Genuine repository acquisition preserved all 79 original QuickGO objects and exported 79 TSV records. The native seed contains 74 rows. The authored review contains 77 contexts: the three pairs with distinct nuclear scope are represented separately, while two provenance-only duplicate pairs retain both originals in the source evidence. The reviewed 77-context representation has now been applied to the genuine seed.
Original fields, donors, qualifiers and extension groupings are preserved. Raw pairs 9/10, 11/12 and 16/17 have separate review rows; pairs 49/50 and 70/71 retain both original records in the archive. The evidence gives explicit zero-based original, native-seed and review indices, plus both zero-based TSV data indices and one-based physical TSV line numbers. Review ordering follows the genuine seed, with scope-specific rows adjacent.
The existing provider credential hold remains in force. Manual original-source reading is documented here; no provider result or retry is claimed. No quotation text or NEW annotation is proposed.
Human promoter repression and binding, SMRT recruitment and FOXP-family association support the transcriptional mechanism. Context-dependent human FBXL7 activation and FOXP1-ES stem-cell biology are retained. Host species, protein construct and natural product are treated separately. The official seven products are Q9H334-1,-3,-4,-5,-6,-7,-8; sequence verification does not establish equal function.
The dated PTHR45796 target proof uses the actual human AN14/PTN002483645 leaf and four literal incoming IBD joins. The off-target chimp alignment/FASTA discrepancy and extra macaque FASTA record are preserved; neither changes the exact human sequence join. Original human self-donor evidence is valid descendant support.
Selected original Methods/Results read: human 677-aa MFH/FOXP1 represses c-fms reporters; a human 431–559 GST fragment and cis-site mutations establish sequence-dependent DNA recognition. Human HL60 differentiation assays are distinct from the mouse Mac-1 upstream experiments.
Access: Selected original.
Assay scope: Human full-length reporter and fragment EMSA; human myeloid differentiation; mouse upstream model.
Sources: pubmed; original full text; doi.
The later recovered original supersedes the earlier access limitation. Selected original Methods were read, combining human FOXP1 with mouse SMRT, plus human THP1 knockdown and promoter recruitment. This supports corepressor binding and transcriptional regulation. The mouse-heart co-IP stage differs between a figure description and Methods; no universal complex stoichiometry or cardiac-growth mechanism is inferred.
Access: Selected original.
Assay scope: Mouse SMRT/human FOXP1 in HEK293 interaction assays; human THP1; separate mouse developmental assays.
Sources: pubmed; original full text; doi; accessed original.
Official identity and authentic abstract verified. The abstract reports FOXP1–androgen-receptor interaction and ligand-dependent repression in prostate cancer cells. Full original Methods remain inaccessible in this packet. Partner class is independently verified; historical FOXP1D nomenclature is not mapped to a current natural product.
Access: Authentic abstract only.
Assay scope: Exact full construct sequence and interaction-assay implementation unresolved.
Sources: pubmed; doi.
The recovered selected original establishes a human FLAG-FOXP1 CD68 transgene in a mouse host, macrophage phenotypes and c-Fms rescue. Cytokine endpoints are assessed separately: Table3 TNF-alpha p=.057 is not a significant result, whereas the separate Fig6D rescue supports that phenotype. In vivo IL1beta and MCP1 results are not substituted for significant in vitro outcomes. Table3 MCP1 is CCL2, not CXCL2; the specific CXCL2 claim remains unverified because supplements were not inspected.
Access: Selected original.
Assay scope: Human protein in transgenic mouse macrophages; no direct human infection experiment.
Sources: pubmed; original full text; doi; accessed original.
Selected original Methods/Results explicitly recover FOXP1 with FOXP2 by nuclear colocalization and co-IP/immunoblot or mass spectrometry in SH-SY5Y cells. The FOXP2-focused title does not make this an incorrect FOXP1 citation. Cellular association is distinguished from purified binary binding.
Access: Selected original.
Assay scope: Human/chimp FOXP2 constructs and endogenous FOXP1 association in human cells.
Sources: pubmed; original full text; doi.
Selected original human FOXP1a WT/R525X reporter experiments directly test SV40 repression in HEK293 cells. The indicated CTBP1-interacting region comes from prior work rather than a new complex experiment in this source. Human developmental findings and the artificial disease construct are not descriptions of all natural products.
Access: Selected original.
Assay scope: Human 677-aa FOXP1a and R525X; reporter and clinical evidence.
Sources: pubmed; original full text; doi.
Selected original human HUVEC and vascular smooth-muscle perturbations measure migration, tube formation and proliferation. SEMA5B expression changes are not alone a direct DNA-binding or rescue demonstration. NM_032682.4 and the reported protein-size wording do not justify a natural-product assignment.
Access: Selected original.
Assay scope: Human vascular cells; transfection/knockdown and cellular endpoints.
