ANKRD11

Summary: ANCO-1 is a nuclear transcriptional coregulator.

Reason: The original abstract explicitly describes nuclear localization and nuclear foci alongside p160-coregulator and HDAC interactions. Nuclear localization is consistent with the defining transcriptional role; the full article was not available for an independent assay-level reanalysis.

Summary: The curated nuclear location agrees with independent localization and function.

Reason: The available abstract concerns ANKRD11 abundance, degradation and human/mouse variants; it does not expose the localization experiment. UniProt attributes nuclear localization and prometaphase chromatin localization to this study. Independent nuclear observations and the transcriptional function corroborate the location, so the experimental curator is not overruled because the full source is unavailable. Those independent observations do not reconstruct this paper’s assay.

Summary: Human neural precursors and neurons contain nuclear ANKRD11.

Reason: The inspected original Figure 2 and human-precursor Results show nuclear ANKRD11 in human ESC-derived cortical precursors and neurons. Mouse precursor experiments separately establish chromatin association and HDAC3 proximity; their species and assay scope are retained. The original human localization was read separately from the abstract-only canonical cache. The attached HPA human-cell evidence corroborates nuclear location; the mouse chromatin/HDAC3 sentence is not used as a quotation for human nuclear localization.

Summary: GFP-ANKRD11 localizes predominantly to nuclei in cortical cultures.

Reason: The original full article reports predominantly nuclear GFP-ANKRD11 in mouse postnatal cortical neurons and glia, with a smaller cytoplasmic pool and depolarization-induced nuclear inclusions. The culture host is specified, but the exact construct sequence species is not stated in the inspected main Methods. Independent human-cell evidence corroborates the human nuclear annotation.

Summary: The combined electronic nucleus annotation agrees with direct target evidence.

Reason: The UniProt nuclear localization and independent human-cell immunofluorescence support the broad nucleus term. The exact historical ARBA condition set was not reconstructed; it is corroborating propagation rather than a new localization experiment.

Summary: The inherited nucleoplasmic location agrees with the target’s nuclear regulatory role.

Reason: PAINT’s ancestral assertion is consistent with direct human ANKRD11 localization and transcriptional function. The target appearing among its own descendant evidence is legitimate experimental grounding, not circularity. The exact ancestral node placement and full family alignment were not independently reconstructed; donor number is not treated as evidence strength.

Summary: Human-cell immunofluorescence supports the main nucleoplasmic location.

Reason: The directly inspected HPA record classifies nucleoplasm as the enhanced main location across multiple antibodies and cell lines. This supports the compartment used by the transcriptional core. The cell-line numeric column reports RNA abundance rather than staining intensity.

Summary: A cytosolic pool is observed alongside the dominant nuclear pool.

Reason: HPA directly reports enhanced cytosolic localization as an additional compartment, with antibody- and cell-line-dependent observations. Retain that experimental localization without inventing a distinct cytosolic mechanism; the characterized transcriptional function is nuclear.

Summary: Dental development is affected by pathogenic human ANKRD11 variants.

Reason: The human KBG cases establish characteristic macrodontia. Retain this supported developmental perturbation phenotype as non-core: a tooth-specific molecular step of ANKRD11 has not been established.

Summary: The skeletal morphogenesis association is compatible with the human disease evidence.

Reason: The electronic ARBA assertion agrees with skeletal abnormalities in human ANKRD11 disease. The historical rule was not reconstructed. Retain the physiological association as non-core rather than interpreting it as a separately demonstrated skeletal biochemical mechanism.

Summary: Human ANKRD11 variants produce skeletal abnormalities.

Reason: The original human case series identifies skeletal anomalies with pathogenic ANKRD11 variants. Retain this supported developmental association as non-core, distinguishing the phenotype from a separately demonstrated skeletal molecular mechanism.

Summary: Head morphogenesis is a broad context of ANKRD11-associated developmental abnormalities.

Reason: The broad electronic annotation is compatible with craniofacial abnormalities in human KBG syndrome. Exact historical ARBA conditions were not recovered. This remains a non-core developmental association; no independent head-specific molecular step is inferred.

Summary: Facial development is affected by pathogenic ANKRD11 variants.

Reason: Human craniofacial findings support the broad developmental association represented by the ARBA annotation. Historical rule conditions were not recovered. The annotation is retained as a phenotypic context without adding a second core mechanism.

Summary: Human KBG syndrome provides perturbation evidence for facial morphogenesis.

Reason: The original human variant series reports characteristic craniofacial findings. Retain the supported facial-development phenotype as non-core while separating this developmental outcome from the protein’s transcriptional coregulator activity.

Summary: ANKRD11 modulates transcription through interactions with transcriptional regulators.

Reason: Nuclear-receptor/p160 interactions and reporter repression, endogenous ANCO-1 perturbation, and independent p53-associated coactivation establish a transcription coregulator function. The unsigned term captures the partner-dependent direction without adding redundant coactivator/corepressor children. Gal4 supplies DNA targeting in the domain assays; those assays do not establish native sequence-specific DNA binding. Partner HDAC/HAT chemistry is not assigned to ANKRD11.

Summary: ANKRD11 directly participates in transcriptional regulation through its coregulator activity.

Reason: ANKRD11 supplies regulatory protein interactions and experimentally mapped repression/activation domains. In PMID:17521611, endogenous ANCO-1 depletion increased progesterone-receptor-dependent reporter transcription, with dose dependence and a second independent shRNA; domain/deletion reporter assays independently support regulatory work by the protein. This is direct transcriptional coregulation, rather than a developmental phenotype or a substrate requirement. The available PMID:18840648 abstract reports ANKRD11-dependent p53 activation of CDKN1A, supporting the unsigned process term across partner contexts. The RNA polymerase II process is distinct from the molecular-function term GO:0003712. No signed child, DNA-binding specificity or partner catalytic activity is inferred. Term-parent, comparator and local GO-CAM checks are documented in the notes.