This guide separates native ETV6, experimental expression constructs, disease fusions and interaction partners. The source annotation objects and normal publication files are preserved. A full original can be recovered independently even when the normal cache contains only an abstract. No publication quotations were added.
Current GO:0000978 describes cis-regulatory sequence-specific DNA binding and is more specific than GO:0000977. GO:0001227 describes the demonstrated Pol II repressor activity. Contextual activation elsewhere is not excluded by retaining this principal activity. Synthetic-probe binding, promoter reporters and native chromatin occupancy remain distinct evidence types.
Both publisher PDF routes returned blocked HTML; the operative evidence comes from the actual author-uploaded text, not those failed files. The exact observed text and read ranges are archived privately. No normal publication cache was replaced.
| Source | Exact target evidence | Interpretation and limits |
|---|---|---|
| PMID:25416956(https://doi.org/10.1016/j.cell.2014.10.050) | Author HI-II-14 PSI: ETV6 ORF 11407 with Q96HA8-1 ORF 4786 (screen 2) and Q9BXS5-1 ORF 206 (screens 1/2), each with array, pooling and validated records. Actual main Results and Methods read. | Human ORFs tested in yeast. Study-wide orthogonal validation is not assigned to each pair. Archived ORFs are not assumed identical to every current product. |
| PMID:26871637(https://doi.org/10.1016/j.cell.2016.01.029) | Actual main alternative-ORF/Y2H Methods and Results read. Official IntAct IM-25013-5015, IM-25013-593 and IM-25013-2701 pair P41212 with A0A0S2Z4M1 and cite Table S2B. | Positive human AXIN1 alternate-product association in yeast. Original workbook access failed; its exact sequence cells were not read. Current A0A0S2Z4M1 is an AXIN1 fragment record, retained literally; no Wnt-role inference. |
| PMID:32296183(https://doi.org/10.1038/s41586-020-2188-x) | Author HuRI PSI: ETV6 11407–PIN1 4406, screen 1, array/pooling/validated records. Main assay/retesting Results and Extended Data 1 caption read. | Binary association, without PIN1 catalysis, native stoichiometry or all-product identity claims. |
| PMID:32911434(https://doi.org/10.1016/j.redox.2020.101686) | Actual main Methods/Results and publisher workbook: Table S1 row 20 is ETV6 Y2H-positive; Table S2 rows 111/164 specify mCherry/FL-V5 ETV6 constructs. | Main Results report a KEAP1-context difference in cellular DULIP association. This is not a purified affinity measurement or evidence for every partner-specific assay or an ETV6 antioxidant function. |
| PMID:33961781(https://doi.org/10.1016/j.cell.2021.04.011) | Actual BioPlex 3.0 293T table has PIN1 bait and ETV6 prey; main clone/cell/AP-MS and gene-aggregation Methods read. | Cellular complex association. No purified binary claim; the missing edge in the captured HCT116 table is not universal negative evidence. |
| PMID:40205054(https://doi.org/10.1038/s41586-025-08878-3) | Exact U2OS AP-MS network edge ETV6–PIN1; actual human ORFeome/HA-Flag purification Methods read. | Both nodes' bait flags do not prove reciprocal pull-downs. The study's imaging, SEC-MS and predicted structures are not automatically evidence for this pair. |
Supported generic interactions remain non-core under the explicit campaign curation instructions. They are not removed because a more informative mechanism has yet to be demonstrated. No new figure-pixel inspection was performed for these screens.
PMID:25581430(https://doi.org/10.1038/ng.3177) — Actual main Methods, Results and Figure 5 caption were read. Full-length human NM_001987.4 constructs in cord-blood CD34-positive HSPCs are distinct from recombinant ETS residues 335–430 used in DNA-binding assays. Mutant-expressing expansion cultures have fewer viable cells than wild-type/empty-vector controls, without reported increased apoptosis. This supports a contextual hematopoietic proliferative role, retained non-core. Mixed HSPCs and viable-cell counts do not separately establish long-term HSC self-renewal or a direct cell-cycle catalytic activity. No figure pixels were inspected.