Sources: pubmed; original full text; doi.
Selected original Results/captions and two exact IntAct records support FOXP1–FOXP2 BRET in both directions with nuclear-localized controls. The complete original protocol was not independently read. CTBP1 experiments directed at FOXP2 are not assigned to FOXP1.
Access: Selected original plus exact IntAct records independently replayed.
Assay scope: Tagged live-cell proximity, not measured isolated affinity.
Sources: pubmed; original full text; doi; accessed original.
The recovered author-hosted original identifies a sequenced human BC152752 677-aa FOXP1 ORF and tests association with FOXP2/FOXP4, nuclear localization and combined-expression responses. Tag orientation differs between some caption wording and Methods; those details are retained in the access ledger. Cotransfection does not establish a pure native heterodimer mechanism.
Access: Selected original.
Assay scope: Human FOXP1 construct in HEK293; co-IP, localization and target-expression comparisons.
Sources: pubmed; doi; accessed original.
Selected original human B-cell experiments show FOXP1-dependent survival and reduced caspase activity in the CD40L/IKK2 context, without additional proliferation. Expression/ChIP-seq support repression of pro-apoptotic genes; direct repression can persist without the survival benefit. These contextual effects are not a universal anti-apoptotic activity.
Access: Selected original.
Assay scope: Human B cells; stimulus-dependent survival and transcriptional regulation.
Sources: pubmed; original full text; doi.
The official original Table S6 HCIP workbook was recovered from BioStudies and its exact FOXP1/FOXP2/FOXP4 rows were read. FOXP1 bait recovers FOXP2 and FOXP4 in chromatin and soluble fractions, with reciprocal recovery; chromatin supports nuclear association. Soluble fractions do not distinguish nuclear and cytosolic pools. Self rows marked Bait are not independent homomerization evidence. The table establishes cellular complex recovery, not isolated binary affinity or current isoform identity. This supersedes the earlier supplement-access gap without changing the original GOA citations or partners.
Access: Original Table S6 HCIP selected rows independently read; selected fractionation/TAP-MS Methods and Discussion read by the coordinating reviewer.
Assay scope: Fraction-specific FOXP1–FOXP2/FOXP4 complex recovery; self-bait detection and soluble-pool limits retained.
Sources: pubmed; original full text; doi; accessed original table s6.
Recovered original selected Methods and Results establish tagged mutant transfection/BRET/localization experiments. Patient lymphoblast RNA undergoes nonsense-mediated decay and mutant RNA is recovered with emetine; the transfection results therefore do not establish abundant mutant protein in the patient. No disease construct is promoted to a natural isoform.
Access: Selected original.
Assay scope: Human WT and artificial V423Hfs*37 constructs; separate patient RNA evidence.
Sources: pubmed; original full text; doi; accessed original.
Recovered institutional original selected functional Results/Methods establish WT FOXP1 repression and nuclear localization, altered activities among patient variants, and WT self/FOXP2 BRET. Variants have distinct mechanisms. Tagged proximity and reporter endpoints are not a native stoichiometry measurement or a survey of all seven products.
Access: Selected original.
Assay scope: Human FOXP1 WT and artificial variants; SV40 reporter, BRET and localization.
Sources: pubmed; doi; accessed original.
Selected original Results/Fig7 show context-dependent FBXL7 activation, regional promoter occupancy and deletion-reporter responses. These do not independently prove a core-promoter-specific DNA-contact boundary. AURKA co-IP/GST capture supports the protein-kinase-binding refinement, while the FBXL7 reporter supports positive regulation of Pol II transcription. Neither assigns kinase activity or a predicted interface to FOXP1.
Access: Selected original.
Assay scope: Cellular transcriptional activation and AURKA association; context-specific direction.
Sources: pubmed; original full text; doi.
The original general Methods and authentic S1/S2 workbook were inspected. S1 construct E285 is a 289-aa FOXP1 DNA-binding fragment matching canonical residues 288–576 and shared by multiple products. Five HT and five MethylHT S2 records yield a common motif. No FOXP1 S3 row was found, so the representative flags are not a final methyl-sensitivity class or quantitative affinity conclusion.
Access: Original Methods and exact original workbook.
Assay scope: Bacterial fragment and sequence-specific in vitro assay; not a unique natural product.
Sources: pubmed; original full text; doi.
The recovered indexed author article and selected supplement supersede abstract-only access. Human FOXP1 siRNA reduces anti-IgM calcium/AKT/ERK signaling without changing surface IgM; CD22 surface abundance increases at 72h and inversely correlates with FOXP1 in CLL. The promoter-binding claim cites earlier work rather than a new assay. DDR-linked regulation is not DNA-repair catalysis, and the observed protein bands are not unique product assignments.
Access: Selected original article and selected supplement.
