Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Akirins are highly conserved nuclear proteins required for NF-kappaB-dependent gene expression in drosophila and mice.
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Human HsAkirin1 and HsAkirin2 show NLS-dependent nuclear localization in HeLa cells.
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Immune rescue/essentiality experiments principally establish Akirin2 functions; the tested Akirin1-null cytokine responses were normal.
Myostatin suppression of Akirin1 mediates glucocorticoid-induced satellite cell dysfunction.
AKIRIN2 controls the nuclear import of proteasomes in vertebrates.
A proteome-scale map of the human interactome network.
Akirin1 (Mighty), a novel promyogenic factor regulates muscle regeneration and cell chemotaxis.
Mighty is a novel promyogenic factor in skeletal myogenesis.
CircEPDR1 regulates proliferation and differentiation of goat skeletal muscle satellite cells through miR-345-3p/Akirin1 axis.
Role of Akirin1 in the regulation of skeletal muscle fiber-type switch.
miR-224 activates cancer-associated fibroblasts to enhance lung cancer cell migration and invasion by targeting Akirin1.
AKIRIN1 primary evidence and phylogenetic scope
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Q9H9L7 inherits the positive muscle/motility assertions from PTN002665250 and nuclear/transcriptional assertions from PTN000329080.
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GO:1902725 concerns satellite-cell identity and is compatible with enhanced terminal myogenesis.
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The generic binary-binding evidence does not justify protein-containing complex binding.
Research Report: Human AKIRIN1 (UniProt Q9H9L7; Akirin-1/Mighty) — functional annotation
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The report emphasizes a promyogenic nuclear cofactor role, while treating detailed immune mechanisms mainly as family/Akirin2 evidence.
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Disease/fertility associations do not establish a new function; the report is a synthesis, not independent experimental proof.
UniProt entry Q9H9L7 (AKIRIN1_HUMAN)