The unchanged seed's displayed UniProt product and the independently catalogued RefSeq transcripts remain separate. Alternative initiation at M43 is supported experimentally, but no invented UniProt isoform identifier or all-function equivalence is introduced. Recovered originals inform reviewer access fields while the fetched source bytes remain unchanged. Only PMID:7761424 has an unresolved full-main-text access gap in this direct lane; PMID:26871637 has an explicitly unresolved supplementary-workbook gap despite accessible main text and exact IntAct target records.
PANTHER PTHR11849 v19 places human leaf PTN002483834 below PTN000218930. The ungapped human MSA is exactly the official 452-residue sequence. Four positive IBD records (transcription-factor activity, nucleus, PolII regulation and differentiation) lie on that path, with no target-path NOT record. Human P41212 appearing in WITH/FROM is valid descendant experimental support. Current mouse P97360 GOA connects the cis-regulatory binding/activation transfers to PMID:17606295 and broad DNA binding to PMID:12527908; the raw mouse Fli1 input extension is retained.
Current ARBA00028973 disjunct 24 (zero-based) matches FunFam 1.10.150.50:FF:000030 and Craniata; ARBA00029016 disjunct 41 matches that FunFam; ARBA00027429 disjunct 215 matches it plus 1.10.10.10:FF:000176. These are actual target cross-references, not guessed InterPro conditions. InterPro target matches include ETS IPR000418, pointed/SAM IPR003118 and family IPR046328. The pointed domain is not independently claimed to contact DNA. Author TFClass hierarchy places ETV6 at 3.5.2.6.1 within ETS 3.5.2; its chromatin assertion is classification-based inference, not a newly claimed ChIP result.
HPA ETV6 antibody HPA000264 recognizes canonical residues 90–210. XML reports nucleoli and cytosol in A-431, U-251MG and U2OS. A-431 and U2OS images were viewed qualitatively. The antibody does not identify a specific natural translation product or pathological fusion; western validation includes additional bands. This independently positive cellular signal does not validate a different source's fusion-to-native projection.
The ten Reactome records below are valid disease-fusion models. Their P41212 referenceEntity legitimately anchors an ETV6 segment. The source defects concern their exported native-protein GOA location assertions, not deletion of the events, fusion entities or ETV6 referenceEntity. Current stored fusion modifications and every participant route are retained in the reproducible private evidence record; no substitute fusion accession or corrected sequence is invented.
| Source event | Representative participant route | Complete P41212 fusion participants |
|---|---|---|
| R-HSA-9703430 | 9703430 → 9703378 → 9703372 → 9703353 → 9703305 | 9703313, 9703318, 9703302, 9703305, 9703308 |
| R-HSA-9703432 | 9703432 → 9703359 → 9703372 → 9703353 → 9703305 | 9703313, 9703318, 9703302, 9703305, 9703308 |
| R-HSA-9703433 | 9703433 → 9703345 → 9703315 | 9703315, 9697944, 9703302, 9703320, 9703307, 9703312 |
| R-HSA-9703434 | 9703434 → 9703358 → 9703356 → 9703378 → 9703372 → 9703353 → 9703305 | 9703313, 9703318, 9703302, 9703305, 9703308 |
| R-HSA-9703435 | 9703435 → 9703372 → 9703353 → 9703305 | 9703313, 9703318, 9703302, 9703305, 9703308 |
| R-HSA-9703437 | 9703437 → 9703409 → 9703354 → 9697944 | 9697944, 9703315, 9703312, 9703320, 9703307, 9703313, 9703318, 9703302, 9703305, 9703308 |
| R-HSA-9703438 | 9703438 → 9703426 → 9703372 → 9703353 → 9703305 | 9703313, 9703318, 9703302, 9703305, 9703308 |
| R-HSA-9703441 | 9703441 → 9703425 → 9703349 → 9703378 → 9703372 → 9703353 → 9703305 | 9703313, 9703318, 9703302, 9703305, 9703308 |
| R-HSA-9673760 | 9673760 → 9673677 → 9673893 | 9673893, 9673898 |
| R-HSA-9673761 | 9673761 → 9673678 → 9673914 → 9673893 | 9673893, 9673898, 9673912, 9673905 |
The table uses the same representative routes as the annotation rationales and source-defect explanations. For R-HSA-9703430, R-HSA-9703432, R-HSA-9703434, R-HSA-9703435, R-HSA-9703438 and R-HSA-9703441, the shared 9703372 container also has a valid alternate branch through 9703373 to 9703313. The representative branch instead passes through 9703353 to 9703305. Both terminals retain a P41212 segment and a foreign FLT3 insertion; neither is native ETV6. Choosing one reproducible route does not exclude the other participants listed in the final column. The ten queries describe one upstream projection issue class across ten exported source rows, not ten independent flaws in the disease-event models.
