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 UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping.
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara.
Automatic assignment of GO terms using logical inference based on inter-ontology links.
Automated transfer of experimentally verified manual GO annotation data to mouse-human orthologs.
UniProtKB record for mouse Surf1 (P09925)
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Mouse SURF1 is a MITRAC component that regulates cytochrome c oxidase assembly.
"Component of the MITRAC (mitochondrial translation regulation assembly intermediate of cytochrome c oxidase complex) complex. Regulates cytochrome c oxidase assembly."
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Mouse SURF1 is a mitochondrial multi-pass membrane protein.
"SUBCELLULAR LOCATION: Mitochondrion membrane; Multi-pass membrane protein."
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Surf1 disruption causes reduced COX activity and mitochondrial stress phenotypes, consistent with an assembly-factor role.
"DISRUPTION PHENOTYPE: Increases lactate levels in blood and brain; decreases COX activity and respiration; in skeletal muscles, results in mitochondrial unfolded protein response."
Falcon deep research report for mouse Surf1
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Falcon verified the target as mouse UniProt P09925 and synthesized SURF1 as a conserved cytochrome c oxidase assembly factor.
"The requested target corresponds to the mammalian SURF1-family protein homologous to yeast Shy1 that functions as a mitochondrial cytochrome c oxidase assembly factor."
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Falcon places Surf1 at the mitochondrial inner membrane and within COX assembly intermediates.
"Surf1 is described as synthesized as a larger precursor with an N-terminal leader peptide that is cleaved, and the mature protein is embedded in the mitochondrial inner membrane where it participates in COX assembly."
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Falcon explicitly distinguishes SURF1 assembly-factor biology from direct enzyme activity.
"Surf1 is not an enzyme catalyzing a chemical transformation; its primary biochemical role is as an inner-membrane assembly factor/chaperone-like protein that promotes correct maturation and/or progression of COX assembly intermediates toward functional holoenzyme."
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Falcon highlights a mechanistic caveat: heme a3-CuB maturation is supported largely by homolog and biochemical model evidence.
"A mechanistic hypothesis supported by biochemical characterization of Surf1p-deficient bacterial oxidase posits that Surf1-family proteins facilitate maturation of the heme a3-CuB catalytic center in COX1."
Curator notes for mouse Surf1
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Local notes summarize Surf1 as a nuclear-encoded assembly factor for cytochrome c oxidase and flag proton transport and ATP synthesis as downstream effects rather than Surf1 core functions.
"NOT core functions: Direct proton transport; direct electron transport; ATP synthesis."
Constitutive knockout of Surf1 is associated with high embryonic lethality, mitochondrial disease and cytochrome c oxidase deficiency in mice.
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Constitutive Surf1 knockout identifies mouse Surf1 as a COX assembly protein and causes isolated COX deficiency.
"We report here the creation of a constitutive knockout mouse for SURF1, a gene encoding one of the assembly proteins involved in the formation of cytochrome c oxidase (COX)."
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Surf1 loss causes severe mouse phenotypes and reduced COX activity but no evidence that SURF1 itself is the COX enzyme.
"The murine phenotype is characterized by the following hallmarks: (1) high post-implantation embryonic lethality, affecting approximately 90% of the Surf1(-/-) individuals; (2) early-onset mortality of post-natal individuals; (3) highly significant deficit in muscle strength and motor performance; (4) profound and isolated defect of COX activity in skeletal muscle and liver, and, to a lesser extent, heart and brain"
Decreased in vitro mitochondrial function is associated with enhanced brain metabolism, blood flow, and memory in Surf1-deficient mice.
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Surf1-deficient brain mitochondria have reduced COX activity, supporting an upstream requirement for functional complex IV.
"ATP production in brain mitochondria isolated from Surf1 KO mice remained unchanged despite a 49% reduction in COX activity, a 24% reduction in state 3 respiration, and a 24% increase in H 2 O 2 production."
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The paper describes Surf1 as participating in efficient assembly and function of cytochrome c oxidase.
"Surf1 participates in the efficient assembly and function of cytochrome C oxidase (COX; mitochondrial Complex IV), which is the terminal enzyme of the electron transport chain and is critical for ATP synthesis."
A mitochondrial protein compendium elucidates complex I disease biology.
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MitoCarta provides high-throughput support for mitochondrial localization.
"We performed mass spectrometry, GFP tagging, and machine learning to create a mitochondrial compendium of 1098 genes and their protein expression across 14 mouse tissues."
Integrated analysis of protein composition, tissue diversity, and gene regulation in mouse mitochondria.
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Mouse mitochondrial proteomics supports broad mitochondrial localization.
"We performed a proteomic survey of mitochondria from mouse brain, heart, kidney, and liver and combined the results with existing gene annotations to produce a list of 591 mitochondrial proteins."