Oncofusion

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Proteinmoderate confidence 3 of 5: One strong study, or several smaller consistent ones.Q47-swi-snf

SMARCD1 (BAF60A) - rank 59 of 17,728, survives the lineage split, and had never been named in this graph or studied in this disease

also called BAF60A · SMRD1_HUMAN

SMARCD1 is the sister part to SMARCD2 in the same slot of the SWI/SNF machine. It has the strongest KMT2A-rearranged dependency signal of any canonical SWI/SNF subunit tested here - and essentially nobody has studied it in leukaemia.

The same thing, for a scientist

SMARCD1 (Q96GM5, 515 aa) is one of three mutually exclusive BAF60 paralogues, shared by cBAF, PBAF and ncBAF [E1]. In the genome-wide KMT2A-rearranged selectivity scan it ranks **59 of 17,728** (0.333rd percentile) with difference **-0.3574** (KMT2A-r mean -0.7416, other leukaemia -0.3841) and an empirical p of 0.0042 - the best-ranked shared SWI/SNF subunit in the whole panel and better than DOT1L (rank 184) [E2]. It is one of only four SWI/SNF genes that **survive the lineage split** (myeloid z -0.86, B-lineage z -1.66) [E3]. Functionally it has one relevant published result: BAF60a was a hit in the 93-hairpin SWI/SNF screen in MLL-AF9 RN2 cells, and BAF60a occupancy was detected at the E1-E5 Myc enhancer cluster in those cells, placing it physically at the locus the enhancer mechanism runs through [E4]. **And then the literature stops: `SMARCD1 AND (MLL OR KMT2A)` returns one record and it title-checks to zero on-beat, while `SMARCD1 AND leukemia` returns 4 [E5].** This entry is the clearest example in the beat of a well-evidenced dependency with no biology written under it.

What it looks like
loading AF-Q96GM5-F1…
AlphaFold AF-Q96GM5-F1 ↗
colourshape

This is a prediction, not a measurement. No one has seen this protein in this shape. The colours say how much the software trusts itself, and that is worth reading before anything else — the orange stretches are places the model is effectively saying this part has no fixed shape.

very high (90+)confident (70–90)low (50–70)very low (<50)
I have never read one of these pictures before

A protein is one long chain of amino acids that folds up. The ribbon traces that chain from one end to the other; it is not a wire, it is a simplification of where the backbone runs. Drag to rotate, scroll to zoom.

Domains are the stretches of chain that do a particular job, and they are what the coloured blocks above the picture mark out. Click one and the view flies to it. In this project the important question about any domain is usually whether the fusion still has it — the labels say lost where it does not.

Anything in yellow sticks is a bound small molecule, which is usually the drug.

Go deeper
The number, in both the ways this project requires

Rank and raw effect, because this project has documented that a z-derived rank in the tail is close to a ranking of narrowness:

SMARCD1SMARCD2SMARCA4MEN1DOT1L
rank / 17,7285951016,3331184
raw difference-0.3574-0.145+0.0791-0.8656-0.231
KMT2A-r mean-0.7416-0.4163-0.4469-1.2629-0.6042
pan-essentiality-0.216-0.1633-0.3636-0.3631-0.148

SMARCD1's difference is more than twice SMARCD2's and about 1.5x DOT1L's, on a pan-essentiality that is not at the floor 2. Lineage-split, it is depleted in both halves, and more in the B-lineage half (-1.66) than the myeloid half (-0.86) - the opposite orientation to SMARCD2, which is the point 3.

What would have to be true for this to be real

Three cautions, all of which this entry would rather state than hide:

  1. A dependency screen measures what a line needs, not what a complex does. Nothing here says SMARCD1 acts through SWI/SNF in these cells.
  2. The BAF60 slot has three occupants. If SMARCD1 is the dominantly expressed one in lymphoid lines, its rank may be reporting expression rather than function - and this beat did not run an expression control.
  3. The only functional evidence is one screen hit and one ChIP-qPCR occupancy panel in a mouse myeloid line 4; nothing has been done in human KMT2A-rearranged cells.

The cheap decisive experiment is therefore an expression-controlled comparison of SMARCD1 against SMARCD2 and SMARCD3 in KMT2A-rearranged B-lineage lines, followed by a degron in one of them.

