AKIRIN1 (Akirin-1/Mighty) is a small nuclear transcriptional cofactor associated with chromatin-dependent gene regulation. Mammalian Akirin1 studies support a promyogenic role involving myogenic gene expression, myoblast migration and differentiation, with proliferation effects that depend on cell state and experimental conditions. Mouse Akirin1 also promotes macrophage chemotaxis and lamellipodium formation through PI3K-dependent actin reorganization; these capacities are inferred to human AKIRIN1 through conserved ancestry. Human AKIRIN1 has direct nuclear-localization evidence, while its detailed transcriptional partners and the connection between nuclear regulation and motility remain incompletely resolved.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0005634 nucleus | IBA GO_REF:0000033 | ACCEPT | Summary: Nuclear localization is supported directly for human AKIRIN1 and by inheritance. Reason: PMID:18066067 expresses tagged HsAkirin1 in HeLa cells and shows NLS-dependent nuclear localization. The source location is retained; the actual PTN000329080 nuclear assertion is also ancestral to the target. Neither broader versus narrower nuclear location nor evidence redundancy changes its biological correctness. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000329080 SUPPORTS TRANSFER The actual PTHR13293 target lineage includes this positive IBD. Exact mouse Akirin1 evidence supports the myogenic/motility branch; the separate innate-immune IRD does not negate this term. Supporting Evidence: PMID:18066067 the nuclear localization of HsAkirin1 and HsAkirin2 file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Nuclear/chromatin/cofactor/transcription assertions descend from PTN000329080. |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IBA GO_REF:0000033 | ACCEPT | Summary: Positive regulation of RNA polymerase II transcription is supported as an inherited Akirin function. Reason: The actual target lineage descends from the positive PTN000329080 IBDs. The Akirin1-specific myogenic transcriptional outcomes and mouse promoter-reporter evidence are compatible with this ancestral judgment. The old rationale overstated direct human AKIRIN1 NF-kappaB evidence: PMID:18066067 tested HsAkirin2 in the fly immune rescue and found normal tested cytokine responses in Akirin1-null mouse cells. The term-specific innate-immune IRD at PTN002665250 does not erase the broader positive cofactor, transcription or chromatin assertions. Detailed recruitment partners in human AKIRIN1 remain incompletely resolved. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000329080 SUPPORTS TRANSFER The actual PTHR13293 target lineage includes this positive IBD. Exact mouse Akirin1 evidence supports the myogenic/motility branch; the separate innate-immune IRD does not negate this term. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Nuclear/chromatin/cofactor/transcription assertions descend from PTN000329080. PMID:30746755 Akirin1 regulated the transcription of muscle-specific RING finger 1 (MuRF-1) file:human/AKIRIN1/AKIRIN1-deep-research-falcon.md the most direct mechanistic NF-ΞΊB/SWI-SNF bridging evidence is from Drosophila Akirin and mammalian Akirin2-centered work |
| GO:0000785 chromatin | IBA GO_REF:0000033 | ACCEPT | Summary: Chromatin association is supported as an inherited Akirin function. Reason: The actual target lineage descends from the positive PTN000329080 IBDs. The Akirin1-specific myogenic transcriptional outcomes and mouse promoter-reporter evidence are compatible with this ancestral judgment. The old rationale overstated direct human AKIRIN1 NF-kappaB evidence: PMID:18066067 tested HsAkirin2 in the fly immune rescue and found normal tested cytokine responses in Akirin1-null mouse cells. The term-specific innate-immune IRD at PTN002665250 does not erase the broader positive cofactor, transcription or chromatin assertions. Detailed recruitment partners in human AKIRIN1 remain incompletely resolved. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000329080 SUPPORTS TRANSFER The actual PTHR13293 target lineage includes this positive IBD. Exact mouse Akirin1 evidence supports the myogenic/motility branch; the separate innate-immune IRD does not negate this term. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Nuclear/chromatin/cofactor/transcription assertions descend from PTN000329080. PMID:30746755 Akirin1 regulated the transcription of muscle-specific RING finger 1 (MuRF-1) file:human/AKIRIN1/AKIRIN1-deep-research-falcon.md the most direct mechanistic NF-ΞΊB/SWI-SNF bridging evidence is from Drosophila Akirin and mammalian Akirin2-centered work |
