Oncofusion

start / graph / gene-exo1

Genemoderate confidence 3 of 5: One strong study, or several smaller consistent ones.Q32-brca1-hr-licensing

EXO1 (Q9UQ84, 846 aa) - the long-range resection nuclease at the bottom of the CTCF cascade, and the point where this graph's two independent 2026 HR papers meet: CtIP starts the resection, EXO1/DNA2 finish it

also called EXO1 · EXOI · HEX1 · Q9UQ84 · EXO1_HUMAN · Exonuclease 1 · Exonuclease I

EXO1 is one of two enzymes that chew back the ends of a broken chromosome far enough for accurate repair to happen. This graph already holds a menin-driven pathway that starts that chewing-back, and EXO1 is the enzyme that finishes it - so two separate stories in this graph turn out to be two halves of the same reaction.

The same thing, for a scientist

**Identity.** Q9UQ84, `EXO1_HUMAN`, **846 aa**, primary gene name EXO1, UniProt gene synonyms **EXOI and HEX1**, 25 PDB entries. The feature table types no classical domains but annotates an N-domain 1-99, an I-domain 138-229, and interaction regions for MSH3 (129-387), MLH1 (388-490 and 787-846) and MSH2 (600-846) [E1]. One reviewed record; `gene_primary` reads back EXO1. **Position in the cascade.** [E2] places EXO1 and DNA2 at the bottom: CTCF-dependent **early** BRCA1/BARD1 recruits SMARCAD1 and EXO1/DNA2, and their recruitment is 'causally linked to defective DNA end resection and dysfunctional HR' when the cascade fails. The paper is explicit about the two-step structure: *'the CTCF-directed HR pathway involves both CtIP-dependent short-range resection and the subsequent EXO1/DNA2-dependent long-range resection'*, and CTCF coordinates CtIP, early BRCA1/BARD1 and BRCA2 through parallel routes that are sequential in function - CtIP initiates, early BRCA1/BARD1 promotes SMARCAD1- and EXO1/DNA2-dependent extensive resection, BRCA2 loads RAD51. Double and triple co-depletion of CtIP, HP1-gamma, BRCA1 or BRCA2 did not worsen resection or HR beyond single depletion. **Why that sentence matters to this graph specifically.** This graph already holds a *separate* 2026 chromatin-primed HR cascade: **menin binds gammaH2A.X through Val371-Gln400, recruits SETD2, SETD2 writes H3K36me3, LEDGF reads it and recruits CtIP** to perform end resection [E3, and `exp-hr-competence-under-menin-inhibition-in-kmt2a-rearranged-blasts`, `mechanism-ledgf-dna-end-resection-and-homologous-recombination`]. **CtIP is the short-range step. EXO1/DNA2 is the long-range step.** The two papers - both *Nucleic Acids Research* 2026, DOIs 10.1093/nar/gkag790 and 10.1093/nar/gkag715 - describe two chromatin-licensing arms feeding consecutive stages of one nuclease reaction, and neither cites the other. That convergence is what `hyp-the-menin-arm-and-the-ctcf-arm-license-consecutive-steps-of-one-resection-reaction` is about. **Dependency: shallow, and shallower in blood.** Mean **-0.1273** over **1,258** screens, 4.3% below -0.5, 0.16% below -1.0; blood mean **-0.0783** with 2.7% below -0.5 [E4]. EXO1 and DNA2 are redundant for long-range resection by design, which is the obvious reason a single knockout costs little. **Literature at this graph's locus: empty, and the operands are large.** `EXO1[tiab] AND KMT2A[tiab]` = 0 and `EXO1[tiab] AND MLL[tiab]` = 0, both with non-empty querytranslations and warninglist 'No items found.'; the bare operands are `EXO1[tiab]` = **1,055** and `MLL[tiab]` = **6,328**. Two large sets with an empty intersection is itself a claim, so the operand check is recorded rather than hidden - and the rule-67 controls through the identical shape return ones (`CTCF[tiab] AND KMT2A[tiab]` = 7, `RAD21[tiab] AND KMT2A[tiab]` = 5) [E5]. **Archive: closed.** ENCODE has no EXO1 target record at all [E6].

