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 assignment of GO terms using logical inference, based on on inter-ontology links

Combined Automated Annotation using Multiple IEA Methods

Six and Eya expression during human somitogenesis and MyoD gene family activation.

SIX1 mutations cause branchio-oto-renal syndrome by disruption of EYA1-SIX1-DNA complexes.

Tyrosine dephosphorylation of H2AX modulates apoptosis and survival decisions.

Biochemical and functional characterization of six SIX1 Branchio-oto-renal syndrome mutations.

Architecture of the human interactome defines protein communities and disease networks.

A reference map of the human binary protein interactome.

Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.

A human homologue of the Drosophila eyes absent gene underlies branchio-oto-renal (BOR) syndrome and identifies a novel gene family.

ATM phosphorylates EYA1-4

Cooperation of six and eya in activation of their target genes through nuclear translocation of Eya.

Eya1-deficient mice lack ears and kidneys and show abnormal apoptosis of organ primordia.

The transcription factor Eyes absent is a protein tyrosine phosphatase.

Eya protein phosphatase activity regulates Six1-Dach-Eya transcriptional effects in mammalian organogenesis.

Branchio-oto-renal syndrome associated mutations in Eyes Absent 1 result in loss of phosphatase activity.

The PI3K/Akt signal hyperactivates Eya1 via the SUMOylation pathway.

Mutations of a human homologue of the Drosophila eyes absent gene (EYA1) detected in patients with congenital cataracts and ocular anterior segment anomalies.

Dephosphorylation of the C-terminal tyrosyl residue of the DNA damage-related histone H2A.X is mediated by the protein phosphatase eyes absent.

Eyes absent represents a class of protein tyrosine phosphatases.

SUMO1 haploinsufficiency leads to cleft lip and palate.

EYA1's Conformation Specificity in Dephosphorylating Phosphothreonine in Myc and Its Activity on Myc Stabilization in Breast Cancer.

Eya3 partners with PP2A to induce c-Myc stabilization and tumor progression.

The Eya1 Phosphatase Mediates Shh-Driven Symmetric Cell Division of Cerebellar Granule Cell Precursors.