa cells. Exact full Methods remain unavailable; this supports contextual growth regulation without making it a universal core function.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: 88.
The authentic abstract and limited original previews report a human F112S family with anterior-segment and dental phenotypes. The detailed clinical table was not inspected; a clinical association is distinct from a direct molecular tooth-development assay. Relevance assessment: A human clinical pedigree supports FOXC1 disease and developmental associations but does not directly establish a molecular tooth-development mechanism.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: 24, 45, 66, 128.
The authentic abstract describes patient variants and localization, binding and transactivation defects, but does not mention a DNA-bending experiment. Later citation text is only corroboration. The exact bending Methods and Results remain unrecovered, so that source-specific bending row is UNDECIDED.
Original-source locator for the selected reading. Author-uploaded original journal text, Michael Walter attribution; Methods plasmids/culture/IF/EMSA/reporter and Results molecular analysis, with figure captions. No image pixels or supplement read.
Identification and analysis of a novel mutation in the FOXC1 forkhead domain.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 25, 26, 95, 129.
Selected original Methods and Results compare human WT, L86F and L86P constructs using COS-7 nuclear localization and extract-based binding with a repeated-site reporter. Extract-based EMSA does not measure purified-protein binding affinity.
Original-source locator for the selected reading. Original journal text uploaded by coauthor Robert Ritch; Methods plasmids/culture/IF/EMSA/reporter, Results molecular analysis and transactivation, selected captions. No image pixels or supplement read.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 27, 49, 91, 130.
Selected original Methods and Results compare human G165R, R169P and M161K with WT. Nuclear localization, DNA binding and transactivation can separate; no universal loss of all functions is inferred from a patient substitution.
Original-source locator for the selected reading. Exact genuine normal full-text cache, lines 67–250: Methods constructs/cells/IF/EMSA/reporter, Results and selected Discussion; figure captions only, not image pixels or supplementary files.
Essential structural and functional determinants within the forkhead domain of FOXC1.
Normal cache full-text flag: true. Reference assessment: VERIFIED. Original raw contexts: 28, 67, 131.
Selected genuine full-text Methods and Results use COS-7 immunofluorescence and extract EMSA plus HeLa reporters to examine engineered forkhead-domain substitutions. The structural template is FOXC2; the model is not a measured FOXC1 structure or proof of native chromatin occupancy.
FOXC1 transcriptional regulatory activity is impaired by PBX1 in a filamin A-mediated manner.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 19, 29, 36, 37, 38, 39, 52, 68, 123, 132.
Selected original assays include human ocular-cell extract capture, HeLa co-immunoprecipitation, mouse C2C12 endogenous association, and FLNA-deficient/reconstituted M2/A7 localization. PBX1a inhibits FOXC1 output in that setting. NFIA is supported at an extract/probe array scope, not as an isolated direct contact. Conditional HP1alpha overlap does not establish constitutive heterochromatin residence.
Original-source locator for the selected reading. Selected original Results and Methods text from author-uploaded paper via web extraction; direct GET returned403 and publisher showed abstract. No full-paper or figure-pixel read claim.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 30, 40, 51, 96, 133.
Selected original assays support FOXC1 association with tested PITX2A, COS-7 nuclear colocalization and reporter modulation. PITX2A represses FOXC1 more strongly than the reverse tested relationship. Extract-assisted binding and tested partner-product scope are retained; this is not a claim about every PITX2 or FOXC1 product.
Original-source locator for the selected reading. Original JBC text exposed in ResearchGate full-text extraction: Methods175–460 and Results555–812 with selected captions. Uploader identity was not independently established. No figure pixels or supplementary files.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 97, 108.
Selected original JBC Methods and Results use human FOXC1 constructs in HeLa cells: EGF signaling changes protein stability and reporter output, with S272A and pathway-inhibitor comparisons.
Original-source locator for the selected reading. Original publisher Methods and Results, including construct, IF, EMSA and reporter sections and captions. No figure pixels or supplement read.
Analyses of a novel L130F missense mutation in FOXC1.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 5, 31, 98, 134.
Selected original Methods and Results compare WT and human L130F using COS-7 localization and extract EMSA plus HeLa reporter assays. The assays support WT nuclear transcription-factor function, with variant-specific limitations.
Original-source locator for the selected reading. Selected original Results/Methods text from author-uploaded original via web extraction. PubMed identity verified. No complete-paper or figure-pixel read claim.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 17, 99.
Selected original experiments combine an engineered inducible FOXC1 fusion for target discovery with endogenous human ocular-cell FOXO1-promoter occupancy, promoter-deletion reporters and FOXC1 knockdown. Zebrafish morpholino outcomes are separate. FOXO1 is a transcriptional target, not an inferred protein-binding partner.
Normal cache full-text flag: true. Reference assessment: VERIFIED. Original raw contexts: auxiliary donor support.
Selected original Methods and Results support mouse endothelial Foxc1 expression/perturbation, Cxcr4 reporter output and CXCL12-dependent migration. The reported promoter ChIP is for Foxc2 only. No direct Foxc1 occupancy claim is transferred from that ChIP.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: 41.