What it looks like
Exonuclease 1846 aa
N-domainN-domain · residues 1–99I-domainI-domain · residues 138–229Interaction with MSH3Interaction with MSH3 · residues 129–387Interaction with MLH1 (N)Interaction with MLH1 (N) · residues 388–490Interaction with MSH2Interaction with MSH2 · residues 600–846InteInteraction with MLH1 (C) · residues 787–8460200400600800

No three-dimensional model is available for this protein, so the map above is the whole picture. That is itself informative: AlphaFold does not model chains this long, and the parts that have been crystallised are held under the entries for the individual domains.

Go deeper
The convergence: two 2026 papers, two chromatin arms, one nuclease reaction
the menin arm [E3]the CTCF arm [E2]
damage sensormenin binds gammaH2A.X via Val371-Gln400CTCF, zinc-finger region, PARylation-independent
writer / eraserSETD2 writes H3K36me3SUV39H1 and SETDB1 write H3K9me; KDM5A removes H3K4me
readerLEDGF/PSIP1HP1-gamma
effector recruitedCtIPearly BRCA1/BARD1, then SMARCAD1 and EXO1/DNA2
resection stepshort-range initiationlong-range extension
venueNucleic Acids Research 2026, 10.1093/nar/gkag790Nucleic Acids Research 2026, 10.1093/nar/gkag715

Both papers were published in the same journal in the same year, neither cites the other, and this graph already holds both of their downstream nodes - gene-rbbp8 for CtIP and mechanism-ledgf-dna-end-resection-and-homologous-recombination for the LEDGF arm. What it did not hold until now is the observation that the two arms are consecutive rather than alternative, which is stated inside 2 in one sentence: 'the CTCF-directed HR pathway involves both CtIP-dependent short-range resection and the subsequent EXO1/DNA2-dependent long-range resection'.

The consequence for this project is in hyp-the-menin-arm-and-the-ctcf-arm-license-consecutive-steps-of-one-resection-reaction, and it is not decorative: menin is the target of the drugs these children receive, and CTCF is the protein at the locus that breaks.

Why an EXO1 entry with almost no leukaemia literature is still worth having

EXO1 has 1,055 title/abstract records and zero paired with KMT2A or MLL. That is not obscurity; it is a specific, bounded hole. EXO1 recruitment is the readout that would score whether an H3K9-axis drug has removed a repair licence - it is the most distal, most interpretable endpoint in the cascade, downstream of every chromatin step and upstream of the HR reporter. An experiment that measures BRCA1 foci is measuring a protein with three known recruitment routes; an experiment that measures EXO1 recruitment is measuring whether resection actually happened.

So this entry exists to name the assay, not to report a finding.

