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
Gene Ontology annotation based on curation of immunofluorescence data
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Molecular cloning of apobec-1 complementation factor, a novel RNA-binding protein involved in the editing of apolipoprotein B mRNA.
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A1CF binds APOB mRNA and docks APOBEC1, providing the minimal noncatalytic RNA-targeting component needed to reconstitute APOB editing in vitro.
"ACF and apobec-1 comprise the minimal protein requirements for apo-B mRNA editing in vitro."
Purification and molecular cloning of a novel essential component of the apolipoprotein B mRNA editing enzyme-complex.
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Recombinant A1CF/ASP stimulates APOBEC1-dependent APOB RNA editing in a purified in-vitro system.
"Purified recombinant glutathione S-transferase (GST)-ASP, but not recombinant GST-KSRP, stimulated recombinant GST-APOBEC-1 to edit apoB RNA in vitro."
Identification of GRY-RBP as an apolipoprotein B RNA-binding protein that interacts with both apobec-1 and apobec-1 complementation factor to modulate C to U editing.
Identification of domains in apobec-1 complementation factor required for RNA binding and apolipoprotein-B mRNA editing.
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A1CF recognizes the APOB mooring region and binds single-stranded, but not double-stranded, APOB RNA with high affinity through all three RRMs and auxiliary residues.
"Here, we show that ACF binds with high affinity to single-stranded but not double-stranded apo-B mRNA."
The apolipoprotein B mRNA editing complex performs a multifunctional cycle and suppresses nonsense-mediated decay.
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The APOBEC1-A1CF complex remains associated with edited APOB RNA, shields the transcript from NMD, and participates in nucleocytoplasmic transport.
"The APOBEC1-ACF complex edits and remains associated with the edited RNA to protect it from NMD."
A novel nuclear localization signal in the auxiliary domain of apobec-1 complementation factor regulates nucleocytoplasmic import and shuttling.
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A 41-residue A1CF auxiliary-domain signal binds TNPO2 and mediates nuclear import and nucleocytoplasmic shuttling.
"a novel 41-residue motif (ANS) in the auxiliary domain of ACF that functions as an authentic nuclear localization signal."
Apobec-1 complementation factor modulates liver regeneration by post-transcriptional regulation of interleukin-6 mRNA stability.
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Mouse A1cf binds an AU-rich IL6 3'-UTR region and stabilizes IL6 mRNA in Kupffer cells during liver regeneration.
"Recombinant ACF bound an AU-rich region in the IL-6 3′-untranslated region with high affinity and IL-6 mRNA half-life was significantly shorter in KC isolated from Acf +/− mice compared with wild-type controls."
Hydroxylation of 5-methylcytosine by TET1 promotes active DNA demethylation in the adult brain.
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The exposed record implicates TET1 and APOBEC1 in mouse neuronal DNA demethylation but does not expose an A1CF-specific experiment.
"Furthermore, Tet1 and Apobec1 are involved in neuronal activity-induced, region-specific, active DNA demethylation and subsequent gene expression in the dentate gyrus of the adult mouse brain in vivo."
C to U RNA editing mediated by APOBEC1 requires RNA-binding protein RBM47.
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RBM47 interacts with A1CF and can replace it as a stronger APOBEC1 editing cofactor, arguing against an universally essential A1CF role.
"RBM47 can substitute for A1CF and is necessary and sufficient for APOBEC1-mediated editing in vitro."
A proteome-scale map of the human interactome network.
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This proteome-scale binary-interaction map is the provenance for several A1CF interaction partners but does not establish an A1CF-specific mechanism.
"Here, we describe a systematic map of ?14,000 high-quality human binary protein-protein interactions."
APOBEC1 complementation factor (A1CF) is dispensable for C-to-U RNA editing in vivo.
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Conditional A1cf loss did not reduce APOBEC1-dependent editing in normal adult mouse liver, intestine, or kidney.
"Taken together, these observations demonstrate that A1CF does not act as the APOBEC1 complementation factor in vivo under normal physiological conditions and suggests new roles for A1CF, specifically within the male adult kidney."
Apobec1 complementation factor (A1CF) and RBM47 interact in tissue-specific regulation of C to U RNA editing in mouse intestine and liver.
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A1CF and RBM47 make independent, partially redundant, tissue-specific contributions to APOBEC1 editing and site selection.
"These data suggest that A1CF and RBM47 each function independently, yet interact in a tissue-specific manner, to regulate the activity and site selection of APOBEC1 dependent C-to-U RNA editing."
Comparison of RNA Editing Activity of APOBEC1-A1CF and APOBEC1-RBM47 Complexes Reconstituted in HEK293T Cells.
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Human A1CF supports APOBEC1-dependent editing in reconstituted HEK293T cells, with substrate selectivity distinct from RBM47.
"human A1CF can mediate APO1 editing activity on APOB RNA in this cell-based assay system"
The RNA-Binding Protein A1CF Regulates Hepatic Fructose and Glycerol Metabolism via Alternative RNA Splicing.
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A1cf regulates hepatocyte-specific alternative splicing, including KHK-C and glycerol-kinase isoforms linked to fructose and glycerol metabolism.
"Our results identify a previously unreported function of A1CF as a regulator of alternative splicing of a subset of genes influencing hepatic glucose production through fructose and glycerol metabolism."
A reference map of the human binary protein interactome.
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HuRI supplies many binary A1CF interaction hits but no partner-specific functional mechanism for A1CF.
"Here we present a human 'all-by-all' reference interactome map of human binary protein interactions, or 'HuRI'."
Enhanced Integrated Gradients: improving interpretability of deep learning models using splicing codes as a case study.
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Independent analysis of A1cf knockout RNA-seq and PAR-CLIP supports direct, position-dependent regulation of liver cassette exons by A1cf.
"Here, we were able to apply EIG to identify A1CF as a regulator of the liver splicing program, then support this result using several lines of experimental and computational evidence based on motif maps, RNA-seq from a A1cf knockout in mouse, and PAR-CLIP binding assays."
HNF1A and A1CF coordinate a beta cell transcription-splicing axis that is disrupted in type 2 diabetes.
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A1CF knockout in human beta-cell models causes a broad alternative-splicing program, including SLC7A2 exon choice, with consequences for arginine-induced insulin secretion.
"A1CFKO cells showed profound alternative splicing changes, with 1,907 differentially spliced events in 1,372 genes"
Binding of A1CF to stem-looped RNA
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Reactome models nuclear binding of A1CF to target stem-looped RNA before APOBEC1 joins the editosome.
"A1CF protein is cytosolic in origin and is translocated to nucleus where it binds to the target RNA."
Binding of APOBEC-1 to form editosome
C4 deamination of cytidine