| GO:0003712 transcription coregulator activity | IBA GO_REF:0000033 | ACCEPT | Summary: Transcription coregulator activity is supported as an inherited Akirin function. Reason: The actual target lineage descends from the positive PTN000329080 IBDs. The Akirin1-specific myogenic transcriptional outcomes and mouse promoter-reporter evidence are compatible with this ancestral judgment. The old rationale overstated direct human AKIRIN1 NF-kappaB evidence: PMID:18066067 tested HsAkirin2 in the fly immune rescue and found normal tested cytokine responses in Akirin1-null mouse cells. The term-specific innate-immune IRD at PTN002665250 does not erase the broader positive cofactor, transcription or chromatin assertions. Detailed recruitment partners in human AKIRIN1 remain incompletely resolved. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN000329080 SUPPORTS TRANSFER The actual PTHR13293 target lineage includes this positive IBD. Exact mouse Akirin1 evidence supports the myogenic/motility branch; the separate innate-immune IRD does not negate this term. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Nuclear/chromatin/cofactor/transcription assertions descend from PTN000329080. PMID:30746755 Akirin1 regulated the transcription of muscle-specific RING finger 1 (MuRF-1) file:human/AKIRIN1/AKIRIN1-deep-research-falcon.md the most direct mechanistic NF-ΞΊB/SWI-SNF bridging evidence is from Drosophila Akirin and mammalian Akirin2-centered work |
| GO:0010592 positive regulation of lamellipodium assembly | IBA GO_REF:0000033 | ACCEPT | Summary: Positive regulation of lamellipodium assembly is supported by the exact mouse Akirin1 ortholog and actual positive ancestry. Reason: Mouse Q99LF1 is Akirin1/Mighty, not Akirin2. Its experimentally curated source annotations cite PMID:19406121, whose abstract reports increased macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. The target lies below the matching PTN002665250 IBD. Nuclear localization does not preclude regulation of cytoskeletal behavior, and viable knockout animals do not refute a cellular capacity. Retain the conserved inference without representing it as a direct human experiment or an identified actin-binding mechanism. Complete source article access remains unavailable, limiting mechanistic detail rather than overturning the positive evidence. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN002665250 SUPPORTS TRANSFER The actual PTHR13293 target lineage includes this positive IBD. Exact mouse Akirin1 evidence supports the myogenic/motility branch; the separate innate-immune IRD does not negate this term. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:19406121 more efficient lamellipodia formation via a PI3 kinase dependent pathway file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Mouse Akirin1 promotes macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. |
| GO:0010759 positive regulation of macrophage chemotaxis | IBA GO_REF:0000033 | ACCEPT | Summary: Positive regulation of macrophage chemotaxis is supported by the exact mouse Akirin1 ortholog and actual positive ancestry. Reason: Mouse Q99LF1 is Akirin1/Mighty, not Akirin2. Its experimentally curated source annotations cite PMID:19406121, whose abstract reports increased macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. The target lies below the matching PTN002665250 IBD. Nuclear localization does not preclude regulation of cytoskeletal behavior, and viable knockout animals do not refute a cellular capacity. Retain the conserved inference without representing it as a direct human experiment or an identified actin-binding mechanism. Complete source article access remains unavailable, limiting mechanistic detail rather than overturning the positive evidence. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN002665250 SUPPORTS TRANSFER The actual PTHR13293 target lineage includes this positive IBD. Exact mouse Akirin1 evidence supports the myogenic/motility branch; the separate innate-immune IRD does not negate this term. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:19406121 more efficient lamellipodia formation via a PI3 kinase dependent pathway file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Mouse Akirin1 promotes macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. |