Facts and figures
uniprotQ9UQ84
uniprot entry nameEXO1_HUMAN
gene symbolEXO1
gene primary readbackEXO1
protein nameExonuclease 1
length AA846
n PDB entries25
how the accession was resolvedgene_exact:EXO1 AND organism_id:9606 AND reviewed:true, fetched live 2026-09-22, returned EXACTLY ONE reviewed human record with gene_primary EXO1; length asserted at 846 aa.
localizationNucleus [ECO:0000269 x3, PubMed:11429708, 14676842, 17426132]. Three experimental citations and no non-nuclear coded location.
subnuclear localizationUniProt's uncoded note is cell-cycle-scoped and is the useful one: EXO1 'colocalizes with PCNA to discrete nuclear foci in S-phase'. That is a replication-associated compartment, not a damage compartment, and it is the strongest single statement in this entry that the cascade is S/G2-restricted. The damage compartment comes only from [E2] - EXO1 recruitment to laser- and nuclease-induced breaks in U2OS, dependent on CTCF-directed early BRCA1/BARD1 and on SMARCAD1. Nothing places EXO1 at the KMT2A locus in any cell type and no public occupancy dataset exists.
localization shown for fusionfalse
cell typeU2OS and HEK-293T only [E2]. 1,258 DepMap lines including 147 haematopoietic and lymphoid [E4]. NO ENCODE experiment in any biosample [E6], no KMT2A-rearranged cell, no infant material, no B-lineage progenitor, and zero records pairing EXO1 with KMT2A or MLL in titles or abstracts [E5].
cell stateS/G2, twice over. Long-range resection commits a break to homologous recombination, which requires a sister chromatid; and UniProt's own note places EXO1 in PCNA-associated S-phase foci. So EXO1's contribution to this cascade exists only in a cycling cell in S or G2. The index disease's putative cell of origin is a fetal progenitor whose cycling state at the moment of translocation is unmeasured, and this is the single biggest obstacle to importing the cascade into this disease - it is stated here rather than in a caveat because it is a property of the biology and not of the study design.
epigenetic readoutNone directly - EXO1 reads no histone mark and writes none. Its position in this graph's epigenetic argument is entirely as the EFFECTOR whose recruitment is the readout of the H3K9me/H3K4me0 state at the break: when UNC-0638, chaetocin or BIX-01294 block H3K9 methylation, BRCA1/BARD1 fails to load and EXO1/DNA2 recruitment is abrogated downstream [E2]. That makes EXO1 recruitment the assay by which an H3K9-axis drug's effect on repair would be scored.
shown for fusionNO - nobody has looked, in any fusion. EXO1[tiab] AND KMT2A[tiab] = 0 and EXO1[tiab] AND MLL[tiab] = 0, both with non-empty querytranslations and warninglist 'No items found.'; EXO1[tiab] AND leukemia[tiab] = 6, none about KMT2A. The bare operand EXO1[tiab] = 1,055, so this is not an unstudied protein - it is a protein nobody has studied in this disease.
archive bound 2026 09 22ENCODE has NO target record for EXO1 - the target.label facet returns HTTP 404 - so no released occupancy dataset exists for it in any biosample. Same for DNA2, SUV39H1 and RBBP8. CORRECTED 2026-09-22: BARD1 is NOT in this class. Measured live, /targets/BARD1-human/ returns HTTP 200 and the 404 came from pinning assay_title=TF+ChIP-seq to the query, so it described the FILTER and not the protein. RAD50 behaves identically (200 bare, 404 filtered). EXO1, DNA2, SUV39H1 and RBBP8 are genuine - 404 on both endpoints.
absence classnever-measured
domains
N-domain1.000N-domain: 1Interaction with MSH3129.0Interaction with MSH3: 129I-domain138.0I-domain: 138Interaction with MLH1 (N)388.0Interaction with MLH1 (N): 388Interaction with MSH2600.0Interaction with MSH2: 600Interaction with MLH1 (C)787.0Interaction with MLH1 (C): 787
gene synonyms in uniprot
[
  "EXOI",
  "HEX1"
]
identifier traps
{
  "registry_check": "Rule 88 read run first over d['collisions'] (177 rows, case-sensitive). 'EXO1' returns zero rows. A substring search for the three-letter fragment 'EXO' does hit the HDGFL2 row, but word-boundary matching returns zero - which is the exact false-positive mode the rule-88 scope note warns about for short tokens, observed here and discarded.",
  "alias_precision_warning": "EXOI and HEX1 are the UniProt synonyms. 'EXOI' differs from 'EXO1' only by letter-I versus digit-1 and is an OCR- and typo-prone pair; 'HEX1' collides with hexokinase and with HEX1/ERH in older literature. Neither retired symbol was searched in this beat, which is recorded as a limit on the absence rather than assumed away.",
  "registry_status": "no EXO1 row exists in data/symbol-collisions.json as of 2026-09-22; no new trap is claimed for this gene."
}
domains — the numbers behind the chart
[
  {
    "name": "N-domain",
    "start": 1,
    "end": 99
  },
  {
    "name": "I-domain",
    "start": 138,
    "end": 229
  },
  {
    "name": "Interaction with MSH3",
    "start": 129,
    "end": 387
  },
  {
    "name": "Interaction with MLH1 (N)",
    "start": 388,
    "end": 490
  },
  {
    "name": "Interaction with MSH2",
    "start": 600,
    "end": 846
  },
  {
    "name": "Interaction with MLH1 (C)",
    "start": 787,
    "end": 846
  }
]
depmap
{
  "n_screens_with_gene_effect": 1258,
  "mean_gene_effect": -0.1273,
  "median_gene_effect": -0.1073,
  "min_gene_effect": -1.1343,
  "max_gene_effect": 0.3749,
  "frac_below_minus_0_5": 0.0429,
  "frac_below_minus_1_0": 0.0016,
  "n_blood_screens": 147,
  "blood_tissue_blocks": [
    "hematopoietic tissue",
    "lymphoid tissue"
  ],
  "blood_mean_gene_effect": -0.0783,
  "blood_frac_below_minus_0_5": 0.0272,
  "n_tissue_blocks_flattened": 29,
  "open_targets_data_version": {
    "year": "26",
    "month": "06",
    "iteration": null
  },
  "depmap_release": null,
  "rule_83": "no DepMap release identifier is present in the payload; the Open Targets data version is recorded and is not a substitute. EXO1's 1,258 screens and DNA2's 80 in the same call are NOT comparable denominators - see `ana-q32-depmap-across-the-hr-licensing-cascade`.",
  "rule_84": "no median-split proportion is reported.",
  "live_zero_screen_control": "POLR2A in the same call returned 0 tissue blocks and 0 screens with a passing approvedSymbol readback.",
  "reading": "shallow and shallower in blood than in the panel. EXO1 and DNA2 are functionally redundant for long-range resection, so a single-gene knockout score is the expected result for a redundant pair and does not measure how much long-range resection matters."
}
How this could bite us back
  • EXO1 is not a target and should not become one here: long-range resection is required for accurate repair, so inhibiting it in a normal progenitor is the same liability this beat is warning about at the H3K9 step, one node further down.
  • EXO1 recruitment is, however, the right ENDPOINT for scoring that liability. Any experiment testing whether UNC0642 or another H3K9-axis inhibitor removes a repair licence should read out EXO1 recruitment or ssDNA resection at a defined break, not BRCA1 foci - BRCA1 has three known recruitment routes and only one of them is in this cascade.
  • Because EXO1 and DNA2 are redundant, a negative EXO1 single-depletion result would not exonerate the cascade; the pair must be depleted together, which is what the source paper does and what any replication must do.
Still open
  1. Does a published AsiSI/DIvA resection dataset cover the KMT2A breakpoint cluster region (GRCh38 chr11 around 118,436,000-118,526,000)? If an AsiSI site lies within or near it, resection kinetics at this graph's locus may already be measurable from deposited data with no wet work. This query was not run in this beat and is the cheapest open item it leaves.
  2. Is EXO1 or DNA2 recruitment to a break reduced by UNC0642 in a haematopoietic cell? [E2] shows the upstream step is blocked by UNC-0638 in U2OS; the downstream, most interpretable readout has not been measured under any G9a inhibitor in any blood cell.
  3. Does long-range resection operate at all in a quiescent fetal haematopoietic progenitor? If it does not, the entire cascade is irrelevant to the genesis of infant t(4;11) however well established it is in cycling cells - and that single fact would settle several arguments in this graph at once.
  4. Are the retired symbols EXOI and HEX1 worth searching? They were not searched here, and this project has previously undercounted a literature tenfold by keying to the current symbol.
Every source behind this entry (6)
  1. E1established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database

