ACTL8

Summary: Retain the broad compartment assignment without treating it as exclusive localization.

Reason: The ancestral actin-family compartment inference is biologically compatible with ACTL8. The local analysis lists human annotation recipients and sequence identities; it does not reconstruct tree topology or establish a node-placement error. Retain this compartment as non-core while the physiological molecular function is unresolved. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The inherited synapse assertion remains unresolved for divergent ACTL8.

Reason: The PAINT cache confirms the IBD at PTN007551913. The local analysis documents sequence/interface divergence and unusual human annotation recipients, but does not reconstruct the family tree or demonstrate a misplaced ancestral assertion. Its ACTR3 control has lower conventional-actin contact conservation yet contributes to a filament branch, so those scores do not prove loss of every structural or filament-associated role. Testis enrichment, a short donor list and lack of a target assay likewise do not establish biological exclusion. The neuronal/postsynaptic context needs target-specific localization or a resolved phylogenetic loss argument; primary tissue enrichment is not evidence of zero neuronal expression. A neutral focused OpenScientist assessment is pending. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: Retain the broad compartment assignment without treating it as exclusive localization.

Reason: The ancestral actin-family compartment inference is biologically compatible with ACTL8. The local analysis lists human annotation recipients and sequence identities; it does not reconstruct tree topology or establish a node-placement error. Retain this compartment as non-core while the physiological molecular function is unresolved. PMID:41129177 independently reports focal cytoplasmic staining in human tumor tissue, providing direct target support. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The inherited membrane assertion remains unresolved for divergent ACTL8.

Reason: The PAINT cache confirms the IBD at PTN007551913. The local analysis documents sequence/interface divergence and unusual human annotation recipients, but does not reconstruct the family tree or demonstrate a misplaced ancestral assertion. Its ACTR3 control has lower conventional-actin contact conservation yet contributes to a filament branch, so those scores do not prove loss of every structural or filament-associated role. Testis enrichment, a short donor list and lack of a target assay likewise do not establish biological exclusion. Peripheral membrane association does not require a transmembrane segment or a conventional cortical actin polymer. A neutral focused OpenScientist assessment is pending. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The inherited axon assertion remains unresolved for divergent ACTL8.

Reason: The PAINT cache confirms the IBD at PTN007551913. The local analysis documents sequence/interface divergence and unusual human annotation recipients, but does not reconstruct the family tree or demonstrate a misplaced ancestral assertion. Its ACTR3 control has lower conventional-actin contact conservation yet contributes to a filament branch, so those scores do not prove loss of every structural or filament-associated role. Testis enrichment, a short donor list and lack of a target assay likewise do not establish biological exclusion. The neuronal/postsynaptic context needs target-specific localization or a resolved phylogenetic loss argument; primary tissue enrichment is not evidence of zero neuronal expression. A neutral focused OpenScientist assessment is pending. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The inherited structural constituent of postsynaptic actin cytoskeleton assertion remains unresolved for divergent ACTL8.

Reason: The PAINT cache confirms the IBD at PTN002631586. The local analysis documents sequence/interface divergence and unusual human annotation recipients, but does not reconstruct the family tree or demonstrate a misplaced ancestral assertion. Its ACTR3 control has lower conventional-actin contact conservation yet contributes to a filament branch, so those scores do not prove loss of every structural or filament-associated role. Testis enrichment, a short donor list and lack of a target assay likewise do not establish biological exclusion. The neuronal/postsynaptic context needs target-specific localization or a resolved phylogenetic loss argument; primary tissue enrichment is not evidence of zero neuronal expression. A neutral focused OpenScientist assessment is pending. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The inherited actin filament assertion remains unresolved for divergent ACTL8.

Reason: The PAINT cache confirms the IBD at PTN002631586. The local analysis documents sequence/interface divergence and unusual human annotation recipients, but does not reconstruct the family tree or demonstrate a misplaced ancestral assertion. Its ACTR3 control has lower conventional-actin contact conservation yet contributes to a filament branch, so those scores do not prove loss of every structural or filament-associated role. Testis enrichment, a short donor list and lack of a target assay likewise do not establish biological exclusion. A neutral focused OpenScientist assessment is pending. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The inherited axonogenesis assertion remains unresolved for divergent ACTL8.

