Gene Ontology annotation through association of InterPro records with GO terms

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 UniPathway vocabulary mapping

Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt

Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara

Automatic Gene Ontology annotation based on Rhea mapping

Combined Automated Annotation using Multiple IEA Methods

The human FA2H gene encodes a fatty acid 2-hydroxylase.

A novel method for the measurement of in vitro fatty acid 2-hydroxylase activity by gas chromatography-mass spectrometry.

Fatty acid 2-hydroxylase, encoded by FA2H, accounts for differentiation-associated increase in 2-OH ceramides during keratinocyte differentiation.

Stereospecificity of fatty acid 2-hydroxylase and differential functions of 2-hydroxy fatty acid enantiomers.

A reference map of the human binary protein interactome.

Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.

Sphingolipid de novo biosynthesis

FA2H hydroxylates 1,2-saturated fatty acids

A mammalian fatty acid hydroxylase responsible for the formation of alpha-hydroxylated galactosylceramide in myelin.

FA2H is responsible for the formation of 2-hydroxy galactolipids in peripheral nervous system myelin.

Absence of 2-hydroxylated sphingolipids is compatible with normal neural development but causes late-onset axon and myelin sheath degeneration.

Central nervous system dysfunction in a mouse model of FA2H deficiency.

Normal fur development and sebum production depends on fatty acid 2-hydroxylase expression in sebaceous glands.

Mutations in the fatty acid 2-hydroxylase gene are associated with leukodystrophy with spastic paraparesis and dystonia.

Mutation of FA2H underlies a complicated form of hereditary spastic paraplegia (SPG35).

Defective FA2H leads to a novel form of neurodegeneration with brain iron accumulation (NBIA).