Facts and figures
uniprotQ96GM5
gene symbolSMARCD1
protein nameSWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily D member 1
length AA515
alphafold IDAF-Q96GM5-F1
accession resolutionUniProt REST gene_exact:SMARCD1 AND organism_id:9606 AND reviewed:true, run 2026-09-20; one reviewed row; gene_primary and length read back from the same record.
complexBAF60 slot, shared by cBAF, PBAF and ncBAF
classificationunwritten, well-ranked dependency: lineage-independent KMT2A-rearranged signal with essentially no primary literature
subnuclear localizationNONE ASSIGNED - A BOUNDED ABSENCE, not a NOT APPLICABLE. SMARCD1 is a soluble nuclear complex subunit, so a subnuclear answer is possible in principle; it has simply never been sought. The one positional measurement that exists is CHROMATIN OCCUPANCY rather than a compartment: BAF60a occupancy was detected at the E1-E5 MYC ENHANCER CLUSTER in MLL-AF9 RN2 cells [E_q91_smarcd1_loc3]. This entry deliberately keeps that apart from a subnuclear assignment, as gene-bicra keeps ncBAF's CTCF-site preference apart from a compartment - an enhancer address is a genomic coordinate, not a place in the nucleus.
localization shown for fusionPARTIAL, AND ONLY AS CHROMATIN OCCUPANCY, IN MLL-AF9 - NOT IN KMT2A::AFF1. BAF60a occupancy at the E1-E5 Myc enhancer cluster in murine MLL-AF9 RN2 cells is the whole of it [E_q91_smarcd1_loc3]; there is no image of the protein in any fusion-bearing cell, and nothing at all in the index fusion or in B-lineage disease. BAF/SWI-SNF in this project's own complex-enrichment analysis of the Skucha 2018 MLL-fusion interactome (analyses/mll-fusion-interactome-complexes/results.json) is 6 of 17 members recovered, p = 9.4e-05 and q_BH = 1.9e-04 AGAINST A 20,431-PROTEIN PROTEOME BACKGROUND - and that background is the one the analysis's own caveat says inflates significance for any complex of abundant nuclear proteins. Re-cast on a realistic denominator the row is NOT SIGNIFICANT: q = 0.0755 against the 5,754-protein nuclear background and q = 0.186 against the 4,600 proteins actually recovered before filtering. Restricted to the INDEX bait (MLL-AF4 = KMT2A::AFF1) only three BAF members appear at all - SMARCB1, SMARCC1, SMARCC2 - and only one of the three has p < 0.05. So nothing in this entry should be read as establishing BAF as a module of the index fusion's interactome; gene-smarcc1 carries the same correction at subunit level.
paralogues
[
  "SMARCD2 (Q92925, 531 aa)",
  "SMARCD3"
]
depmap
{
  "rank": 59,
  "of": 17728,
  "percentile": 0.333,
  "difference": -0.3574,
  "mean_kmt2a_r": -0.7416,
  "mean_other_leukaemia": -0.3841,
  "pan_essentiality_all_lines": -0.216,
  "empirical_p_vs_scan": 0.004174,
  "lineage_split_z_myeloid": -0.86,
  "lineage_split_z_b_lineage": -1.66,
  "verdict": "lineage-independent"
}
literature size
{
  "query": "SMARCD1 AND (MLL OR KMT2A)",
  "records": 1,
  "on_beat_after_title_check": 0,
  "second_query": "SMARCD1 AND leukemia",
  "second_records": 4,
  "alias_query": "BAF60A AND (MLL OR KMT2A)",
  "alias_records": 0,
  "date": "2026-09-20",
  "tool": "PubMed E-utilities esearch"
}
depmap kmt2a selectivity
{
  "chronos_mean_kmt2a_rearranged": -0.7416,
  "chronos_mean_other_leukaemia": -0.3841,
  "difference": -0.3574,
  "pan_essentiality_all_lines": -0.216,
  "selectivity_rank": 59,
  "rank_denominator": 17728,
  "provenance": "Joined 2026-09-21 from analyses/depmap-kmt2a-selective-scan-full (generated 2026-09-19T10:12:06Z), the project's own genome-wide scan over 11 KMT2A-rearranged and 43 other leukaemia DepMap lines. NOT re-fetched and NOT independent of that scan: every caveat it carries applies here, including that the KMT2A-rearranged arm is a small number of lines drawn from nine individuals, that the rank denominator is 17,728 genes, and that a difference is not a dependency. Added because only 26 of 308 gene entries carried this number, which made any KMT2A-selectivity question answerable for 8% of the corpus.",
  "how_to_read": "A negative difference means MORE required in KMT2A-rearranged lines than in other leukaemia lines. A rank near 17,728 is ANTI-selective. Neither is evidence of a fusion-driven dependency on its own: check pan_essentiality_all_lines before calling anything selective, and note that a paralogue-redundant gene can score near zero for reasons that have nothing to do with this disease - see ana-the-paralogue-redundancy-excuse-is-not-tested-and-my-proxy-decided-the-answer."
}
localization
{
  "CONSTITUTIVE": "NUCLEUS, and the experimental support UniProt cites for it contains no localisation experiment. UniProt Q96GM5 (fetched live 2026-09-21) carries exactly ONE location value, 'Nucleus', with two attributions: ECO:0000269 to PubMed:8804307 and a bare ECO:0000305 (curator inference). PubMed:8804307 is Wang et al. 1996, the paper that ISOLATED THE cDNAs for BAF155, BAF170 and BAF60 and characterised mammalian SWI/SNF complex composition by antibody-column co-purification. Its abstract describes cDNA cloning, complex membership and TISSUE expression and DESCRIBES NO SUBCELLULAR LOCALISATION EXPERIMENT AT ALL [E_q91_smarcd1_loc1]. A RULE-91 INSTANCE of the same shape tranche 3 found for BICRA: a co-purification paper cited as the experimental source of a compartment.",
