Oncofusion

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Genemoderate confidence 3 of 5: One strong study, or several smaller consistent ones.Q136-interactome-tail-size-and-abundance

ELF1 - a direct transcriptional target of MLL fusion proteins and HOXA9 that is ALSO a BioID neighbour of KMT2A, and that is focally deleted in paediatric AML without a KMT2A rearrangement

also called E74 like ETS transcription factor 1 · E74-like factor 1 · Elf1

ELF1 is a transcription factor that leukaemia-causing MLL fusion proteins switch on directly, and it is also one of eleven factors whose neighbourhood contained KMT2A in a proximity screen. So the fusion turns ELF1 up, and ELF1 sits next to the protein the fusion is made from - which is a loop worth understanding, even though the proximity half of it is very weak evidence.

The same thing, for a scientist

ELF1 (HGNC:3316, ENSG00000120690, UniProt **P32519**, 619 aa, 13q14.11) is an ETS-family transcription activator with a single ETS DNA-binding domain at residues 208-290 [E4]. It enters this project on one curated row - IntAct **IM-28767**, **MI:1314 BioID**, **MI:1060 spoke**, **ELF1 bait / KMT2A prey**, MI-score 0.27, HEK293 Flp-In - one of the eleven TF baits recovering KMT2A, and **NOT RESOLVED** at p = 0.151 under a both-margins null [E1][E2][E3]. **What lifts it out of that block is not the row.** Varghese, Garcia-Cuellar and Slany report that **Elf1 is a direct downstream target of HoxA9 and of leukemogenic MLL fusion proteins**, is consistently over-expressed in AML regardless of genotype, and that ChIP places Elf1 on archetypical myeloid enhancers and promoters **co-localising with HoxA9 and Meis1**, where it controls an innate-immunity programme [E5]. **HOXA9 and MEIS1 are the canonical effectors of KMT2A-rearranged leukaemia and both have entries here.** Against that sits a second, opposite-signed literature: **focal deletion of ELF1 is disproportionately prevalent in paediatric relative to adult AML** [E6], and the pedatric AML subgroups carrying RB1/ELF1 co-deletion are found **only in patients without RUNX1::RUNX1T1, CBFB::MYH11 or KMT2A rearrangement** [E7]. **The gene is up in KMT2A-rearranged disease and lost in a different paediatric AML, and both findings are in the last eight years.**

What it looks like
ELF1 - a direct transcriptional target of MLL fusion proteins and HOXA9 that is ALSO a BioID neighbour of KMT2A, and that is focally deleted in paediatric AML without a KMT2A rearrangement619 aa
ETS (DNA binding)ETS (DNA binding) · residues 208–2900200400600

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 interaction row, and why it is the weakest part of this entry

One IntAct row, IMEx IM-28767: MI:1314 BioID, MI:1060 spoke, roles MI:0496 bait (ELF1) / MI:0498 prey (KMT2A), host taxid:9606(Homo sapiens HEK293flp-in embryonic kidney cell), MI-score 0.27 (the deposition-wide floor) 2.

ELF1 recovered 85 preys of 946 in that arm, ranking 34th of 102 baits; KMT2A is recovered by 11 of the 102. Holding both margins, p = 0.151: NOT RESOLVED - neither promoted nor declined 3. For context, this beat's regression shows KMT2A's 11-of-102 is 0.9x what its size and abundance predict in that panel (p = 0.42), so KMT2A is not even unusually recoverable there. The ELF1-KMT2A row carries essentially no information on its own.

gene-elf2 already asked whether the three ETS rows in this screen - ELF1, ELF2, FEV - are one observation or three, and named it an analysis rather than an entry. The analysis has now been run and the answer is that they are ordered but not separated: ELF1 p = 0.151, ELF2 p = 0.141, FEV p = 0.386 (FEV falls to EXPLAINED because it labelled 197 preys, the second-widest bait in the panel). On the interaction evidence alone ELF1 and ELF2 are indistinguishable.

The reason to write ELF1: it is downstream of the fusion, not just beside KMT2A

This is the finding that reached this beat only through the historical gene symbol. ELF1[tiab] AND KMT2A[tiab] returns 2 records; ELF1[tiab] AND MLL[tiab] returns 1, and it is the decisive one 8.