    EXO1 is UniProt Q9UQ84, entry name EXO1_HUMAN, 846 amino acids, primary gene name EXO1 with gene synonyms EXOI and HEX1, recommended protein name 'Exonuclease 1'; the feature table annotates an N-domain 1-99, an I-domain 138-229, and interaction regions with MSH3 (129-387), MLH1 (388-490 and 787-846) and MSH2 (600-846); it cross-references 25 PDB entries; its coded subcellular location is Nucleus with three ECO:0000269 citations (PubMed:11429708, 14676842, 17426132) and an uncoded note that it colocalizes with PCNA to discrete nuclear foci in S-phase.

    UniProtKB Q9UQ84 (EXO1_HUMAN) - Exonuclease 1, Homo sapiens · UniProt Consortium · UniProt Knowledgebase 2026
    What this evidence cannot show

    A database record fetched 2026-09-22 with gene_exact:EXO1 AND organism_id:9606 AND reviewed:true returning exactly one reviewed record. UniProt types no classical catalytic domain for EXO1 - the nuclease activity is not captured as a Domain feature - so the domains array here is regions and interaction spans, not a catalytic-domain map. The three MMR interaction regions (MSH2, MSH3, MLH1) are a reminder that EXO1's largest published role is mismatch repair, not resection.

    Evidence that argues against this (1)
    • The interaction regions annotated on this record are all mismatch-repair partners. A reader taking EXO1 from this entry into an HR argument should know that the protein's dominant annotated context in the database is MMR, and that its HR role is not represented in the feature table at all. UniProt Consortium 2026
  2. E2strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    EXO1 and DNA2 are the long-range resection effectors at the bottom of the CTCF-directed cascade. In U2OS and HEK-293T cells, failure of the CTCF-recruited repressive chromatin assembly abrogates recruitment of the exonucleases EXO1/DNA2, which is causally linked to defective DNA end resection and dysfunctional HR; recruitment of SMARCAD1 and EXO1/DNA2 relies on CTCF-dependent EARLY BRCA1/BARD1 rather than on CTCF-independent late BRCA1/BARD1; the CTCF-directed HR pathway involves both CtIP-dependent short-range resection and the subsequent EXO1/DNA2-dependent long-range resection; CTCF coordinates recruitment of CtIP, early BRCA1/BARD1 and BRCA2 to DSBs through multiple parallel routes that are sequentially linked in function, with CtIP in initial resection, early BRCA1/BARD1 promoting SMARCAD1- and EXO1/DNA2-dependent extensive resection, and BRCA2 mediating RAD51 loading; and double or triple co-depletion of CtIP, HP1-gamma, BRCA1 or BRCA2 did not further aggravate end resection or HR efficiency beyond single depletion of each.