  "what_can_be_defended": "SMARCD1 is a subunit of nuclear chromatin-remodelling complexes and its occupancy has been mapped on chromatin by ChIP in a fusion-bearing cell [E_q91_smarcd1_loc3], which is a stronger positional statement than any microscopy in the record. Nobody has imaged the protein."
}
cell type
{
  "PARALOGUE_TISSUE_SPLIT_IS_THE_ANSWER_AND_IT_WAS_IN_THE_FOUNDING_PAPER": "BAF60a (SMARCD1) is expressed in ALL TISSUES EXAMINED, whereas BAF60b is expressed preferentially in MUSCLE and BAF60c preferentially in PANCREAS; and BAF60a is present within the 2,000-kD BRG1 complex while BAF60b is in a distinct complex sharing some but not all subunits [E_q91_smarcd1_loc1]. That partly answers this entry's own first open question - which BAF60 paralogue is expressed in a blast - in the direction of SMARCD1, at bulk-tissue resolution and in 1996.",
  "in_a_fusion_cell": "MURINE MLL-AF9 RN2 acute myeloid leukaemia cells: BAF60a was a hit in the 93-hairpin SWI/SNF shRNA screen and its occupancy was detected at the Myc enhancer cluster there [E_q91_smarcd1_loc3]. Myeloid, murine, MLL-AF9 - not the index fusion and not B-lineage.",
  "never": "No human haematopoietic cell, no B-lineage cell, and no measurement of SMARCD1 protein abundance or compartment in any KMT2A::AFF1 sample."
}
cell state
{
  "not_recorded": "No cell-cycle, damage, differentiation or stress-dependent redistribution of SMARCD1 has been reported anywhere this beat could reach; UniProt records no induced localisation and no location note.",
  "the_state_that_matters_here_is_untested": "The dependency signal that put SMARCD1 in this graph is a CRISPR knockout rank. Whether the protein's abundance or its enhancer occupancy changes under menin inhibition - the state this project cares about most - has never been measured."
}
localization bounded absence
{
  "date": "2026-09-22",
  "tool": "NCBI esearch db=pubmed",
  "run_by": "Q91",
  "queries": [
    {
      "query": "SMARCD1[tiab]",
      "querytranslation": "\"SMARCD1\"[Title/Abstract]",
      "count": 87,
      "role": "operand control"
    },
    {
      "query": "BAF60a[tiab]",
      "querytranslation": "\"BAF60a\"[Title/Abstract]",
      "count": 60,
      "role": "second operand control on the name the founding literature uses"
    },
    {
      "query": "SMARCD1[tiab] AND (nuclear[tiab] OR localization[tiab])",
      "querytranslation": "\"SMARCD1\"[Title/Abstract] AND (\"nuclear\"[Title/Abstract] OR \"localization\"[Title/Abstract])",
      "count": 7
    },
    {
      "query": "BAF60a[tiab] AND (nuclear[tiab] OR localization[tiab])",
      "querytranslation": "\"BAF60a\"[Title/Abstract] AND (\"nuclear\"[Title/Abstract] OR \"localization\"[Title/Abstract])",
      "count": 14
    },
    {
      "query": "SMARCD1[tiab] AND MLL[tiab]",
      "querytranslation": "\"SMARCD1\"[Title/Abstract] AND \"MLL\"[Title/Abstract]",
      "count": 0
    },
    {
      "query": "BAF60a[tiab] AND MLL[tiab]",
      "querytranslation": "\"BAF60a\"[Title/Abstract] AND \"MLL\"[Title/Abstract]",
      "count": 0
    },
    {
      "query": "SMARCD1[tiab] AND KMT2A[tiab]",
      "querytranslation": "\"SMARCD1\"[Title/Abstract] AND \"KMT2A\"[Title/Abstract]",
      "count": 1
    }
  ],
  "reading": "BOTH fusion-scoped queries return ZERO while this entry's own E4 - PMID 24285714, Role of SWI/SNF in acute leukemia maintenance and enhancer-mediated Myc regulation - is an MLL-AF9 paper that names BAF60a as a screen hit and maps its occupancy. The paper is unreachable from either symbol because its abstract frames everything at the level of SWI/SNF. This is rule 64 and rule 71 demonstrated inside a single entry, against a paper the entry already cites. Titles and abstracts only (rule 80).",
  "absence_class": "never-measured"
}
How this could bite us back
  • No SMARCD1-directed chemical matter exists; a rank is not a target.
  • Two other paralogues occupy the same slot, so a selective agent would be exposed to substitution - and because nobody has measured which paralogue leukaemic complexes use, there is no assay to detect the switch.
  • SMARCD1's KMT2A-r mean of -0.74 is a strong dependency; its pan-essentiality of -0.22 means normal-tissue exposure is a real question that a leukaemia-only panel cannot answer.
Still open
  1. Which BAF60 paralogue is expressed in KMT2A-rearranged B-lineage blasts, and does SMARCD1's DepMap rank survive an expression control?
  2. Does acute SMARCD1 degradation in a KMT2A::AFF1 B-ALL line phenocopy the CRISPR result, and does it move HOXA9/MEIS1 or only MYC-adjacent programmes?
  3. Is SMARCD1 the BAF60 paralogue in leukaemic ncBAF? If so, its rank and BRD9's are measuring the same complex and should not be counted as independent evidence.
Every source behind this entry (8)
  1. E1established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database