Varghese et al. (Slany lab) report that Elf1, normally predominantly expressed in monocytes, "was not only a direct downstream target of homeobox A9 (HoxA9) and leukemogenic mixed-lineage leukemia (MLL) fusion proteins but it was also consistently overexpressed in acute myeloid leukemia (AML) regardless of the underlying genotypic alteration"; ChIP localised Elf1 to archetypical myeloid enhancers and promoters as defined by co-localisation with HoxA9 and Meis1; perturbation and ectopic expression showed Elf1 controls a transcriptional programme dominated by innate-immunity genes; and Elf1 was required for the rapid transcriptional response of myeloid cells to lipopolysaccharide, with upregulation of NfkB and RelB, confirmed in Elf1 genetic knockout myelocytes 5.

Why this matters here. This graph's model of KMT2A::AFF1 output runs through a HOXA9/MEIS1 programme. A factor that is (i) directly induced by MLL fusion proteins, (ii) occupies the same myeloid enhancers as HOXA9 and MEIS1, and (iii) turns up in a proximity screen beside KMT2A describes a feed-forward shape: the fusion drives the factor, the factor occupies the fusion's target enhancers. None of that requires the BioID row to be real, and the entry does not use the row to support it.

The opposite-signed literature, which is not a contradiction but is not nothing

The TARGET paediatric AML landscape (~1,000 COG participants, whole-genome, targeted DNA, mRNA, microRNA and CpG methylation) reports that somatic structural variants including focal deletions of MBNL1, ZEB2 and ELF1 were disproportionately prevalent in young individuals as compared with adults 6. A later Japanese AML-05 series (n = 328) found TP53 and RB1 alterations in 2.1% and 1.8% of cases, with RB1 frequently co-deleted with its neighbouring gene ELF1 and both classes of alteration present only in patients without RUNX1::RUNX1T1, CBFB::MYH11 or KMT2A rearrangements; RB1-altered patients had 0% five-year overall survival 7.

ELF1 is at 13q14.11 and RB1 at 13q14.2, so the co-deletion is positional, not necessarily functional, and the paper frames it that way.

How to hold the two together. In KMT2A-rearranged AML, ELF1 is reported induced by the fusion. In a small, KMT2A-rearrangement-negative, very poor-prognosis paediatric AML subgroup, ELF1 is deleted alongside RB1. Those are different diseases and the findings do not collide - but a gene that is up in one arm and gone in another is not a simple candidate for anything, and this entry does not treat it as one.

A third context, in the other lineage: ELF1 is named as one of the T-ALL master transcription factors, with ERG and ETS1, that activate a super-enhancer driving IRF2BP2, which is required for T-ALL cell growth and survival 9. This graph carries gene-erg.

Localization, subnuclear compartment, cell type, epigenetics

Subcellular (UniProt): Nucleus, with no evidence code - an uncoded annotation, which this graph already knows is not a measurement 4.

Subnuclear (HPA immunofluorescence): nucleoplasm, main and only location, reliability Supported 10. No speckle, nucleolar or nuclear-body call. KMT2A's own HPA main call is also nucleoplasm, so bait and prey share a compartment - which is what makes a proximity row look informative when it is not.

Domain architecture: a single ETS DNA-binding domain, 208-290, with disordered stretches at 158-199, 300-366 and 564-592. No chromatin reader, no catalytic domain 4.

Cell type. Two different answers, and keeping them apart is the point of this entry. Of the interaction observation: HEK293 Flp-In embryonic kidney, over-expressed tagged construct - not blood, not leukaemic, not KMT2A-rearranged. Of the biology: Elf1 is normally predominantly expressed in monocytes, and the MLL-fusion-target result is in myeloid cells with ChIP and genetic knockout 5.

Cell state: the functional result is state-dependent in a way that is unusual and worth recording - Elf1's requirement is most visible in the rapid transcriptional response to lipopolysaccharide, i.e. under acute innate-immune stimulation rather than at baseline, which the authors present as an example of a common haematopoietic enhancer where redundant factor binding matters only under particular conditions 5.

Epigenetic role: ELF1 has no chromatin-modifying or chromatin-reading activity. Its chromatin relevance is occupancy: ChIP places it at myeloid enhancers and promoters co-bound by HOXA9 and MEIS1 5.