Assay scope: Human WSU-NHL/primary CLL; signaling, surface CD22 and expression endpoints.
Sources: pubmed; doi; accessed original.
Selected original Methods directly test FOXP1 and WT/variant TBR1 proximity by BRET in HEK293 with controls. Official partner metadata supports the Pol II transcription-factor binding class. These are tagged-cell assays rather than isolated affinity or a demonstrated native developmental heterocomplex.
Access: Selected original.
Assay scope: FOXP1 NM_032682 and TBR1 constructs; human cell host.
Sources: pubmed; original full text; doi.
Three exact 42-field IntAct records recover the FOXP1–FOXP2 pair from this source in tagged affinity-purification assays, including HEK293T and HCT116 conditions. The original dataset projection is positive source-specific evidence; this consultation does not claim a complete paper/supplement reread or direct binary contact.
Access: Exact original curated interaction records independently replayed.
Assay scope: AP association with spoke expansion; cell-line-specific records retained.
Sources: pubmed; original full text; doi.
Selected original author-paper pages establish the human H9/CA1 exon18b switch, forkhead-fragment PBM/EMSA and isoform RNAi. LIF-free maintenance, teratoma and reprogramming experiments are mouse CGR8/MEF assays. FOXP1-ES can repress many targets while supporting selected pluripotency genes; anti-FOXP1 ChIP is not intrinsically isoform-specific.
Access: Selected original.
Assay scope: Human splice/biochemical experiments and separate mouse pluripotency endpoints.
Sources: pubmed; doi; accessed original.
Original mouse conditional-deletion, adoptive-transfer and Foxp1A/D experiments show restraint of Tfh differentiation and IL21 production. The current mouse positive-IL21 annotation conflicts with the measured direction. Human ISS is preserved while a review proposes the negative direction. Mouse A/D construct names are not mapped to human isoforms.
Access: Selected original; independently read Results320–371/Methods405–445.
Assay scope: Mouse T-cell perturbation and regional Il21 occupancy; no direct human T-cell assay.
Sources: pubmed; original full text; doi.
Official identity and abstract explicitly report rat Foxp1 expression in striatal development despite the Foxp2-focused title. Original Methods/Results were not recovered. Expression alone does not establish participation in striatal development; independent mouse perturbation evidence is now documented under PMID:25266127.
Access: Authentic abstract only; original access failed.
Assay scope: Rat donor IEP; original-source functional participation remains unresolved, independently corroborated by the mouse developmental study.
Sources: pubmed; doi.
Official abstract describes Foxp1/Foxp2/Foxp4 expression patterns in the developing rat forebrain. Original Methods/Results remain unavailable in this packet. This source alone does not establish functional participation; independent mouse forebrain perturbation evidence is now documented under PMID:29138280. No wrong-paralog inference is made from the title.
Access: Authentic abstract only; original access failed.
Assay scope: Rat donor IEP expression mapping.
Sources: pubmed; doi.
The newly acquired full original supersedes the earlier abstract-only access limit. Selected rat hormone-treatment, Western blot, qRT-PCR and co-IP Methods and Results were read. DHT increases Foxp1 mRNA/protein in striatum and decreases both in cerebellar vermis; cortical Foxp1 mRNA decreases while protein is unchanged. The AR co-IP detects Foxp2, not Foxp1; Foxp1 coexpression is a separate observation. These source-specific expression responses support the existing non-core response judgment without transferring a paralog interaction or asserting a human assay.
Access: Selected original Methods/Results/Discussion read from the genuinely acquired full-text cache; no figure pixels or supplements.
Assay scope: Androgen-treated neonatal rat brain; region-specific Foxp1 expression response, with Foxp2-specific AR co-IP kept separate.
Sources: pubmed; original full text; doi.
Selected original main Methods/Results/Fig7 show rat cardiomyocyte Foxp1 knockdown increases cell size and H2O2 survival; restoring Foxp1 opposes hypertrophy and chelerythrine protection. The H2O2 result points to unread Online VIII G. The exact overexpression sequence and H2O2 programmed-death readout remain unresolved.
Access: Selected indexed original main; actual supplement blocked.
Assay scope: Neonatal rat cells; growth versus proliferation distinguished.
Sources: pubmed; original full text; doi.
The original XML Methods/Results/captions were read. In primary rat cortical neurons, human recombinant TNF and XPO1 inhibitors alter FOXP1 immunofluorescence with several other proteins. Rat injury experiments also measure nuclear FOXP1. The intervention targets export, not FOXP1 itself; the specific contribution of FOXP1 to the protective response is unresolved.
Access: Selected original Methods/Results/Fig2–3 captions/Discussion.
Assay scope: Rat cells and animals; human TNF reagent is not a human FOXP1 construct.
Sources: pubmed; original full text; doi.