    SMARCD1 is UniProt Q96GM5, 515 aa, primary gene SMARCD1, synonym BAF60A; it is one of three mutually exclusive BAF60 paralogues shared across cBAF, PBAF and ncBAF.

    UniProtKB Q96GM5 (SMRD1_HUMAN) · UniProt Consortium · UniProtKB 2026
    What this evidence cannot show

    gene_exact:SMARCD1 AND organism_id:9606 AND reviewed:true, run 2026-09-20; one reviewed row; gene_primary and length read back from the fetched record. SMARCD1 (515) and SMARCD2 (531) differ by 16 residues, so length is a weak discriminator between them.

    Evidence that argues against this (1)
    • ncBAF composition was defined as containing 'BAF60' without specifying the paralogue, so which SMARCD sits in ncBAF in a given cell is not established by that work. Alpsoy A et al. 2018
  2. E2moderate confidence 3 of 5: One strong study, or several smaller consistent ones.dataset

    SMARCD1 ranks 59 of 17,728 for KMT2A-rearranged selectivity (0.333rd percentile) with difference -0.3574, KMT2A-r mean -0.7416, other-leukaemia mean -0.3841, pan-essentiality -0.216, empirical p 0.0042.

    Genome-wide KMT2A-rearranged selectivity scan, 17,728 genes (DepMap Chronos via Open Targets) · Oncofusion knowledge graph, analyses/depmap-kmt2a-selective-scan-full/run.py · DepMap Chronos gene effect via Open Targets GraphQL 2026
    What this evidence cannot show

    11 index against 43 comparator leukaemia lines, none infant-derived; Cellosaurus fusion annotation may be incomplete; DepMap release version not stated by the API. Empirical p is the fraction of scanned genes with an equally extreme difference, i.e. a genome-wide background, not an independent null.

