id: A0A9L0JEY6
gene_symbol: PARD3B
taxon:
  id: NCBITaxon:9793
  label: Equus asinus
status: COMPLETE
description: 'Assessment of 2 ProtNLM2 GO predictions for donkey PARD3B (A0A9L0JEY6). Anchoring junction
  is correct but less precise than the bicellular tight junction annotation already in donkey GOA (LSP).
  Cell cycle is uncertain (UNC): a mouse Par3L knockout shows increased mitotic cells with aberrant spindles, but this loss-of-function phenotype does not establish a direct cell-cycle role. Non-GO ProtNLM2 outputs,
  not scored: subcellular locations ''Endomembrane system'' and ''Cell junction'', both matching locations
  reported for human PARD3B.'
source_documents:
- projects/PROTNLM_EVALUATION/donkey40/donkey40-predictions.tsv
- genes/EQUAS/PARD3B/PARD3B-goa.tsv
- genes/EQUAS/PARD3B/PARD3B-bioinformatics/Q8TEW8-uniprot.txt
- genes/EQUAS/PARD3B/PARD3B-bioinformatics/RESULTS.md
predictions:
- source_method: ProtNLM2
  source_version: UniProt API snapshot 2026-10-14
  predicted_term:
    id: GO:0007049
    label: cell cycle
  predicted_term_type: GO_BP
  review:
    assessment: UNC
    confidence_score: 1
    summary: The broad term cell cycle is not in donkey GOA, and no experimental GO annotation for human
      or mouse PARD3B places it in a cell-cycle process. Human PARD3B is described as a putative adapter
      in asymmetric cell division through its interaction with Inscuteable. The only direct cell-division
      evidence is a mouse knockout phenotype, in which Par3L-null intestinal epithelium has more mitotic
      cells and a higher fraction of defective spindles, accompanied by tumours. This is a loss-of-function
      phenotype in a tumour-prone tissue; it does not show which step of the cell cycle PARD3B performs or
      whether the spindle defects are direct, and the PARD3B-specific mechanism defined so far (LKB1 binding
      and restraint of its kinase activity) is a signalling role, not a cell-cycle step. The gene review
      removes the related TreeGrafter centrosome-localization term because it is a PARD3-derived transfer.
      The prediction is plausible but neither established nor refuted by the available evidence.
    supported_by:
    - reference_id: file:EQUAS/PARD3B/PARD3B-bioinformatics/Q8TEW8-uniprot.txt
      supporting_text: Putative adapter protein involved in asymmetrical cell
    - reference_id: file:EQUAS/PARD3B/PARD3B-bioinformatics/RESULTS.md
      supporting_text: Apart from protein binding and generic complex/cell-junction rows, no experimental
        GO annotation exists for either PARD3B ortholog.
    - reference_id: PMID:41274508
      supporting_text: Further analysis of the gastrointestinal track
        in the Par3L KO mice found increased mitotic cells, which have significantly
        higher ratios of aberrant spindles compared to that of the WT mice.
    - reference_id: PMID:24859006
      supporting_text: Unexpectedly, Par3L, but not Par3, binds to the tumour suppressor protein Lkb1 and
        inhibits its kinase activity.
- source_method: ProtNLM2
  source_version: UniProt API snapshot 2026-10-14
  predicted_term:
    id: GO:0070161
    label: anchoring junction
  predicted_term_type: GO_CC
  review:
    assessment: LSP
    confidence_score: 2
    summary: Human PARD3B colocalizes with TJP1 at epithelial tight junctions, and donkey GOA already
      contains bicellular tight junction (GO:0005923), which is a GO descendant of anchoring junction.
      The prediction is therefore correct but less precise than an existing supported annotation.
    supported_by:
    - reference_id: file:EQUAS/PARD3B/PARD3B-bioinformatics/Q8TEW8-uniprot.txt
      supporting_text: Colocalizes with TJP1 to epithelial tight junctions.
    - reference_id: file:EQUAS/PARD3B/PARD3B-bioinformatics/RESULTS.md
      supporting_text: aligned pairs 1202; identical 1061; identity over aligned pairs 88.27%
references:
- id: file:EQUAS/PARD3B/PARD3B-bioinformatics/Q8TEW8-uniprot.txt
  title: UniProt record for human PARD3B (Q8TEW8)
  findings: []
- id: file:EQUAS/PARD3B/PARD3B-bioinformatics/RESULTS.md
  title: 'PARD3B: donkey-human sequence comparison'
  findings: []
- id: PMID:41274508
  title: Polarity protein Par3L deletion causes chromosomal segregation defects and tumorigenesis.
  findings: []
- id: PMID:24859006
  title: The Par3-like polarity protein Par3L is essential for mammary stem cell maintenance.
  findings: []