The authentic abstract explicitly identifies human C1QBP/p32 as a FOXC1 partner and reports confirmation assays and transcriptional modulation. Full Methods and construct details were not independently recovered; retain the contextual association without a guessed receptor or catalytic subtype.
Severe molecular defects of a novel FOXC1 W152G mutation result in aniridia.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: 6, 32, 100, 135.
The authentic abstract reports the human W152G variant and molecular defects. Exact cell hosts and controls were not recovered. Independent original WT studies support the shared transcription-factor function, without claiming replay of this particular assay.
Normal cache full-text flag: true. Reference assessment: VERIFIED. Original raw contexts: auxiliary donor support.
Selected original Methods and Results combine human regional-variation evidence with mouse mesenchymal Foxc1 loss and cerebellar consequences. The developmental contribution is non-cell-autonomous from surrounding mesenchyme, not evidence that Foxc1 acts intrinsically in cerebellar neurons.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: 33, 101, 136.
Only authentic bibliographic identification of the P297S letter was recovered; there is no abstract and the full original was inaccessible. Its three experimental contexts remain UNDECIDED.
Original-source locator for the selected reading. Original publisher indexed Methods, Results and captions; direct page access failed403. The follow-up indexed query explicitly confirms the 4T1 mouse model. No supplement or figure pixels inspected.
FOXC1 is a potential prognostic biomarker with functional significance in basal-like breast cancer.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 70, 77, 137.
Selected original Methods and Results include human MDA-MB-231 overexpression, separate mouse 4T1 knockdown and human nuclear immunohistochemistry. These contexts do not establish a universal cancer phenotype or all-product behavior. No supplementary data or image pixels were inspected.
Normal cache full-text flag: true. Reference assessment: VERIFIED. Original raw contexts: auxiliary donor support.
Selected original Results and Discussion show that mouse corneal neural-crest stromal Foxc1 loss promotes blood and lymphatic growth; endothelial deletion alone does not reproduce it. SU5416 reduces the blood-vessel genotype difference, with no significant corresponding lymphatic rescue. The experiments concern the cornea, whereas GO:0036438 explicitly concerns lens transparency; those transfers remain UNDECIDED.
Global landscape of HIV-human protein complexes.
Normal cache full-text flag: false. Reference assessment: VERIFIED. Original raw contexts: 42.
Original Methods describe HIV-human affinity-purification mass spectrometry and MiST filtering. Three exact positive IntAct records establish the FOXC1/tagged HIV retropepsin-fragment pair; one curated pulldown record points to Figure S11a. The supplementary figure was not read. These data do not establish direct contact, native cleavage or protease inhibition. Relevance assessment: The broad interactome and exact positive curated pair records corroborate a peripheral FOXC1 association, without establishing its core transcriptional mechanism.
Normal cache full-text flag: true. Reference assessment: VERIFIED. Original raw contexts: 71, 74, 78.
Selected genuine full-text Results and Methods show context-dependent proliferation, partial epithelial-mesenchymal changes and migration in the described cancer cell lines. Knockdown causes G1 arrest without increased apoptosis. Snail, Twist and TGF-beta lie upstream in the tested comparisons; direct FOXC1 occupancy at MMP or VEGF promoters was not shown.
Foxc1 is a critical regulator of haematopoietic stem/progenitor cell niche formation.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: auxiliary donor support.
The authentic abstract describes Foxc1-dependent mesenchymal hematopoietic niche formation, CAR-cell identity and support of stem/progenitor abundance. A niche cell can regulate differentiation in another cell; the unresolved issue is the exact positive-differentiation endpoint and assay.
Proteomic analyses reveal distinct chromatin-associated and soluble transcription factor complexes.
Normal cache full-text flag: true. Reference assessment: UNVERIFIED. Original raw contexts: 43.
Selected original Methods describe tagged transcription-factor purification from soluble and chromatin fractions in HEK293T cells and a modified SAINT filter. The exact high-confidence FOXC1-PBX1 row could not be recovered; attempted workbook downloads were HTML challenges. Other-factor validation does not verify this pair, and the distinct 2005 PBX1 study cannot replay this source. Relevance assessment: The original methods inform the interaction-screen context, but the exact FOXC1–PBX1 table entry remains unrecovered; this is supporting methodological context rather than independently verified target-pair evidence.
Original-source locator for the selected reading. Selected original Methods and Results, as described below.
Normal cache full-text flag: true. Reference assessment: VERIFIED. Original raw contexts: 7, 34, 102, 138.
Selected original Methods and Results use human FOXC1 WT and variant constructs in HEK293T localization, extract EMSA and CXCR4-promoter reporter assays. The WT activation/binding evidence is distinct from the clinical severity of individual variants.
The transcription factor Foxc1 is necessary for Ihh-Gli2-regulated endochondral ossification.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: auxiliary donor support.