| GO:0014839 myoblast migration involved in skeletal muscle regeneration | IBA GO_REF:0000033 | ACCEPT | Summary: Myoblast migration is supported by the exact mouse Akirin1 ortholog and actual positive ancestry. Reason: Mouse Q99LF1 is Akirin1/Mighty, not Akirin2. Its experimentally curated source annotations cite PMID:19406121, whose abstract reports increased macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. The target lies below the matching PTN002665250 IBD. Nuclear localization does not preclude regulation of cytoskeletal behavior, and viable knockout animals do not refute a cellular capacity. Retain the conserved inference without representing it as a direct human experiment or an identified actin-binding mechanism. Complete source article access remains unavailable, limiting mechanistic detail rather than overturning the positive evidence. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN002665250 SUPPORTS TRANSFER The actual PTHR13293 target lineage includes this positive IBD. Exact mouse Akirin1 evidence supports the myogenic/motility branch; the separate innate-immune IRD does not negate this term. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:19406121 more efficient lamellipodia formation via a PI3 kinase dependent pathway file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Mouse Akirin1 promotes macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. |
| GO:0045663 positive regulation of myoblast differentiation | IBA GO_REF:0000033 | ACCEPT | Summary: AKIRIN1 is a conserved positive regulator of myoblast differentiation. Reason: The matching mouse Akirin1 primary studies directly connect its overexpression to earlier MyoD expression and enhanced terminal myogenesis. The target inherits the positive PTN002665250 assertion, and the direct C2C12 experiments in PMID:23516508 support the same promyogenic capacity under glucocorticoid stress. These are active gene-regulatory effects, not merely the consequences of generic viability. Muscle differentiation is a well-supported biological role and is retained as core with its ortholog-inference scope. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN002665250 SUPPORTS TRANSFER The actual PTHR13293 target lineage includes this positive IBD. Exact mouse Akirin1 evidence supports the myogenic/motility branch; the separate innate-immune IRD does not negate this term. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:18255059 enhanced and accelerated differentiation and hypertrophy of myotubes file:human/AKIRIN1/AKIRIN1-deep-research-falcon.md promyogenic nuclear factor |
| GO:1902723 negative regulation of skeletal muscle satellite cell proliferation | IBA GO_REF:0000033 | ACCEPT | Summary: Retain context-dependent negative regulation of satellite-cell proliferation. Reason: The original dismissal treated positive proliferation under glucocorticoid rescue as a universal sign. Mouse Akirin1 source PMID:18255059 instead reports earlier cell-cycle withdrawal during differentiation, and the actual target descends from the negative-proliferation IBD at PTN002665250. Independently, goat Akirin1 overexpression reduces proliferation markers and EdU/CCK-8 outcomes in PMID:40211850. These results can coexist with improved proliferation in the distinct C2C12 dexamethasone experiment of PMID:23516508. Retain the inherited capacity with state and assay limits; the evidence does not imply constitutive suppression in every muscle-cell context. Propagation Review Root cause: NO FAILURE CORE Sources checked: PANTHER:PTN002665250 SUPPORTS TRANSFER The actual PTHR13293 target lineage includes this positive IBD. Exact mouse Akirin1 evidence supports the myogenic/motility branch; the separate innate-immune IRD does not negate this term. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:18255059 early withdrawal of myoblasts from the cell cycle PMID:40211850 adding Akirin1 restrained newly formed cells and viable cells |
| GO:0005634 nucleus | IEA GO_REF:0000044 | ACCEPT | Summary: Nuclear localization is supported directly for human AKIRIN1 and by inheritance. Reason: PMID:18066067 expresses tagged HsAkirin1 in HeLa cells and shows NLS-dependent nuclear localization. The source location is retained; the actual PTN000329080 nuclear assertion is also ancestral to the target. Neither broader versus narrower nuclear location nor evidence redundancy changes its biological correctness. Supporting Evidence: PMID:18066067 the nuclear localization of HsAkirin1 and HsAkirin2 file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Nuclear/chromatin/cofactor/transcription assertions descend from PTN000329080. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: Retain the verified binary interaction as non-core, without an unsupported complex-binding replacement. Reason: Remove the generic protein-binding annotation because it does not describe a specific molecular function. The interaction evidence and source attribution are retained; this curation action does not assert that the reported association is false. The inspected evidence does not justify an informative replacement function for this particular row. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-uniprot.txt Q9H9L7; Q9HD26: GOPC; NbExp=3; IntAct=EBI-10309796, EBI-349832 file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The real binary interaction is retained as evidence, but it does not support the old replacement GO:0044877 protein-containing complex binding. |