Reason: The PAINT cache confirms the IBD at PTN007551913. The local analysis documents sequence/interface divergence and unusual human annotation recipients, but does not reconstruct the family tree or demonstrate a misplaced ancestral assertion. Its ACTR3 control has lower conventional-actin contact conservation yet contributes to a filament branch, so those scores do not prove loss of every structural or filament-associated role. Testis enrichment, a short donor list and lack of a target assay likewise do not establish biological exclusion. The neuronal/postsynaptic context needs target-specific localization or a resolved phylogenetic loss argument; primary tissue enrichment is not evidence of zero neuronal expression. A neutral focused OpenScientist assessment is pending. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The inherited protein kinase binding assertion remains unresolved for divergent ACTL8.

Reason: The PAINT cache confirms the IBD at PTN007551913. The local analysis documents sequence/interface divergence and unusual human annotation recipients, but does not reconstruct the family tree or demonstrate a misplaced ancestral assertion. Its ACTR3 control has lower conventional-actin contact conservation yet contributes to a filament branch, so those scores do not prove loss of every structural or filament-associated role. Testis enrichment, a short donor list and lack of a target assay likewise do not establish biological exclusion. Protein kinase binding is a defined interaction class, not generic protein binding; the source experiment and conserved interface need assessment. A neutral focused OpenScientist assessment is pending. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The inherited NuA4 histone acetyltransferase complex assertion remains unresolved for divergent ACTL8.

Reason: The PAINT cache confirms the IBD at PTN007551913. The local analysis documents sequence/interface divergence and unusual human annotation recipients, but does not reconstruct the family tree or demonstrate a misplaced ancestral assertion. Its ACTR3 control has lower conventional-actin contact conservation yet contributes to a filament branch, so those scores do not prove loss of every structural or filament-associated role. Testis enrichment, a short donor list and lack of a target assay likewise do not establish biological exclusion. Complex membership can be inherited phylogenetically. The named ACTB/ACTL6A subunits in a descriptive definition do not logically exclude another subunit; no ACTL8-specific loss has been demonstrated. A neutral focused OpenScientist assessment is pending. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The inherited cell motility assertion remains unresolved for divergent ACTL8.

Reason: The PAINT cache confirms the IBD at PTN007551913. The local analysis documents sequence/interface divergence and unusual human annotation recipients, but does not reconstruct the family tree or demonstrate a misplaced ancestral assertion. Its ACTR3 control has lower conventional-actin contact conservation yet contributes to a filament branch, so those scores do not prove loss of every structural or filament-associated role. Testis enrichment, a short donor list and lack of a target assay likewise do not establish biological exclusion. Cancer-cell migration phenotypes support a connection but do not yet identify ACTL8’s work in the motility machinery or a specific regulatory step. A neutral focused OpenScientist assessment is pending. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: Retain the broader cytoskeletal inference consistently with the actin-cytoskeleton annotation.

Reason: The UniProt cytoskeletal statement is a similarity inference and the parent compartment is compatible with the retained IBA. This is not independent experimental confirmation and does not prove a particular filament-assembly mechanism. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The inherited postsynaptic actin cytoskeleton organization assertion remains unresolved for divergent ACTL8.

Reason: The automatic MF-to-BP inference depends on GO:0098973, now UNDECIDED. Neither conventional-actin interface divergence nor tissue enrichment establishes loss of all postsynaptic structural contributions, so the derived process is also unresolved rather than confidently removed. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The CERT1 interaction remains a lead, but generic protein binding is uninformative.

Reason: The interaction-screen evidence is not declared false. Remove the generic term under project policy; orthogonal validation and functional assays are needed before assigning a more informative molecular function. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The CERT1 interaction remains a lead, but generic protein binding is uninformative.

Reason: The interaction-screen evidence is not declared false. Remove the generic term under project policy; orthogonal validation and functional assays are needed before assigning a more informative molecular function. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.

Summary: The inherited epithelial cell differentiation assertion remains unresolved for divergent ACTL8.

Reason: PMID:21492153 reports differentially regulated proteins during Caco-2 differentiation. The cached abstract does not resolve the ACTL8-specific result or mechanistic participation. Tissue enrichment does not disprove expression in this cell line, and lack of full text prevents a confident exclusion or functional upgrade. The previous donor-by-donor records are preserved in the linked superseded-assessment artifact. The existing RESULTS analysis also preserves filament-interface and DNase-I-loop comparisons. Those site-specific differences motivate a test of altered assembly; sequence identity or recipient counts alone do not establish loss of this particular ancestral function.