    Evidence that argues against this (1)
    • No expression control was run. If SMARCD1 is the dominant BAF60 paralogue in the index lines and SMARCD2 in the comparators, the difference would be an expression artefact rather than a selectivity result, and nothing in this scan can exclude that. Oncofusion knowledge graph et al. 2026
  3. E3moderate confidence 3 of 5: One strong study, or several smaller consistent ones.dataset

    SMARCD1 is one of only four SWI/SNF panel genes depleted in both halves of the lineage-split KMT2A-rearranged arm (myeloid z -0.86, B-lineage z -1.66), the others being BRD9, BICRA and SS18.

    SWI/SNF panel lineage-split DepMap dependency scan, 28 genes · Oncofusion knowledge graph, analyses/swi-snf-lineage-split/run.py · DepMap Chronos gene effect via Open Targets GraphQL 2026
    What this evidence cannot show

    Eight myeloid and five B-lineage index lines; z is in SDs of the 43-line comparator arm and is not an effect size. The B-lineage half is five lines, none infant.

    Evidence that argues against this (1)
    • SMARCD1 is also depleted in the two myeloid non-KMT2A reference lines (OCI-AML3 -1.07, U-937 -0.86), so the dependency is not confined to the rearrangement even though it is present in both of its lineage halves. Oncofusion knowledge graph et al. 2026
  4. E4strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    BAF60a was a hit in the 93-hairpin SWI/SNF shRNA screen in MLL-AF9/NrasG12D RN2 cells, and BAF60a occupancy was detected by ChIP at the E1-E5 distal Myc enhancer cluster in the same cells.

    Role of SWI/SNF in acute leukemia maintenance and enhancer-mediated Myc regulation. · Shi J, Whyte WA, Zepeda-Mendoza CJ, Milazzo JP, et al. · Genes Dev 2013
    PMID 24285714DOI
    What this evidence cannot show

    Mouse line; the occupancy detection is in a supplementary figure and is qualitative rather than quantified against a control locus in the main text. It establishes presence at the enhancers, not a requirement of SMARCD1 for their activity.

    Evidence that argues against this (1)
    • BAF250a (ARID1A) occupancy was detected at the same elements in the same experiment, so the observation identifies a SWI/SNF complex at the locus rather than a SMARCD1-specific function. Xiu Y et al. 2018
  5. E5moderate confidence 3 of 5: One strong study, or several smaller consistent ones.database

    SMARCD1 has no primary literature in KMT2A-rearranged leukaemia: `SMARCD1 AND (MLL OR KMT2A)` returns 1 record which title-checks to 0 on-beat (PMID 38114583, a neurodevelopmental de novo variant cohort naming SMARCD1 in a gene list), and `SMARCD1 AND leukemia` returns 4.

    What this evidence cannot show

    Bounded absence. Bounded to PubMed on 2026-09-20 over SMARCD1 and BAF60A. The single MLL/KMT2A hit was fetched in full and is a neurodevelopmental cohort paper that lists SMARCD1 and KMT2A among 46 genes - a co-mention, not a study. The four `SMARCD1 AND leukemia` records were NOT individually title-checked, so the statement about them is weaker than the statement about the conjunction, and the item is graded moderate for that reason.

    Evidence that argues against this (1)
    • The BAF60a result in PMID 24285714 is exactly the kind of finding a symbol query cannot reach, because the paper names the subunit only in BAF nomenclature. So the literature is not as empty as the count implies - it is unindexed. Shi J et al. 2013
  6. E_q91_smarcd1_loc1established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.database

    UniProtKB Q96GM5 (SMRD1_HUMAN, primary gene SMARCD1, 515 aa, read back live 2026-09-21) carries ONE subcellular location value, 'Nucleus', attributed to ECO:0000269 PubMed:8804307 plus a bare ECO:0000305. There is no location note, no annotated NLS and no isoform-scoped comment. PubMed:8804307 (Wang et al., Genes Dev 1996) isolated cDNAs for human BAF155, BAF170 and BAF60, showed the two SWI3 homologues copurify on antibody columns, and reported that BAF60a is expressed in ALL TISSUES EXAMINED while BAF60b is preferentially muscle and BAF60c preferentially pancreas, and that BAF60a is present within the 2,000-kD BRG1 complex whereas BAF60b is in a distinct complex. Its abstract reports no subcellular localisation experiment of any kind.

    What this evidence cannot show

    The abstract was read; the full text was not reached, so a fractionation panel inside the paper cannot be excluded and this is stated as 'no localisation experiment in reachable text' rather than 'none in the paper'. That is the same bound tranche 3 applied to BICRA, where the full text WAS read and contained zero microscopy.

