| Topic | Key findings | Evidence type | Source (first author year) | Publication date | URL | Notes/limitations |
|---|---|---|---|---|---|---|
| identity/domains | ABTB1 is the human gene/protein targeted here (approved symbol ABTB1; synonym BPOZ), encoding an ankyrin repeat and BTB domain-containing protein; Open Targets lists ENSG00000114626 with approved name “ankyrin repeat and BTB domain containing 1.” (pqac-00000006, pqac-00000017) | Database annotation / target curation | Open Targets | 2025 platform paper; underlying evidence earlier | https://platform.opentargets.org/target/ENSG00000114626 | Database-level identity support; does not by itself prove mechanism. |
| identity/domains | BTB/POZ-domain proteins are a large eukaryotic family proposed to act as substrate-specific adaptors for CUL3 ubiquitin ligases; this family-level model is consistent with ABTB1’s BTB/POZ architecture. (pqac-00000001, pqac-00000005, pqac-00000012, pqac-00000013) | Biochemical complex biology / family inference | Geyer 2003 | Sep 2003 | https://doi.org/10.1016/S1097-2765(03)00341-1 | Evidence is family-level and yeast-centered; not direct human ABTB1 biochemistry. |
| molecular function | ABTB1 is described as a tumor suppressor and mediator of PTEN growth-suppressive signaling; prior work cited in later papers reports that ABTB1 overexpression decreases proliferation and inhibits G1/S progression in vitro. (pqac-00000008, pqac-00000016, pqac-00000024) | Functional cell biology / literature synthesis | Bousquet 2012; Nätkin 2023 | Nov 2012; Feb 2023 | https://doi.org/10.3324/haematol.2011.061515 ; https://doi.org/10.1371/journal.pone.0281645 | Primary direct mechanistic substrate of ABTB1 remains unclear in available context. |
| regulation | In myeloid cells, ABTB1 is a direct miR-125b target: ABTB1 mRNA was down-regulated 3.9-fold, protein decreased by ~60% with miR-125b overexpression, and increased ~40% with miR-125b inhibitor; luciferase assays validated direct 3'UTR targeting. (pqac-00000008, pqac-00000020, pqac-00000022, pqac-00000023) | Expression analysis / reporter assay / immunoblot | Bousquet 2012 | Nov 2012 | https://doi.org/10.3324/haematol.2011.061515 | Strong evidence for post-transcriptional regulation; effect shown in hematopoietic model rather than all tissues. |
| pathways | ABTB1 is repeatedly linked to PTEN growth-suppressive signaling; in prostate cancer transcriptomic analysis it remained androgen receptor (AR)-associated under androgen-deprivation adaptation. (pqac-00000016, pqac-00000018, pqac-00000024) | Expression/pathway analysis | Nätkin 2023 | Feb 2023 | https://doi.org/10.1371/journal.pone.0281645 | Pathway placement is partly based on prior literature cited by authors rather than direct pathway biochemistry in this paper. |
| localization | Direct ABTB1 localization evidence was limited in the retrieved human-focused context; no robust subcellular localization for human ABTB1 was established from the cited excerpts. (pqac-00000024) | Evidence gap | — | — | — | Important limitation: localization should not be overstated from current context. |
| disease/clinical associations | In prostate cancer, ABTB1 low vs high expression was associated with better progression-free survival in TCGA-based Cox analysis; authors therefore suggested ABTB1 inhibition might suppress prostate cancer cell proliferation. (pqac-00000018, pqac-00000025) | Expression/survival analysis | Nätkin 2023 | Feb 2023 | https://doi.org/10.1371/journal.pone.0281645 | Association is correlative and context-specific; contrasts with anti-proliferative narrative in other systems, implying context dependence or isoform complexity. |
| disease/clinical associations | Open Targets reports ABTB1 associations with refractive error, asthma, neurodegenerative disease, abnormality of refraction, and sialolithiasis, supported by GWAS credible sets and a glutamatergic-neuron CRISPRi screen. (pqac-00000017) | Genetic association / functional genomics | Open Targets | 2025 platform paper; evidence PMIDs earlier | https://platform.opentargets.org/target/ENSG00000114626 | Platform scores support prioritization, but causal mechanism and effect sizes are not provided in the retrieved context. |
| quantitative stats | Prostate cancer progression-free survival: ABTB1 low vs high expression HR 0.46, 95% CI 0.28–0.74, p=0.0013. (pqac-00000025) | Multivariable survival statistic | Nätkin 2023 | Feb 2023 | https://doi.org/10.1371/journal.pone.0281645 | Statistic comes from table image extraction; clinical endpoint defined as biochemical relapse or clinical tumor progression. |
| quantitative stats | Open Targets association scores for ABTB1 include refractive error 0.2878, asthma 0.2681, neurodegenerative disease 0.1988, abnormality of refraction 0.1418, and sialolithiasis 0.0452; individual evidence scores included 0.77882, 0.72245, and 0.52786 for specific evidence items. (pqac-00000017) | Prioritization scores / platform metrics | Open Targets | 2025 platform paper | https://platform.opentargets.org/target/ENSG00000114626 | Scores are platform-derived prioritization metrics, not direct effect sizes like odds ratios or hazard ratios. |


*Table: This table summarizes the main experimentally or computationally supported functional annotation evidence for human ABTB1 (UniProt Q969K4). It highlights what is known with direct support, what remains inferential, and where the strongest quantitative evidence currently lies.*