FUT4 - the myeloid alpha-1,3-fucosyltransferase, a hub gene of the KMT2A-rearranged expression module, and the gene HGNC once officially called CD15

[
  "CD15",
  "FCT3A",
  "ELFT"
]

{
  "chronos_mean_kmt2a_rearranged": -0.0971,
  "chronos_mean_other_leukaemia": -0.1878,
  "difference": 0.0907,
  "pan_essentiality_all_lines": -0.1162,
  "selectivity_rank": 16678,
  "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."
}

{
  "subcellular": "GOLGI APPARATUS, GOLGI STACK MEMBRANE, as a SINGLE-PASS TYPE II MEMBRANE PROTEIN. UniProt P22083 (fetched 2026-09-21) gives exactly this and nothing else, with Golgi apparatus and Membrane as its cellular-component keywords. FUT4 is a type II membrane glycosyltransferase: N-terminal cytoplasmic tail, one transmembrane span, catalytic domain in the Golgi lumen.",
  "subnuclear": "NOT APPLICABLE - AND THIS IS A CATEGORY STATEMENT, NOT A GAP. A single-pass type II Golgi membrane protein has no nuclear pool and therefore no subnuclear compartment. This is the distinction the Q71 brief asked to be made explicitly: FUT4 is NOT APPLICABLE, whereas FANCF, RELB and RYBP in this same tranche are UNPUBLISHED. Recording the two as the same kind of blank would be wrong.",
  "the_enzyme_is_not_its_product": "The enzyme sits in the Golgi; its PRODUCT, the Lewis-x/CD15 carbohydrate epitope, is displayed on glycoconjugates at the PLASMA MEMBRANE, which is where flow cytometry reads it and where an antibody therapeutic would act. Two different compartments, one gene, and the graph's plasma-membrane localization entry is about the second. Conflating them is the localisation form of the rule-69 error that FUT4 'is' CD15.",
  "explicit_no": "No localisation of FUT4 has been measured in any KMT2A-rearranged cell; the compartment above is the generic annotation for the enzyme class. Golgi sub-compartment (cis/medial/trans) is not resolved in the UniProt record.",
  "how_shown": "UniProt P22083 SUBCELLULAR LOCATION comment with topology, fetched 2026-09-21",
  "systems": "database annotation; no KMT2A-rearranged system",
  "shown_for_fusion_localisation": "no",
  "node": "localization-plasma-membrane-leukaemic-surface-antigens"
}

{
  "evidence_class_key": "concept-expressed-required-maintains-three-evidence-classes",
  "identifier_note": "FUT4 (P22083, 530 aa, 'Alpha-(1,3)-fucosyltransferase 4', synonyms ELFT and FCT3A) is the MYELOID alpha-1,3-fucosyltransferase and is not FUT7 (the leukocyte enzyme that predominates at PSGL-1) or FUT9 (which carries much of the human E-selectin ligand activity) [E_q71_ct1]. Brief rule 69 records the separate and more dangerous trap: HGNC lists CD15 as a PREVIOUS OFFICIAL SYMBOL of FUT4, and FUT4 helps BUILD Lewis-x rather than encoding it - so a flow report saying CD15 is reporting a carbohydrate epitope, not this gene's expression. FUT4 versus FUT9 is 530 against 359 aa, which rule 69 calls genuinely safe on length.",
  "expressed_in": {
    "class": 1,
    "summary": "MYELOID. FUT4 is the alpha-1,3-fucosyltransferase of white cells, functional in human leukocytic HL-60 and in murine neutrophils [E_q71_ct1], and this entry already records it as a hub gene of the KMT2A-rearranged expression module. This is the only gene in this tranche whose EXPRESSION is genuinely lineage-restricted rather than ubiquitous.",
    "nodes": [
      "cell-type-gmp",
      "cell-type-monocyte"
    ]
  },
  "required_in": {
    "class": 2,
    "claim": "In HUMAN HL-60 leukocytic cells and murine neutrophils, FUT4 makes a MINOR contribution to selectin-ligand biosynthesis, with FUT7 predominating at PSGL-1 and FUT9 carrying E-selectin ligand activity in human cells [E_q71_ct1]. This is a requirement for LEUKOCYTE ADHESION in inflammation, not for survival, and not in a KMT2A-rearranged cell.",
    "pmids": [
      "23192350"
    ],
    "system_named_in_the_claim": "human HL-60 myeloid leukaemia cells and murine bone-marrow neutrophils - no KMT2A rearrangement"
  },
  "not_required_in": {
    "claim": "ANTI-SELECTIVE, and barely a dependency at all. Chronos -0.0971 in the KMT2A-rearranged arm against -0.1878 in other leukaemias, difference +0.0907, rank 16,678 of 17,728, pan-essentiality -0.1162. Both arms are within noise of zero, so this is a NON-DEPENDENCY ranked on a dependency scale - the same category as SIRT1 and ATM in this tranche, though here both arms are weakly negative rather than positive.",
    "and_that_is_the_right_answer": "FUT4 is a marker gene and a hub of an expression module. Being a hub of a co-expression module is not being a dependency, and the scan correctly says so. This entry should be read as an antigen and expression-signature entry, not a target entry."
  },
  "context": "human myeloid leukocytes and murine neutrophils; this project's DepMap scan for the (non-)dependency"
}

{
  "evidence_class_key": "concept-expressed-required-maintains-three-evidence-classes",
  "maintains_state": {
    "class": 3,
    "states": [],
    "claim": "NO CELL STATE IN THIS GRAPH'S VOCABULARY IS MAINTAINED BY FUT4 on published evidence. The function documented is construction of selectin ligands for leukocyte rolling [E_q71_ct1] - an adhesion property of mature myeloid cells, and a general inflammatory-biology function rather than anything to do with this fusion.",
    "pmids": [
      "23192350"
    ],
    "system_named_in_the_claim": "human HL-60 cells and murine neutrophils in leukocyte-adhesion assays"
  },
  "confidence": "strong",
  "caveats": "No FUT4 measurement exists in a KMT2A-rearranged cell. The adhesion biology is inflammation, not leukaemia. And the human and murine answers differ, which the paper itself makes the point of.",
  "counter_evidence": {
    "note": "Two independent reasons not to build a FUT4 story here. First, within its own enzyme family FUT4 is the minor contributor - FUT7 predominates at PSGL-1 and FUT9 carries E-selectin ligand activity in human cells. Second, this graph's scan places FUT4 at rank 16,678 of 17,728 with both arms within noise of zero. A hub gene of an expression module that is neither the dominant enzyme nor a dependency is a marker, and the entry is correct to be titled for the naming problem rather than for a mechanism.",
    "citation": {
      "title": "Silencing α1,3-fucosyltransferases in human leukocytes reveals a role for FUT9 enzyme during E-selectin-mediated cell adhesion.",
      "authors": "Buffone A, Mondal N, Gupta R, McHugh KP, Lau JT, Neelamegham S",
      "year": 2013,
      "venue": "J Biol Chem",
      "pmid": "23192350",
      "doi": "10.1074/jbc.M112.400929",
      "type": "paper"
    }
  }
}

{
  "open_targets_dataversion": "26.06",
  "note": "Added by Q71 per brief rule 83; Open Targets dataVersion fetched live 2026-09-21 as year 26 month 06. Scan denominator for this gene: n_all_lines 1208."
}