The immutable existing-main event record identifies FOXP1-ES in its title. The abbreviated summary is not a complete isoform-specific event audit. Independent human nuclear localization and the original stem-cell study support the shared location; the unrestricted GOA product is preserved.
Access: Read immutable existing-main cached event; no remote full event expansion.
Sources: event.
The immutable event summary describes NANOG promoter regulation without a detailed FOXP1 participant assertion. It is not evidence of a wrong citation. Independent human FOXP1 localization supports the same nucleoplasmic term; a complete event participant audit remains a source follow-up.
Access: Read immutable existing-main cached event; no remote full event expansion.
Sources: event.
The original main Methods, developmental Results and Figure 1–2 captions were read. Mouse Nestin-Cre Foxp1 deletion reduces the striatal region from early postnatal stages, with no detected E18 difference, and changes striatal transcription and neuronal morphology. This independently supports the existing striatum-development term. The broad neural-lineage deletion does not isolate a cell-autonomous striatal mechanism or demonstrate endogenous human developmental necessity. The original rat IEP source remains separately access-limited.
Access: Selected original main sections and captions; no image pixels or supplementary materials inspected.
Sources: PubMed; original full text; DOI.
Selected Results s1a/s1b/s1g/s1h/s1j and Methods s3a/s3c/s3g/s3l/s3m/s3n/s3r were read. Emx1-Cre Foxp1 deletion changes mouse neocortical size, lamination and neuronal positioning; WT FOXP1, unlike K636R, restores the experimental migration phenotype. The human neurosphere comparison uses mutant overexpression and is not endogenous human FOXP1 depletion. Some regional effects may be non-cell-autonomous, and the tagged constructs are not assigned to current natural products from nomenclature alone.
Access: Selected original main Methods, Results and captions; no image pixels or supplementary tables inspected.
Sources: PubMed; original full text; DOI.
Private source pins and exact paragraph/record ledgers remain separate from these public locators. The access descriptions distinguish selected original sections, curated interaction records and abstract-only material; they do not imply that every experiment or supplement was inspected.
Thirty-two normal sources are present: twenty-seven publication caches, two Reactome records and three PTHR45796 files. Seven existing main sources were reused byte-for-byte; twenty-five qualified absent sources were fetched through the unforced repository tooling, including two targeted developmental papers added during review follow-up. No provider was run. A cache full-text flag describes the cached payload, not which Methods, Results, tables or figures were read. Separately accessible originals support several papers whose normal caches contain only abstracts. PMID:25247470 became available as full text during genuine acquisition and its selected original sections were then read.
| Reference | Normal cache has full text | Actual reading scope |
|---|---|---|
| PMID:15286807 | yes | Selected original |
| PMID:18347093 | no | Selected original |
| PMID:18640093 | no | Authentic abstract only |
| PMID:18799727 | no | Selected original |
| PMID:19907493 | yes | Selected original |
| PMID:20950788 | yes | Selected original |
| PMID:24023716 | yes | Selected original |
| PMID:24893771 | yes | Selected original plus exact IntAct records independently replayed |
| PMID:25027557 | no | Selected original |
| PMID:25267198 | yes | Selected original |
| PMID:25609649 | yes | Original Table S6 HCIP selected rows independently read; selected fractionation/TAP-MS Methods and Discussion read by the coordinating reviewer. |
| PMID:25853299 | yes | Selected original |
| PMID:26647308 | no | Selected original |
| PMID:28218735 | no | Selected original |
| PMID:28473536 | yes | Original Methods and exact original workbook independently checked |
| PMID:30111844 | no | Selected original article and selected supplement |
| PMID:30250039 | yes | Selected original |
| PMID:33961781 | yes | Exact original curated interaction records independently replayed |
| PMID:21924763 | no | Selected original |
| PMID:24859450 | yes | Selected original; independent reading of Results320–371/Methods405–445 |
| PMID:12815709 | no | Authentic abstract only; original access failed |
| PMID:18561326 | no | Authentic abstract only; original access failed |
| PMID:25247470 | yes | Selected original Methods/Results/Discussion read from the genuinely acquired full-text cache; no figure pixels or supplements. |
| PMID:26333362 | yes | Selected indexed original main; actual supplement blocked |
| PMID:26842647 | yes | Selected original Methods/Results/Fig2–3 captions/Discussion |
| PMID:25266127 | yes | Selected developmental Methods/Results and Figure 1–2 captions |
| PMID:29138280 | yes | Selected forebrain, migration and construct Methods/Results/captions |
The genuine current family fetch contains 23 listed members and a 190-node PAINT slice with eight IBD rows. Its human entry is Q9H334, 677 aa. The separate dated tree/MSA proof establishes the human leaf and four incoming assertions; its off-target chimp and macaque discrepancies remain recorded. The normal family files are not rewritten to resemble that historical proof.