The authentic abstract supports mouse Foxc1 involvement in Ihh-Gli2-dependent endochondral ossification. The downloaded purported original PDF was a challenge response. Exact core-promoter binding Methods were not recovered, and the separate human GLI2 paper cannot supply that assay.
Original-source locator for the selected reading. Selected original Methods and Results, as described below.
FOXC1 Activates Smoothened-Independent Hedgehog Signaling in Basal-like Breast Cancer.
Normal cache full-text flag: true. Reference assessment: VERIFIED. Original raw contexts: 44, 89, 139.
Selected original Results and Methods include reciprocal purified His-FOXC1/GST-GLI2 pulldowns and endogenous BT549 co-immunoprecipitation, with GLI2 occupancy and signaling readouts. The proposed allosteric-opening model is an inference, not an experimentally resolved structure. GLI2 DNA binding is not automatically FOXC1 occupancy of the same motifs.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: 8, 35, 103, 140.
The authentic abstract compares four human patient variants using prediction, modeling and functional assays. Full Methods were not recovered; do not transfer uninspected host, control or product details.
Forkhead Box C1 Regulates Human Primary Keratinocyte Terminal Differentiation.
Normal cache full-text flag: true. Reference assessment: VERIFIED. Original raw contexts: 90, 104.
Selected original human primary-keratinocyte experiments support late FLG, IVL and LOR expression and terminal differentiation after FOXC1 perturbation. Early keratins and cell-cycle readouts were unaffected. The ChIP assays concern KLF4/ZNF750 at the FOXC1 promoter, not FOXC1 occupancy at GRHL3.
Foxc1 and Foxc2 are necessary to maintain glomerular podocytes.
Normal cache full-text flag: false. Reference assessment: UNVERIFIED. Original raw contexts: auxiliary donor support.
The authentic abstract and limited previews support dose-dependent mouse Foxc1/Foxc2 podocyte integrity. The precise negative RNA-polymerase-II regulation assay was not recovered. Inhibition of FOXC1 by its partners does not supply the missing direction.
The reviewed UniProt Q12948 sequence is 553 amino acids long and has no enumerated alternative natural products. Patient substitutions, engineered deletions, inducible fusions and bacterial forkhead-domain constructs are not natural product records. The nuclear annotation extension preserves the tested PITX2 partner context without inventing a FOXC1 isoform.
The official PAINT family tree and MSA contain 1,182 nodes. The target sequence matches human Q12948 exactly. Each of the six incoming IBA contexts has a positive IBD origin on its actual target path. The family cache preserves eight original records, including two off-path fungal negated IRD records. QuickGO contexts 12 and 69 retain an additional RGD:621723 donor and different dates from the inspected IBD snapshot; the discrepancy is recorded without claiming a cause or altering either source.
Current Human Protein Atlas text corroborates nucleoplasm localization with antibody HPA040670: A-431 and U2OS show nucleoplasm, and U-251MG lists nucleoplasm and cytosol. Image pixels, antibody specificity and the historical GOA version were not replayed. The existing nucleoplasm row remains non-core; no cytosol row was added.
Official ontology paths establish GO:0001228 is_a GO:0000981 is_a GO:0003700 and GO:0000978 is_a GO:0000977 is_a GO:0000976. DNA bending remains a distinct assertion. GO:0010628 is not an ancestor of GO:0045944 in the inspected hierarchy, so that pair is not treated as a formal redundancy. GO:0036438 refers to lens transparency and cannot be equated with corneal transparency.
For PMID:11782474, the original author-uploaded Results/Figure 5E and Discussion were inspected for the inhibitory mechanism. The paper tests residues 215–366 coupled to GAL4 DNA-binding and activation domains: the segment attenuates activation-domain-driven output but did not lower the constitutive SV40 baseline with the GAL4 DNA-binding domain alone. The conclusion is modular attenuation, not a demonstrated independent full-length DNA-binding repressor mode. The original URL and section locators are in the source guide; the normal cache remains abstract-only and unchanged.
For PMID:15684392, the original TF–TF array Methods, Results and Figures 5/7 captions identify the NFIA-associated signal and explicitly separate the PBX1 co-immunoprecipitation/inhibition follow-up. The specific binding replacement uses NFIA's established transcription-factor class while preserving the extract/probe-complex limitation and absence of an NFIA inhibitory effect in the reported assay.
For PMID:22171010, the previously read corneal Results/Discussion and the official lens-specific GO definition now support structured probable source-defect queries. The original donor is UniProt-assigned, not MGI-assigned. No supplementary experiments, replacement term or upstream reporting action is newly claimed.
The selected original PMID:26565916 Results/Methods support both FOXC1–GLI2 association and a GLI2-dependent increase in DNA-binding and transcriptional readouts in human cancer models. This supports the second core and the ACCEPT decision for positive regulation of DNA binding. The structural-opening explanation remains inferred. The distinct PMID:15684392 PBX1a source supports the narrower Pol-II DNA-binding-transcription-factor binding class, with nuclear-extract association and tested-product limitations retained.