| GO:0010592 positive regulation of lamellipodium assembly | IEA GO_REF:0000107 | ACCEPT | Summary: Positive regulation of lamellipodium assembly is supported by the exact mouse Akirin1 ortholog and actual positive ancestry. Reason: Mouse Q99LF1 is Akirin1/Mighty, not Akirin2. Its experimentally curated source annotations cite PMID:19406121, whose abstract reports increased macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. The target lies below the matching PTN002665250 IBD. Nuclear localization does not preclude regulation of cytoskeletal behavior, and viable knockout animals do not refute a cellular capacity. Retain the conserved inference without representing it as a direct human experiment or an identified actin-binding mechanism. Complete source article access remains unavailable, limiting mechanistic detail rather than overturning the positive evidence. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:19406121 more efficient lamellipodia formation via a PI3 kinase dependent pathway file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Mouse Akirin1 promotes macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. |
| GO:0010759 positive regulation of macrophage chemotaxis | IEA GO_REF:0000107 | ACCEPT | Summary: Positive regulation of macrophage chemotaxis is supported by the exact mouse Akirin1 ortholog and actual positive ancestry. Reason: Mouse Q99LF1 is Akirin1/Mighty, not Akirin2. Its experimentally curated source annotations cite PMID:19406121, whose abstract reports increased macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. The target lies below the matching PTN002665250 IBD. Nuclear localization does not preclude regulation of cytoskeletal behavior, and viable knockout animals do not refute a cellular capacity. Retain the conserved inference without representing it as a direct human experiment or an identified actin-binding mechanism. Complete source article access remains unavailable, limiting mechanistic detail rather than overturning the positive evidence. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:19406121 more efficient lamellipodia formation via a PI3 kinase dependent pathway file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Mouse Akirin1 promotes macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. |
| GO:0014839 myoblast migration involved in skeletal muscle regeneration | IEA GO_REF:0000107 | ACCEPT | Summary: Myoblast migration is supported by the exact mouse Akirin1 ortholog and actual positive ancestry. Reason: Mouse Q99LF1 is Akirin1/Mighty, not Akirin2. Its experimentally curated source annotations cite PMID:19406121, whose abstract reports increased macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. The target lies below the matching PTN002665250 IBD. Nuclear localization does not preclude regulation of cytoskeletal behavior, and viable knockout animals do not refute a cellular capacity. Retain the conserved inference without representing it as a direct human experiment or an identified actin-binding mechanism. Complete source article access remains unavailable, limiting mechanistic detail rather than overturning the positive evidence. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:19406121 more efficient lamellipodia formation via a PI3 kinase dependent pathway file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Mouse Akirin1 promotes macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. |
| GO:0045663 positive regulation of myoblast differentiation | IEA GO_REF:0000107 | ACCEPT | Summary: AKIRIN1 is a conserved positive regulator of myoblast differentiation. Reason: The matching mouse Akirin1 primary studies directly connect its overexpression to earlier MyoD expression and enhanced terminal myogenesis. The target inherits the positive PTN002665250 assertion, and the direct C2C12 experiments in PMID:23516508 support the same promyogenic capacity under glucocorticoid stress. These are active gene-regulatory effects, not merely the consequences of generic viability. Muscle differentiation is a well-supported biological role and is retained as core with its ortholog-inference scope. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:18255059 enhanced and accelerated differentiation and hypertrophy of myotubes file:human/AKIRIN1/AKIRIN1-deep-research-falcon.md promyogenic nuclear factor |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IEA GO_REF:0000107 | ACCEPT | Summary: Positive regulation of RNA polymerase II transcription is supported as an inherited Akirin function. Reason: The actual target lineage descends from the positive PTN000329080 IBDs. The Akirin1-specific myogenic transcriptional outcomes and mouse promoter-reporter evidence are compatible with this ancestral judgment. The old rationale overstated direct human AKIRIN1 NF-kappaB evidence: PMID:18066067 tested HsAkirin2 in the fly immune rescue and found normal tested cytokine responses in Akirin1-null mouse cells. The term-specific innate-immune IRD at PTN002665250 does not erase the broader positive cofactor, transcription or chromatin assertions. Detailed recruitment partners in human AKIRIN1 remain incompletely resolved. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Nuclear/chromatin/cofactor/transcription assertions descend from PTN000329080. PMID:30746755 Akirin1 regulated the transcription of muscle-specific RING finger 1 (MuRF-1) file:human/AKIRIN1/AKIRIN1-deep-research-falcon.md the most direct mechanistic NF-ΞΊB/SWI-SNF bridging evidence is from Drosophila Akirin and mammalian Akirin2-centered work |
| GO:1902723 negative regulation of skeletal muscle satellite cell proliferation | IEA GO_REF:0000107 | ACCEPT | Summary: Retain context-dependent negative regulation of satellite-cell proliferation. Reason: The original dismissal treated positive proliferation under glucocorticoid rescue as a universal sign. Mouse Akirin1 source PMID:18255059 instead reports earlier cell-cycle withdrawal during differentiation, and the actual target descends from the negative-proliferation IBD at PTN002665250. Independently, goat Akirin1 overexpression reduces proliferation markers and EdU/CCK-8 outcomes in PMID:40211850. These results can coexist with improved proliferation in the distinct C2C12 dexamethasone experiment of PMID:23516508. Retain the inherited capacity with state and assay limits; the evidence does not imply constitutive suppression in every muscle-cell context. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:18255059 early withdrawal of myoblasts from the cell cycle PMID:40211850 adding Akirin1 restrained newly formed cells and viable cells |
| GO:1902725 negative regulation of satellite cell differentiation | IEA GO_REF:0000107 | ACCEPT | Summary: Retain reduced satellite/reserve-cell differentiation, distinct from increased terminal myogenesis. Reason: GO:1902725 negatively regulates GO:0014816, which defines acquisition of satellite-cell features. The old review conflated this with a satellite-derived myoblast differentiating into a myotube. The exact mouse Q99LF1 MGI IMP source is PMID:18255059. Related primary work in the Dyer 2006 thesis describes reduced reserve-cell populations and reduced Sca-1/CD34 in Mighty-overexpressing C2C12 cultures alongside increased myotube fusion. This is consistent with the standing curator-supported transfer; the positive myogenesis result does not contradict it. The original journal full text remains unavailable and reserve-cell markers are not lineage tracing, so the precise mechanism remains a follow-up, not a confident reversal of the annotation. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md It is not synonymous with a satellite-derived myoblast forming a myotube. file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md This corroborates the compatibility of reduced satellite/reserve identity with positive terminal myogenesis. PMID:18255059 enhanced and accelerated differentiation and hypertrophy of myotubes |
| GO:0005654 nucleoplasm | IDA GO_REF:0000052 | ACCEPT | Summary: Retain the directly curated nucleoplasmic location. Reason: The immunofluorescence-derived IDA supports nucleoplasm and is compatible with independently observed human AKIRIN1 nuclear localization. The precise source image has not been re-scored here; no conflicting localization evidence warrants overruling the curator. Supporting Evidence: PMID:18066067 the nuclear localization of HsAkirin1 and HsAkirin2 |
| GO:0045663 positive regulation of myoblast differentiation | ISS GO_REF:0000024 | ACCEPT | Summary: AKIRIN1 is a conserved positive regulator of myoblast differentiation. Reason: The matching mouse Akirin1 primary studies directly connect its overexpression to earlier MyoD expression and enhanced terminal myogenesis. The target inherits the positive PTN002665250 assertion, and the direct C2C12 experiments in PMID:23516508 support the same promyogenic capacity under glucocorticoid stress. These are active gene-regulatory effects, not merely the consequences of generic viability. Muscle differentiation is a well-supported biological role and is retained as core with its ortholog-inference scope. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:18255059 enhanced and accelerated differentiation and hypertrophy of myotubes file:human/AKIRIN1/AKIRIN1-deep-research-falcon.md promyogenic nuclear factor |