Facts and figures
hgnc IDHGNC:3316
symbolELF1
ensembl gene IDENSG00000120690
uniprotP32519
length AA619
chromosomal location13q14.11
entrez ID1997
identifier provenanceHGNC REST fetch/symbol/ELF1 and UniProtKB P32519 retrieved live 2026-09-23; Ensembl id taken from the HGNC record. HGNC lists no previous symbol and no alias symbol for ELF1, so no alias search was possible or needed. ELF1 is named in 3 node files by word-boundary match, all of which enumerate the eleven TF baits; no entry existed.
subnuclear location hpaNucleoplasm (main, reliability Supported, no additional location)
cell type of the observationHEK293 Flp-In embryonic kidney - not blood, not leukaemic, not KMT2A-rearranged
cell type of the biologymonocytes and myeloid cells; Elf1 is normally predominantly expressed in monocytes
cell state of the biologythe Elf1 requirement is most visible under acute innate-immune stimulation - the rapid transcriptional response to lipopolysaccharide, with NfkB and RelB upregulation - rather than at baseline
epigenetic roleNone as a writer, eraser or reader. Chromatin relevance is occupancy: ChIP places ELF1 at archetypical myeloid enhancers and promoters co-bound by HOXA9 and MEIS1.
shown for fusionPARTIAL - shown as a DIRECT TARGET of leukemogenic MLL fusion proteins in PMID 40780499, fusion not named in the abstract and the Slany laboratory's usual systems are murine MLL-ENL and MLL-AF9; NOT shown for KMT2A::AFF1 and NOT shown as a physical partner of any fusion. The proximity row is wild-type KMT2A in HEK293.
evidence classinteraction: single publication, single method, spoke-expanded BioID proximity, no orthogonal validation. Biology: independent ChIP and genetic-knockout work in myeloid cells, read at abstract level only.
prev and alias symbols
[]
domains
[
  {
    "name": "ETS (DNA binding)",
    "start": 208,
    "end": 290
  }
]
interaction with project baits
[
  {
    "core_protein": "KMT2A",
    "core_uniprot": "Q03164",
    "partner_experimental_role": "bait",
    "core_experimental_role": "prey",
    "method": "MI:1314 proximity-dependent biotin identification",
    "expansion": "MI:1060 spoke",
    "mi_score": 0.27,
    "imex": "IM-28767",
    "pmid": "35140242",
    "host_cell": "HEK293 Flp-In embryonic kidney",
    "n_rows": 1,
    "n_publications": 1
  }
]
adjudication
{
  "verdict": "NOT RESOLVED",
  "p_pair_both_margins_held": 0.151,
  "bait_preys_recovered": 85,
  "bait_selectivity_rank_in_panel": "34 of 102 (1 = widest labeller)",
  "prey_baits_recovering_it": 11,
  "of_panel": 102,
  "ets_block_comparison": {
    "ELF1": 0.151,
    "ELF2": 0.141,
    "FEV": 0.386
  },
  "why_written_anyway": "ELF1 is a DIRECT TRANSCRIPTIONAL TARGET of MLL fusion proteins and HOXA9 and co-occupies myeloid enhancers with HOXA9 and MEIS1 (PMID 40780499) - a relationship to the fusion that is independent of, and far stronger than, the proximity row",
  "source": "analyses/interactome-tail-size-and-abundance-adjudication/pair_null.json"
}
relationship to the fusion
{
  "direction": "DOWNSTREAM - induced by MLL fusion proteins, not a component of the complex",
  "evidence": "PMID 40780499, direct HoxA9 and MLL-fusion target, ChIP co-localisation with HoxA9 and Meis1 at myeloid enhancers",
  "which_fusion": "'leukemogenic MLL fusion proteins' as stated in the abstract; the specific fusion is NOT named there and KMT2A::AFF1 is NOT established",
  "opposite_signed_finding": "focal ELF1 deletion is enriched in paediatric versus adult AML (PMID 29227476) and RB1/ELF1 co-deletion occurs only in paediatric AML WITHOUT a KMT2A rearrangement (PMID 37102302)"
}
subcellular location uniprot
[
  "Nucleus (NO evidence code - uncoded annotation, not a measurement)"
]
literature queries
{
  "ELF1_AND_KMT2A": {
    "n": 2,
    "pmids": [
      "37102302",
      "29227476"
    ],
    "querytranslation": "\"ELF1\"[Title/Abstract] AND \"KMT2A\"[Title/Abstract]"
  },
  "ELF1_AND_MLL": {
    "n": 1,
    "pmids": [
      "40780499"
    ],
    "querytranslation": "\"ELF1\"[Title/Abstract] AND \"MLL\"[Title/Abstract]"
  },
  "note": "THE TWO HIT SETS ARE DISJOINT. A beat querying only the modern symbol would have found ELF1 solely as a gene DELETED in KMT2A-rearrangement-negative AML and would have concluded the opposite of the MLL-operand paper."
}
How this could bite us back
  • ELF1's own paper describes it as occupying a COMMON haematopoietic enhancer with redundant transcription-factor binding, required only under particular conditions. A factor that is redundant at baseline is one a cell can lose without noticing, which is the classic shape of a target that fails.
  • ELF1 is required for the rapid myeloid response to lipopolysaccharide. Any agent that suppressed it would plausibly blunt innate immune responsiveness in a patient population that dies of infection during induction, and this graph already tracks infection toxicity in infant ALL.
  • ELF1 is focally deleted in a poor-prognosis paediatric AML subgroup. If loss of ELF1 is compatible with - or contributes to - aggressive leukaemia, then suppressing it is not obviously a therapeutic direction at all, and the sign of any intervention is unresolved.
Still open
  1. Which MLL fusion was used in the experiments showing Elf1 is a direct fusion target? The abstract says 'leukemogenic MLL fusion proteins' and names none. If it is MLL-ENL or MLL-AF9 in mouse, the claim does not transfer to human KMT2A::AFF1 infant ALL without a test, and reading the full text is a one-hour job that would settle it.
  2. Is ELF1 induced in KMT2A::AFF1 B-lineage blasts, or is the induction myeloid-restricted? Elf1 is normally a monocyte factor and the fusion-target work is in myeloid cells; the index disease is pro-B arrested. An ELF1 query against an existing infant-ALL expression dataset decides whether this entry is about the index disease at all.
  3. Does the feed-forward shape close? The fusion induces ELF1; ELF1 occupies HOXA9/MEIS1 enhancers; a proximity screen puts ELF1 beside KMT2A. If ELF1 also occupied the fusion's own target loci in a KMT2A-rearranged cell, that would be a loop rather than three coincidences - and the ChIP to test it already exists as a method in the cited paper.
  4. Is the ELF1 focal deletion in paediatric AML a passenger of RB1 loss? ELF1 sits at 13q14.11 and RB1 at 13q14.2, and the cohort paper attributes the prognosis to RB1. Separating them needs cases with ELF1 loss and intact RB1, which the published cohorts may already contain.
Every source behind this entry (10)
  1. E1established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.paper