The protein-bearing participant routes are complete: 116 fully captured participant objects plus GDP 29420 and GTP 29438 as two inline terminal chemical leaves (118 reachable identifiers). The chemical leaves do not introduce another protein participant. Each of the 14 reachable P41212 sequence entities carries a foreign-protein insertion; no native P41212 participant was found. The event roots have no regulator branches. Earlier rate-limited child requests were retained, then independently recovered by paced retries before this conclusion.
Defining examples are 9703289 (FLT3/P36888 residues 570–993 inserted at 337), 9703285 (ETV6 residue 336 replaced by AGCS), 9673894 (PDGFRB/P09619 residues 527–1106 inserted at 155), and 9673897 (PDGFRA/P16234 residues 552–1089 inserted at 385). The API field referenceSequence supplies these insertion partners; it must not be replaced by an assumed secondReferenceSequence. Some FLT3 display ranges disagree with stored insertion ranges, including the display of 9703313. Both fields remain preserved; no corrected fusion sequence is asserted.
The official canonical sequence is 452 residues. Absence of a UniProt alternative-products comment does not exclude other natural products. The independently captured transcript/RefSeq models and the historical M1/M43 translation evidence are preserved separately; pathological ETV6 kinase fusions are not normal splice products. No identical function or localization is assigned to every model.
The annotation proposals add no publication quotations. PMID:12527908 remains full-text unavailable, while the separately recovered human originals and the complete PMC donor original have the precise read scopes above. Genuine normal publication records are preserved unchanged, including metadata that may differ from separately recovered access. The two donor publication additions were fetched normally without overwriting any of the 52 accepted normal sources.
The direct-original and database readers inspected different bounded portions of the shared human papers. Their full labelled assessments are retained in the reference reviews; one reader's additional text access is not represented as figure-pixel inspection by the other. No paper figure pixels were inspected in either lane. The HPA A-431 and U2OS images were inspected qualitatively by the database lane. PMID:7761424 and PMID:12527908 remain full-main-text unavailable; the PMID:26871637 workbook remains unavailable despite accessible main text and exact target records. The canonical 452-residue product, historical M43 initiation and the seven RefSeq models are not asserted functionally equivalent.
One nuclear ETS-site-dependent repressor activity is represented by GO:0001227, acting in GO:0000122 at the nucleus. Current official definitions and typed ancestry were checked. Cis-DNA recognition and corepressor association support this mechanism; they are not split into redundant core activities. No speculative complex membership is asserted.
Additional synthesis reading used the observed author-upload text of PMID:12588862(https://doi.org/10.1074/jbc.M300592200), Methods and Results/Figures 4–6, and PMID:12590135(https://doi.org/10.1074/jbc.M212935200), Methods and Results/Figures 6–7. The first includes native U2OS nuclear co-immunoprecipitation, human-protein domain mapping, GST/reticulocyte pull-downs and the additive human-TEL/L3MBTL1 effect on a rat promoter in mouse NIH3T3 cells. The second distinguishes transfected HDAC9/ΔCD variants from an endogenous C-terminal antibody that cannot identify MITR. Neither establishes ETV6 deacetylase activity or one permanent multicomponent complex. No figure pixels or supplements were inspected during this synthesis.
The family segregation, variant and HSPC sections of PMID:25581430(https://doi.org/10.1038/ng.3177), including Figures 1–5 captions and Methods, support familial thrombocytopenia with hematologic malignancy predisposition. They do not resolve the individual roles of every natural ETV6 product. The historical M1(M43A)/M43 reporter comparison and mouse S1A positive Fli1 context retain the species, promoter and construct limits described above. Questions and experiments address these boundaries without manufacturing new annotations.
The original publication and database reference assessments retain their access limits. This guide is cited as a local reference so that the Reactome participant routes and independent HPA observations are traceable from the annotation rationales. It does not turn the antibody signal into a product-resolved localization assay or establish a new core at the cytosol.