| GO:0045944 positive regulation of transcription by RNA polymerase II | ISS GO_REF:0000024 | ACCEPT | Summary: Positive regulation of RNA polymerase II transcription is supported as an inherited Akirin function. Reason: The actual target lineage descends from the positive PTN000329080 IBDs. The Akirin1-specific myogenic transcriptional outcomes and mouse promoter-reporter evidence are compatible with this ancestral judgment. The old rationale overstated direct human AKIRIN1 NF-kappaB evidence: PMID:18066067 tested HsAkirin2 in the fly immune rescue and found normal tested cytokine responses in Akirin1-null mouse cells. The term-specific innate-immune IRD at PTN002665250 does not erase the broader positive cofactor, transcription or chromatin assertions. Detailed recruitment partners in human AKIRIN1 remain incompletely resolved. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Nuclear/chromatin/cofactor/transcription assertions descend from PTN000329080. PMID:30746755 Akirin1 regulated the transcription of muscle-specific RING finger 1 (MuRF-1) file:human/AKIRIN1/AKIRIN1-deep-research-falcon.md the most direct mechanistic NF-ΞΊB/SWI-SNF bridging evidence is from Drosophila Akirin and mammalian Akirin2-centered work |
| GO:0010592 positive regulation of lamellipodium assembly | ISS GO_REF:0000024 | ACCEPT | Summary: Positive regulation of lamellipodium assembly is supported by the exact mouse Akirin1 ortholog and actual positive ancestry. Reason: Mouse Q99LF1 is Akirin1/Mighty, not Akirin2. Its experimentally curated source annotations cite PMID:19406121, whose abstract reports increased macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. The target lies below the matching PTN002665250 IBD. Nuclear localization does not preclude regulation of cytoskeletal behavior, and viable knockout animals do not refute a cellular capacity. Retain the conserved inference without representing it as a direct human experiment or an identified actin-binding mechanism. Complete source article access remains unavailable, limiting mechanistic detail rather than overturning the positive evidence. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:19406121 more efficient lamellipodia formation via a PI3 kinase dependent pathway file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Mouse Akirin1 promotes macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. |
| GO:0010759 positive regulation of macrophage chemotaxis | ISS GO_REF:0000024 | ACCEPT | Summary: Positive regulation of macrophage chemotaxis is supported by the exact mouse Akirin1 ortholog and actual positive ancestry. Reason: Mouse Q99LF1 is Akirin1/Mighty, not Akirin2. Its experimentally curated source annotations cite PMID:19406121, whose abstract reports increased macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. The target lies below the matching PTN002665250 IBD. Nuclear localization does not preclude regulation of cytoskeletal behavior, and viable knockout animals do not refute a cellular capacity. Retain the conserved inference without representing it as a direct human experiment or an identified actin-binding mechanism. Complete source article access remains unavailable, limiting mechanistic detail rather than overturning the positive evidence. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:19406121 more efficient lamellipodia formation via a PI3 kinase dependent pathway file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Mouse Akirin1 promotes macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. |
| GO:0014839 myoblast migration involved in skeletal muscle regeneration | ISS GO_REF:0000024 | ACCEPT | Summary: Myoblast migration is supported by the exact mouse Akirin1 ortholog and actual positive ancestry. Reason: Mouse Q99LF1 is Akirin1/Mighty, not Akirin2. Its experimentally curated source annotations cite PMID:19406121, whose abstract reports increased macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. The target lies below the matching PTN002665250 IBD. Nuclear localization does not preclude regulation of cytoskeletal behavior, and viable knockout animals do not refute a cellular capacity. Retain the conserved inference without representing it as a direct human experiment or an identified actin-binding mechanism. Complete source article access remains unavailable, limiting mechanistic detail rather than overturning the positive evidence. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:19406121 more efficient lamellipodia formation via a PI3 kinase dependent pathway file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Mouse Akirin1 promotes macrophage and myoblast chemotaxis with PI3K-dependent actin reorganization and lamellipodia formation. |