    Göös et al. identified 6,703 BioID and 1,536 AP-MS protein-protein interactions for 109 human transcription factors in HEK293 Flp-In cells; in the resulting IntAct deposition IM-28767, ELF1 is one of eleven transcription-factor baits whose BioID neighbourhood contained KMT2A.

    Human transcription factor protein interaction networks. · Göös H, Kinnunen M, Salokas K, Tan Z, Liu X, Yadav L, Zhang Q, Wei GH, Varjosalo M · Nat Commun 2022
    PMID 35140242DOI
    What this evidence cannot show

    Abstract read; full text and supplementary tables not read. The eleven-bait figure was RE-DERIVED from the deposition by this beat (102 bait symbols, 946 human preys, KMT2A recovered by 11) and not quoted from the prior entry, which the prior entry itself asked for. Every bait is an over-expressed tagged construct in embryonic kidney cells.

    Evidence that argues against this (1)
    • Eleven of 102 unrelated transcription factors recovering the same large nuclear protein is at least as consistent with KMT2A being a generally recoverable prey as with eleven specific relationships. This beat measured that KMT2A's 11-of-102 is 0.9x what its size and abundance predict in this panel, so it is not even an unusually recoverable prey here - the rows are simply uninformative. source 2026
  2. E2established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database

    IntAct serves the ELF1-KMT2A record as PSI-MI MI:1314 proximity-dependent biotin identification, MI:1060 spoke expansion, ELF1 experimental role MI:0496 bait and KMT2A MI:0498 prey, MI-score 0.27, host taxid:9606 Homo sapiens HEK293flp-in embryonic kidney cell, IMEx IM-28767, publication PMID 35140242.

    What this evidence cannot show

    Retrieved live 2026-09-23; 8,331 rows fetched against an endpoint-declared count of 8,331. Rule 93: PSICQUIC is a floor relative to IntAct REST and a REST query on this pair was not run. Spoke expansion means the binary pair was never measured.

