Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword 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
A human IAP-family gene, apollon, expressed in human brain cancer cells.
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Identified Apollon/BIRC6 as a human IAP family member with a BIR domain and UBC domain, expressed in brain cancer cells.
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Antisense knockdown of Apollon sensitizes SNB-78 brain cancer cells to cisplatin and camptothecin-induced apoptosis.
Nrdp1-mediated degradation of the gigantic IAP, BRUCE, is a novel pathway for triggering apoptosis.
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Nrdp1/RNF41 associates with BRUCE and catalyzes its ubiquitination and proteasomal degradation.
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BRUCE normally inhibits apoptosis; decreasing BRUCE by RNAi or Nrdp1 overexpression promotes apoptosis.
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Apoptotic stimuli induce proteasomal degradation of BRUCE but not XIAP or c-IAP1.
Dual role of BRUCE as an antiapoptotic IAP and a chimeric E2/E3 ubiquitin ligase.
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BRUCE inhibits caspase activity and apoptosis in a BIR domain-dependent manner.
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BRUCE functions as a chimeric E2/E3 ubiquitin ligase with Smac as a substrate.
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BRUCE is antagonized by Smac binding, HtrA2 protease, and caspase-mediated cleavage.
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BRUCE is a 528 kDa peripheral membrane protein of the trans-Golgi network.
Final stages of cytokinesis and midbody ring formation are controlled by BRUCE.
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BRUCE is a major regulator of abscission during cytokinesis.
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BRUCE exhibits cell cycle-dependent localization: pericentriolar in interphase, spindle poles in metaphase, midbody/midbody ring in telophase/cytokinesis.
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BRUCE depletion causes defective abscission, cytokinesis-associated apoptosis, and disrupts midbody ring formation and ubiquitin relocalization.
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BRUCE interacts with KIF23/MKLP1, USP8/UBPY, survivin, MEK1, RAB8, RAB11, PLK1, SEC6, and SEC8.
IAPs: more than just inhibitors of apoptosis proteins.
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Review discussing IAP family roles beyond apoptosis inhibition, including cell proliferation, differentiation, signaling, and immune response.
Defining the membrane proteome of NK cells.
A human interactome in three quantitative dimensions organized by stoichiometries and abundances.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Structures of BIRC6-client complexes provide a mechanism of SMAC-mediated release of caspases.
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Cryo-EM structure of BIRC6 reveals antiparallel homodimer with central substrate-binding cavity accommodating Smac/DIABLO.
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BIRC6 ubiquitinates caspases-3, -7, -9 and their procaspases via UBA6 as E1.
Structural basis for regulation of apoptosis and autophagy by the BIRC6/SMAC complex.
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BIRC6 ubiquitinates the autophagy protein MAP1LC3B; inhibited by Smac.
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Cryo-EM structure reveals multiple domains including WD40, BIR, and UBC.
Structural basis for SMAC-mediated antagonism of caspase inhibition by the giant ubiquitin ligase BIRC6.
ALK mutants bind type I TKIs
Deep research on BIRC6 function (Falcon)
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BIRC6 is a cell-fate rheostat coordinating apoptosis-autophagy balance through caspase-9 regulation and LC3 K51 ubiquitylation.
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BIRC6 mono-ubiquitinates LC3 at K51 in cooperation with UBA6, suppressing autophagy.
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BIRC6 ubiquitinates Axin to activate Wnt/beta-catenin signaling in RCC cells.
Manual PROTEOSTASIS PN review notes for BIRC6
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PN review supports replacing the broad BIRC6 ubiquitin-protein transferase activity annotation with GO:0061630 ubiquitin protein ligase activity.
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BIRC6 autophagy evidence concerns LC3 ubiquitination and autophagy suppression, not lysosome-autophagosome SNARE or docking/fusion activity.
BRUCE regulates DNA double-strand break response by promoting USP8 deubiquitination of BRIT1.