Gene Ontology annotation through association of InterPro records with GO terms

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

GO_REF:0000052

Gene Ontology annotation based on curation of immunofluorescence data

GO_REF:0000107

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

GO_REF:0000120

Combined Automated Annotation using Multiple IEA Methods

PMID:10964512

Succinyl-CoA:3-ketoacid CoA transferase (SCOT): cloning of the human SCOT gene, tertiary structural modeling of the human SCOT monomer, and characterization of three pathogenic mutations.

SCOT activity is the main determinant of the ketolytic capacity of tissues; pathogenic mutations abolish or reduce enzyme activity and cause episodic ketoacidosis (SCOT deficiency).

"the main determinant of the ketolytic capacity of tissues"

PMID:11756565

Cloning and characterization of a human orthologue of testis-specific succinyl CoA: 3-oxo acid CoA transferase (Scot-t) cDNA.

The SCOT-t protein localizes to the mitochondria-containing midpiece of ejaculated spermatozoa.

"the protein was localized to the midpiece of ejaculated spermatozoa"

PMID:34800366

Quantitative high-confidence human mitochondrial proteome and its dynamics in cellular context.

OXCT1 is identified as a component of the high-confidence human mitochondrial proteome.

PMID:8751852

Succinyl CoA: 3-oxoacid CoA transferase (SCOT): human cDNA cloning, human chromosomal mapping to 5p13, and mutation detection in a SCOT-deficient patient.

SCOT mediates the rate-determining step of ketolysis in extrahepatic tissues, esterifying acetoacetate to CoA for energy production; expressed in heart, leukocytes and fibroblasts but not liver (HepG2).

"rate-determining step of ketolysis in extrahepatic"
SCOT mRNA is undetectable in the human hepatoma cell line HepG2, consistent with liver's inability to utilize ketone bodies.

"no signal is detectable in the human hepatoma cell line HepG2"

PMID:9671268

Succinyl-CoA:3-ketoacid CoA transferase (SCOT) deficiency: two pathogenic mutations, V133E and C456F, in Japanese siblings.

SCOT is the key enzyme of ketone-body utilization; loss-of-function mutations produce no detectable SCOT activity and cause episodes of severe ketoacidosis.

"the key enzyme of ketone body utilization"

Reactome:R-HSA-74177

OXCT dimers transfer CoA from SUCC-CoA to ACA, forming ACA-CoA

OXCT1/OXCT2 dimers catalyze the first, rate-limiting step of ketone-body utilization in peripheral tissues, transferring CoA from succinyl-CoA to acetoacetate to form acetoacetyl-CoA and succinate, in the mitochondrial matrix.

"catalysing the first rate-limiting step of ketone body utilisation in peripheral tissues"

Reactome:R-HSA-9838035

CLPXP binds mitochondrial matrix proteins

Reactome:R-HSA-9838081

LONP1 degrades mitochondrial matrix proteins

Reactome:R-HSA-9838093

LONP1 binds mitochondrial matrix proteins

Reactome:R-HSA-9838289

CLPXP degrades mitochondrial matrix proteins