    Evidence that argues against this (1)
    • MI-score 0.27 is the deposition-wide value on every row in this arm and carries no pair-specific information. source 2026
  3. E3moderate confidence 3 of 5: One strong study, or several smaller consistent ones.dataset

    In IM-28767's BioID arm ELF1 recovered 85 of 946 human preys, ranking 34th of 102 baits by reach, while KMT2A is recovered by 11 of the 102; under a null holding both margins ELF1 recovering KMT2A has p = 0.151 (NOT RESOLVED), against ELF2 at 0.141 and FEV at 0.386 (EXPLAINED).

    What this evidence cannot show

    20,000 draws, seed 20260923. A Bonferroni threshold over the 62 pairs tested is 0.0008 and nothing survives it, so these are an ordering rather than a test. The null assumes preys are drawn independently given their degrees, which is false when baits share a complex.

    Evidence that argues against this (1)
    • ELF1 and ELF2 separate by 0.010 in p. That is not a separation. Any entry that reads ELF1's row as better than ELF2's is reading noise, and this entry rests its case entirely on the independent MLL-fusion-target literature instead. source 2026
  4. E4moderate confidence 3 of 5: One strong study, or several smaller consistent ones.database

    UniProt P32519 is 619 aa with a single ETS DNA-binding domain at residues 208-290 and disordered regions at 158-199, 300-366 and 564-592, and assigns subcellular location Nucleus with no evidence code.

    What this evidence cannot show

    Fetched live 2026-09-23. The nucleus call is UNCODED - no ECO term at all - so it is a curator assertion and not a measurement, and this graph has already measured that roughly a quarter of its UniProt localisation annotations are of this kind.

    Evidence that argues against this (1)
    • An uncoded location for a transcription factor is close to a tautology: curators assign nucleus because the protein binds DNA. It is not independent evidence of where the protein is under any particular condition. source 2026
  5. E5strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    Elf1, normally predominantly expressed in monocytes, is a direct downstream target of HoxA9 and of leukemogenic MLL fusion proteins and is consistently overexpressed in AML regardless of the underlying genotypic alteration; chromatin immunoprecipitation localises Elf1 to archetypical myeloid enhancers and promoters as defined by co-localisation with HoxA9 and Meis1; in perturbation and ectopic expression experiments Elf1 controls a transcriptional programme dominated by innate-immunity genes, and Elf1 is required for the rapid transcriptional response of myeloid cells to lipopolysaccharide including upregulation of NfkB and RelB, confirmed in myelocytes with a genetic knockout of Elf1.

    The myeloid transcription factor Elf1 regulates genes with function in innate immunity. · Varghese P, Garcia-Cuellar MP, Slany RK · Exp Hematol 2025
    PMID 40780499DOI
    What this evidence cannot show

    ABSTRACT ONLY - the full text was not read. The abstract does not state which MLL fusion was used, in which cell system, or whether the human index fusion KMT2A::AFF1 was among them; the phrase is 'leukemogenic mixed-lineage leukemia (MLL) fusion proteins', and the Slany laboratory's standard system is murine MLL-ENL and MLL-AF9. Treat 'direct target of MLL fusions' as established for the fusion class tested in that paper and NOT for KMT2A::AFF1. This paper was reachable ONLY through the operand MLL; ELF1 AND KMT2A does not return it.

    Evidence that argues against this (1)
    • The paper's own framing is that Elf1 occupies a COMMON haematopoietic enhancer where transcription-factor binding is redundant and matters only under particular conditions, and that its programme is innate immunity rather than self-renewal. A factor that is induced by the fusion but functionally redundant at baseline is a poor candidate for a fusion-specific dependency. source 2025
  6. E6established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.paper

    In the COG-NCI TARGET paediatric AML landscape of nearly 1,000 Children's Oncology Group participants, somatic structural variants including new gene fusions and focal deletions of MBNL1, ZEB2 and ELF1 were disproportionately prevalent in young individuals as compared with adults, while DNMT3A and TP53 mutations common in adults were conspicuously absent from virtually all paediatric cases.

    PMID 29227476DOI
    What this evidence cannot show

    Abstract read; full text not read. The abstract does not give the frequency of ELF1 focal deletion, does not state whether the deleted cases are KMT2A-rearranged, and does not separate ELF1 deletion from the neighbouring RB1 locus. This is paediatric AML; the index disease of this project is infant B-ALL.