| GO:1902723 negative regulation of skeletal muscle satellite cell proliferation | ISS GO_REF:0000024 | ACCEPT | Summary: Retain context-dependent negative regulation of satellite-cell proliferation. Reason: The original dismissal treated positive proliferation under glucocorticoid rescue as a universal sign. Mouse Akirin1 source PMID:18255059 instead reports earlier cell-cycle withdrawal during differentiation, and the actual target descends from the negative-proliferation IBD at PTN002665250. Independently, goat Akirin1 overexpression reduces proliferation markers and EdU/CCK-8 outcomes in PMID:40211850. These results can coexist with improved proliferation in the distinct C2C12 dexamethasone experiment of PMID:23516508. Retain the inherited capacity with state and assay limits; the evidence does not imply constitutive suppression in every muscle-cell context. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md The current PTHR13293 tree places human leaf PTN002491310 below PTN002665250. PMID:18255059 early withdrawal of myoblasts from the cell cycle PMID:40211850 adding Akirin1 restrained newly formed cells and viable cells |
| GO:1902725 negative regulation of satellite cell differentiation | ISS GO_REF:0000024 | ACCEPT | Summary: Retain reduced satellite/reserve-cell differentiation, distinct from increased terminal myogenesis. Reason: GO:1902725 negatively regulates GO:0014816, which defines acquisition of satellite-cell features. The old review conflated this with a satellite-derived myoblast differentiating into a myotube. The exact mouse Q99LF1 MGI IMP source is PMID:18255059. Related primary work in the Dyer 2006 thesis describes reduced reserve-cell populations and reduced Sca-1/CD34 in Mighty-overexpressing C2C12 cultures alongside increased myotube fusion. This is consistent with the standing curator-supported transfer; the positive myogenesis result does not contradict it. The original journal full text remains unavailable and reserve-cell markers are not lineage tracing, so the precise mechanism remains a follow-up, not a confident reversal of the annotation. Supporting Evidence: file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md It is not synonymous with a satellite-derived myoblast forming a myotube. file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md This corroborates the compatibility of reduced satellite/reserve identity with positive terminal myogenesis. PMID:18255059 enhanced and accelerated differentiation and hypertrophy of myotubes |
| GO:0005634 nucleus | IDA PMID:18066067 Akirins are highly conserved nuclear proteins required for N... | ACCEPT | Summary: Nuclear localization is supported directly for human AKIRIN1 and by inheritance. Reason: PMID:18066067 expresses tagged HsAkirin1 in HeLa cells and shows NLS-dependent nuclear localization. The source location is retained; the actual PTN000329080 nuclear assertion is also ancestral to the target. Neither broader versus narrower nuclear location nor evidence redundancy changes its biological correctness. Supporting Evidence: PMID:18066067 the nuclear localization of HsAkirin1 and HsAkirin2 file:human/AKIRIN1/AKIRIN1-primary-and-phylogeny-scope.md Nuclear/chromatin/cofactor/transcription assertions descend from PTN000329080. |
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Download this section (compressed HTML)Q: Which human AKIRIN1 partners and transcriptional targets connect its nuclear cofactor role to PI3K-dependent lamellipodium formation and chemotaxis inferred from the mouse ortholog?
Q: How do AKIRIN1 dosage, glucocorticoid exposure and cell state determine proliferation versus cell-cycle exit and satellite/reserve-cell commitment? Full-text curator follow-up on PMID:18255059 should resolve the exact assay underlying GO:1902725 without conflating satellite identity with terminal myogenesis.
Experiment: Measure AKIRIN1-dependent transcription, cell-cycle exit, terminal myogenesis and reserve-cell fate in matched human myogenic cultures across differentiation and glucocorticoid conditions, using perturbation/rescue and lineage-resolved readouts.
Experiment: Test endogenous AKIRIN1 recruitment partners and target-gene occupancy while measuring lamellipodium dynamics and chemotaxis, separating nuclear regulation from possible cytoplasmic actions.
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