    Evidence that argues against this (1)
    • The defence of this annotation would be that a protein purified out of a nuclear extract as part of a nuclear complex is obviously nuclear, so the citation is a formality. That defence fails on this project's own recent evidence. SMARCB1, a core subunit of the SAME complexes with the SAME purification history, is CYTOPLASMIC in 19% of primary atypical teratoid/rhabdoid tumours because a C-terminal truncation unmasks a nuclear export signal - a 102-tumour series. Complex membership does not guarantee a compartment, and for BAF subunits specifically there is a documented, clinically consequential exception. The right inference from an uninformative annotation is that the question is open, not that it is settled. Pathak R et al. 2021
  7. E_q91_smarcd1_loc3strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper

    In MURINE MLL-AF9 RN2 acute myeloid leukaemia cells, BAF60a was a hit in a 93-hairpin SWI/SNF-directed shRNA screen and BAF60a OCCUPANCY was detected at the E1-E5 MYC ENHANCER CLUSTER, placing SMARCD1 physically at the locus through which the SWI/SNF enhancer mechanism in this leukaemia runs.

    Role of SWI/SNF in acute leukemia maintenance and enhancer-mediated Myc regulation. · Shi J, Whyte WA, Zepeda-Mendoza CJ, Milazzo JP et al. · Genes Dev 2013
    PMID 24285714DOI
    What this evidence cannot show

    Murine, myeloid, MLL-AF9 - not the index fusion and not B-lineage (rule 73). It is a genomic address by ChIP, not a subcellular or subnuclear localisation, and this entry keeps the two apart deliberately. The screen readout is proliferation, not localisation.

    Evidence that argues against this (1)
    • This occupancy is the entry's strongest positional fact and it must not be promoted into a statement about the fusion's BAF dependency, because the complex-level statistics do not support one. BAF/SWI-SNF in this project's own complex-enrichment analysis of the Skucha 2018 MLL-fusion interactome (analyses/mll-fusion-interactome-complexes/results.json) is 6 of 17 members recovered, p = 9.4e-05 and q_BH = 1.9e-04 AGAINST A 20,431-PROTEIN PROTEOME BACKGROUND - and that background is the one the analysis's own caveat says inflates significance for any complex of abundant nuclear proteins. Re-cast on a realistic denominator the row is NOT SIGNIFICANT: q = 0.0755 against the 5,754-protein nuclear background and q = 0.186 against the 4,600 proteins actually recovered before filtering. Restricted to the INDEX bait (MLL-AF4 = KMT2A::AFF1) only three BAF members appear at all - SMARCB1, SMARCC1, SMARCC2 - and only one of the three has p < 0.05. So nothing in this entry should be read as establishing BAF as a module of the index fusion's interactome; gene-smarcc1 carries the same correction at subunit level. A single subunit's occupancy at one enhancer cluster in one murine myeloid line is compatible with BAF being present at active enhancers generally, which is what BAF does everywhere, and the enrichment analysis cannot distinguish that from a fusion-specific association. Skucha A et al. 2018
  8. E_q91_smarcd1_loc4moderate confidence 3 of 5: One strong study, or several smaller consistent ones.database

    Counted absence, 2026-09-22, querytranslation read back on every line. SMARCD1[tiab] = 87 and BAF60a[tiab] = 60 as operand controls; SMARCD1[tiab] AND MLL[tiab] = 0; BAF60a[tiab] AND MLL[tiab] = 0; SMARCD1[tiab] AND KMT2A[tiab] = 1. No subnuclear compartment has ever been assigned to SMARCD1.

    What this evidence cannot show

    Bounded by titles and abstracts (rule 80). Both the HGNC symbol and the field's own name were run; BAF60A in upper case, SMARCD1's UniProt entry name SMRD1 and the yeast/complex name SWP73 were not.

    Evidence that argues against this (1)
    • These two zeros are a demonstration that this entry's own bibliography refutes them, and that is the reason to record them. PMID 24285714, cited above as E_q91_smarcd1_loc3 and already this entry's E4, IS an MLL-AF9 paper that names BAF60a and maps its occupancy - and it is unreachable from BOTH symbols because its abstract frames the work as 'SWI/SNF' rather than naming a subunit. Rule 64 predicts precisely this and it fires here on a paper the entry was already citing. Any beat that bounds a BAF subunit in this disease by its symbol alone will produce a confident zero over a literature that exists. Shi J et al. 2013
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