    Evidence that argues against this (1)
    • The same paper reports that deletions, mutations and promoter hypermethylation converge on a cluster of zinc-finger-encoding genes ASSOCIATED WITH KMT2A REARRANGEMENTS - a different gene set from ELF1. The KMT2A-associated signal in this cohort is not the ELF1 deletion. source 2017
  7. E7strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    In 328 paediatric AML patients from the Japanese AML-05 trial, TP53 alterations were found in 7 patients (2.1%) and RB1 alterations in 6 (1.8%), TP53 and RB1 were frequently co-deleted with their neighbouring genes PRPF8 and ELF1 respectively, these alterations were found only in patients without RUNX1::RUNX1T1, CBFB::MYH11 or KMT2A rearrangements, and RB1-altered patients had 0% five-year overall survival against 71.8% for others.

    TP53 and RB1 alterations characterize poor prognostic subgroups in pediatric acute myeloid leukemia. · Hara Y, Shiba N, Yoshida K, Yamato G, Kaburagi T, Shiraishi Y, et al. · Genes Chromosomes Cancer 2023
    PMID 37102302DOI
    What this evidence cannot show

    Abstract read; full text not read. n = 6 for RB1 alterations, so the 0% survival figure rests on six patients. ELF1 is described as a NEIGHBOURING gene co-deleted with RB1 (13q14.11 and 13q14.2), and the paper attributes the prognosis to RB1, not to ELF1 - nothing here shows ELF1 loss is itself consequential.

    Evidence that argues against this (1)
    • This is the direct counterweight to E5. Where the Slany work has ELF1 induced by MLL fusions, this cohort has ELF1 deleted - and specifically in the patients WITHOUT a KMT2A rearrangement. The two findings are in different subgroups and do not collide, but a gene that is up in one arm and gone in another is not a clean candidate for anything. source 2025
  8. E8established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database

    PubMed returns 2 records for ELF1 AND KMT2A in titles and abstracts (PMID 37102302 and PMID 29227476) and 1 record for ELF1 AND MLL (PMID 40780499); the single most informative paper about ELF1 and this project's biology is reachable only through the historical operand MLL.

    What this evidence cannot show

    Neither query is a zero, so no absence is being claimed. Both translations are non-empty. Bounded by titles and abstracts; ELF1 has 57 records against leukaemia/haematopoietic terms and only these three name the fusion gene under either symbol.

    Evidence that argues against this (1)
    • The two KMT2A-operand hits and the one MLL-operand hit do not overlap at all. A beat that queried only the modern symbol would have found ELF1 exclusively as a deleted gene in KMT2A-rearrangement-negative AML, and would have concluded the opposite of what the MLL-operand paper reports. source 2026
  9. E9moderate confidence 3 of 5: One strong study, or several smaller consistent ones.paper

    A previously unreported super-enhancer region in T-cell acute lymphoblastic leukaemia patient samples and cell lines activates IRF2BP2 and is regulated by the T-ALL master transcription factors ERG, ELF1 and ETS1; IRF2BP2 is dispensable for normal T cell development but crucial for T-ALL cell growth and survival in vitro and in vivo.

    PMID 39454110DOI
    What this evidence cannot show

    Abstract read; full text not read. This is T-ALL, a different lineage from the index B-lineage disease, and ELF1 appears here as one of three named master factors without separation of their individual contributions. It is included to show ELF1 is lineage-relevant in acute leukaemia generally, not to make a claim about KMT2A.

    Evidence that argues against this (1)
    • Being named among the master transcription factors of a leukaemia subtype is a common designation and ELF1's specific contribution is not isolated in this work. ERG, which this graph already carries an entry for, is the better-established member of that trio. source 2024
  10. E10moderate confidence 3 of 5: One strong study, or several smaller consistent ones.database

    The Human Protein Atlas assigns ELF1 a main subcellular location of nucleoplasm with no additional location, reliability 'Supported', and classes it as a transcription factor with molecular function activator and DNA-binding.

    What this evidence cannot show

    Antibody-based immunofluorescence in a small cell-line panel, not in myeloid or leukaemic cells. 'Supported' is the middle reliability tier.

    Evidence that argues against this (1)
    • KMT2A's HPA main location is also nucleoplasm. A shared compartment call for bait and prey is exactly what makes an uninformative proximity row look informative, and it is the reason this entry does not lean on the BioID row. source 2026
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