    CTCF primes repressive chromatin for rapid BRCA1/BARD1 recruitment to drive homologous recombination repair of DNA double-strand breaks. · Hwang SY, Choi D, Choi MJ, Jo HR, Jeong JH, Kang MA, Lee JS · Nucleic Acids Research 2026
    PMID 42475683DOI
    What this evidence cannot show

    U2OS reporter lines (AsiSI-ER, LacI-FokI-DD, DR-GFP, EJ5-GFP) and HEK-293T only. Resection and HR efficiency are reporter and imaging readouts in an osteosarcoma line; no haematopoietic cell, no fusion, no KMT2A locus. The epistasis argument rests on NON-ADDITIVITY of co-depletions, which is a weaker inference than an ordered rescue: non-additivity is consistent with one pathway but also with a shared ceiling or with incomplete knockdown. Several of the load-bearing panels are supplementary (S8-S10). DOI taken from PubmedData/ArticleIdList only.

    Evidence that argues against this (1)
    • The same paper's own framing is that CtIP, early BRCA1/BARD1 and BRCA2 reach DSBs through 'distinct parallel routes, rather than a single epistatic linear pathway'. So the sequential model is a functional interpretation laid over a parallel recruitment architecture, and an intervention that removes one chromatin arm may not remove the resection step it is assigned to. Hwang SY et al. 2026
  3. E3strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    A second, independent 2026 chromatin-primed HR cascade converges on the step immediately upstream of EXO1/DNA2: menin directly recognises histone H2A.X via its Val371-Gln400 motif with the interaction markedly promoted by DNA damage; SETD2 is recruited to damage sites by menin and catalyses H3K36me3 reprogramming at local chromatin; LEDGF reads H3K36me3 and recruits CtIP as the effector to perform DNA end resection, activating the RPA2/RAD51 pathway; genetic ablation of Men1 caused spontaneous lung carcinogenesis with severe genomic instability; and pharmacologically restoring H3K36me3 rescued impaired HR repair in Men1-deficient cells.

    The tumor suppressor menin is a key scaffold mediator for homologous recombination repair. · Lian A, Zhu X, Jin B, Gu G, Xu B, Zhang L, Lin X, Zhu X, Jin G · Nucleic Acids Research 2026
    PMID 42578372DOI
    What this evidence cannot show

    Abstract read and identifiers fetched fresh from efetch in this beat; full text not read here. The in vivo system is a Men1-ablation LUNG carcinogenesis model, not a haematopoietic one and not a KMT2A-rearranged one. This paper is already cited in this graph on `exp-hr-competence-under-menin-inhibition-in-kmt2a-rearranged-blasts`, `gene-rbbp8` and `gene-topbp1`; it is cited here only for the convergence claim, and the convergence is my inference from reading the two abstracts side by side, not a statement either paper makes. Neither paper cites the other.

    Evidence that argues against this (1)
    • The two cascades could be alternatives rather than consecutive steps: both are described by their own authors as sufficient to explain an HR defect, and a cell in which either arm alone abolishes resection is not a cell in which they act in series. Distinguishing 'consecutive' from 'redundant-parallel' requires a double perturbation that neither paper performed. Hwang SY et al. 2026
  4. E4strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.database

    EXO1 is a shallow CRISPR dependency and shallower in blood than in the panel: flattening every tissue block gives 1,258 screens with a gene effect, mean -0.1273, median -0.1073, minimum -1.1343, maximum 0.3749, with 4.29% of lines below -0.5 and 0.16% below -1.0; in the 147 hematopoietic and lymphoid screens the mean is -0.0783 with 2.7% below -0.5.

