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
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
E2F-dependent accumulation of hEmi1 regulates S phase entry by inhibiting APC(Cdh1).
Prophase destruction of Emi1 by the SCF(betaTrCP/Slimb) ubiquitin ligase activates the anaphase promoting complex to allow progression beyond prometaphase.
Role of Polo-like kinase in the degradation of early mitotic inhibitor 1, a regulator of the anaphase promoting complex/cyclosome.
Plk1 regulates activation of the anaphase promoting complex by phosphorylating and triggering SCFbetaTrCP-dependent destruction of the APC Inhibitor Emi1.
The evi5 oncogene regulates cyclin accumulation by stabilizing the anaphase-promoting complex inhibitor emi1.
Emi1 stably binds and inhibits the anaphase-promoting complex/cyclosome as a pseudosubstrate inhibitor.
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EMI1 binds the APC/C and CDH1, occupies the D-box receptor site competing with substrates, and its ZBR antagonizes APC/C E3 ligase activity; mutation of the ZBR converts EMI1 into a D-box-dependent APC/C substrate.
The APC/C inhibitor, Emi1, is essential for prevention of rereplication.
Selective role for RGS12 as a Ras/Raf/MEK scaffold in nerve growth factor-mediated differentiation.
Emi1 is needed to couple DNA replication with mitosis but does not regulate activation of the mitotic APC/C.
A bacterial effector targets Mad2L2, an APC inhibitor, to modulate host cell cycling.
Loss of Emi1-dependent anaphase-promoting complex/cyclosome inhibition deregulates E2F target expression and elicits DNA damage-induced senescence.
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Loss of EMI1-dependent APC/C inhibition deregulates E2F targets, causes replication stress and DNA damage, and elicits cellular senescence; EMI1 normally maintains genome integrity and prevents senescence.
The Cdc14B-Cdh1-Plk1 axis controls the G2 DNA-damage-response checkpoint.
Emi1 preferentially inhibits ubiquitin chain elongation by the anaphase-promoting complex.
Electron microscopy structure of human APC/C(CDH1)-EMI1 reveals multimodal mechanism of E3 ligase shutdown.
Atomic structure of the APC/C and its mechanism of protein ubiquitination.
A High-Density Map for Navigating the Human Polycomb Complexome.
Two Transcripts of FBXO5 Promote Migration and Osteogenic Differentiation of Human Periodontal Ligament Mesenchymal Stem Cells.
EMI1 switches from being a substrate to an inhibitor of APC/C(CDH1) to start the cell cycle.
A reference map of the human binary protein interactome.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
The SCF Complex Is Essential to Maintain Genome and Chromosome Stability.
Multimodal cell maps as a foundation for structural and functional genomics.
Falcon deep research report for human FBXO5
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EMI1/FBXO5 is a high-affinity pseudosubstrate inhibitor of APC/C (especially APC/C-CDH1), required during interphase to permit cyclin accumulation and mitotic entry rather than functioning as an enzyme.
"**Emi1/FBXO5 acts as a principal interphase inhibitor of APC/C**, particularly **APC/C activated by Cdh1 (APC/C^CDH1)**, thereby preventing premature degradation of cyclins and enabling progression toward mitosis"
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Inhibition is multimodal, using a C-terminal D-box that competes at the APC/C D-box receptor and a zinc-binding region (ZBR) that provides additional inhibition and protects EMI1 from being processed as an APC/C substrate.
"Mutating the ZBR converts Emi1 into an APC/C substrate** that becomes efficiently ubiquitinated in a D-box-dependent manner, while wild-type Emi1 is a poor substrate, supporting the pseudosubstrate-inhibitor model in which the ZBR "protects" Emi1 from APC/C-mediated ubiquitination"
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A 2024 study frames EMI1/FBXO5 as a possible F-box substrate receptor of an SCF^EMI1 complex with RAD51 cited as a substrate, but this is a recent and far less established role than its core APC/C-inhibitory function.
"a 2024 study explicitly frames **EMI1 (FBXO5)** as an **F-box protein** that can serve as the variable substrate receptor in an **SCF^EMI1** ubiquitin ligase complex (core SCF components SKP1–CUL1–RBX1 plus the F-box protein) and cites **RAD51** as an SCF^EMI1 substrate targeted for proteolytic degradation"
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EMI1 abundance is dosage-sensitive for genome stability; reduced EMI1 in colonic epithelium increases chromosome instability, DNA damage, and transformation, consistent with its role coupling replication to mitosis.
"**reduced EMI1 expression drives chromosome instability (CIN)** and is associated with DNA damage and transformation phenotypes in colonic epithelial contexts"
Down Regulation of Emi1 through Phosphorylation of Emi1
Association of Emi1 with Cdh1
Phosphorylation of the Emi1 DSGxxS degron by Cyclin B:Cdc2
Ubiquitination of Emi1 by SCF-beta-TrCP
Phosphorylation of the Emi1 DSGxxS degron by Plk1
SCF-mediated degradation of Emi1
Phosphorylated Emi1 binds the beta-TrCP in the SCF complex
Association of Emi1 with Cdc20
FBXO5 gene expression is stimulated by E2F1