    Open Targets Platform GraphQL API, target.depMapEssentiality with all tissue blocks flattened, plus meta.dataVersion · Open Targets Platform; Broad Institute DepMap · Open Targets Platform 2026
    What this evidence cannot show

    Rule 83: no DepMap release identifier in the payload; Open Targets data version year 26, month 06. Rule 84: no median-split proportion is reported. The live zero-screen control fired - POLR2A returned 0 blocks and 0 screens in the same call with a passing symbol readback. EXO1 and DNA2 are redundant for long-range resection, and the screens carry no exogenous genotoxin, so this is the least informative condition for a resection nuclease.

    Evidence that argues against this (1)
    • DNA2, EXO1's redundant partner, returns a mean of -2.71 in the same call - but over only 80 screens in 17 tissue blocks against EXO1's 1,258 in 29. The two figures come from different denominators and must not be read as 'DNA2 matters and EXO1 does not'; see `ana-q32-depmap-across-the-hr-licensing-cascade`. Open Targets Platform; Broad Institute DepMap 2026
  5. E5strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.database

    No published title or abstract pairs EXO1 with this graph's gene, and the zero is not an instrument failure. Measured live 2026-09-22 with one [tiab] tag per term and every querytranslation read back: EXO1[tiab] AND KMT2A[tiab] returns 0 with translation '"EXO1"[Title/Abstract] AND "KMT2A"[Title/Abstract]' and warninglist outputmessages 'No items found.'; EXO1[tiab] AND MLL[tiab] returns 0 the same way; EXO1[tiab] AND leukemia[tiab] returns 6. The bare operands are EXO1[tiab] 1,055, MLL[tiab] 6,328 and KMT2A[tiab] 1,653. Rule-67 positive controls through the IDENTICAL SYMBOL[tiab] AND TOKEN[tiab] shape return non-zero: CTCF[tiab] AND KMT2A[tiab] 7, RAD21[tiab] AND KMT2A[tiab] 5.

    NCBI E-utilities esearch over PubMed, db=pubmed, retmode=json, querytranslation read back for every query · National Center for Biotechnology Information · NCBI Entrez Programming Utilities 2026
    What this evidence cannot show

    Titles and abstracts only - rule 80: an EXO1 measurement in a supporting figure of a KMT2A paper would be invisible to every query above. The retired synonyms EXOI and HEX1 were NOT searched, so the name list is incomplete and the absence is bounded by the current symbol alone. Two large operands with an empty intersection is recorded explicitly because rule 67 says that is a claim needing its own evidence; here the evidence is that the shape returns ones for CTCF and RAD21.

    Evidence that argues against this (1)
    • TOP2B[tiab] AND KMT2A[tiab] returns 0 through the identical shape, although the TOP2B-KMT2A relationship is central to this disease - because that literature writes 'MLL' and 'topoisomerase II'. So a symbol-pair zero in this shape demonstrably CAN be false as a conclusion while being accurate as a measurement, and the EXO1 zero inherits that limitation. National Center for Biotechnology Information 2026
  6. E6strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.database

    ENCODE holds no released TF ChIP-seq experiment for EXO1 and no target record for it at all - the target.label facet returns HTTP 404 - as it does for DNA2, SUV39H1 and RBBP8. CORRECTED 2026-09-22: BARD1 is NOT in this class. Measured live, /targets/BARD1-human/ returns HTTP 200 and the 404 came from pinning assay_title=TF+ChIP-seq to the query, so it described the FILTER and not the protein. RAD50 behaves identically (200 bare, 404 filtered). EXO1, DNA2, SUV39H1 and RBBP8 are genuine - 404 on both endpoints. In the same census BRCA1 has 7, CBX3 4, CBX1 2, CBX5 4, KDM5A 3, TRIM28 5, SETDB1 5 and CTCF 502.

    What this evidence cannot show

    Counted 2026-09-22 on the released TF ChIP-seq facet only. GEO, ChIP-Atlas and ReMap were not swept. A 404 means no ENCODE target record, which is a different negative from a searched zero and is recorded as such. Note also that ChIP-seq is arguably the wrong assay for a resection nuclease - END-seq, BLESS or qPCR-based resection assays at a defined break are what would answer the question, and none of those was searched for either.

    Evidence that argues against this (1)
    • For EXO1 the right archive is not a ChIP-seq archive. Resection at a defined break is measured by ssDNA-resection qPCR in the AsiSI/DIvA system, and DIvA datasets are deposited in GEO. A DIvA-based resection map covering chr11q23 may already exist and would answer part of this beat's locus question without any new experiment - that query was NOT run here. NCBI Gene Expression Omnibus 2026
Connected to