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
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
p28 Bap31, a Bcl-2/Bcl-XL- and procaspase-8-associated protein in the endoplasmic reticulum.
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BAP31 is an ER membrane protein associated with BCL2, BCL-XL and procaspase-8 in the reported experiments.
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Caspase cleavage produces fragments including p20; p20 expression induces apoptotic effects in the tested cells.
BAP31 interacts with Sec61 translocons and promotes retrotranslocation of CFTRDeltaF508 via the derlin-1 complex.
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BAP31 associates with Sec61beta/TRAM and Derlin-1 machinery and binds the N-terminal region of CFTR F508del.
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BAP31 depletion reduces CFTR F508del degradation and permits some mutant CFTR to reach the cell surface, supporting client handling in ER quality control.
Fis1 and Bap31 bridge the mitochondria-ER interface to establish a platform for apoptosis induction.
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Intact FIS1-BAP31 complexes recruit procaspase-8; deletion of the relevant BAP31 cytoplasmic segment disrupts recruitment.
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Caspase cleavage generates ER-associated p20, which contributes to calcium-dependent mitochondrial apoptotic responses.
BAP31 regulates mitochondrial function via interaction with Tom40 within ER-mitochondria contact sites.
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Endogenous DSP-crosslinked co-immunoprecipitation in human U2OS cells supports BAP31 association with TOMM40 and NDUFS4.
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BAP31 depletion changes mitochondrial distribution and turnover of NDUFS4 and NDUFB11; VDAC1 association does not show the same localization phenotype.
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The observed localization and turnover effects do not constitute a direct kinetic pore or motor assay.
Identification of major proteins in the lipid droplet-enriched fraction isolated from the human hepatocyte cell line HuH7.
The yeast split-ubiquitin membrane protein two-hybrid screen identifies BAP31 as a regulator of the turnover of endoplasmic reticulum-associated protein tyrosine phosphatase-like B.
Huntingtin interacting proteins are genetic modifiers of neurodegeneration.
Role of syntaxin 18 in the organization of endoplasmic reticulum subdomains.
Defining the membrane proteome of NK cells.
Transmembrane and coiled-coil domain family 1 is a novel protein of the endoplasmic reticulum.
Interaction between human BAP31 and respiratory syncytial virus small hydrophobic (SH) protein.
Histone Interaction Landscapes Visualized by Crosslinking Mass Spectrometry in Intact Cell Nuclei.
A reference map of the human binary protein interactome.
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
OpenCell: Endogenous tagging for the cartography of human cellular organization.
Differential CFTR-Interactome Proximity Labeling Procedures Identify Enrichment in Multiple SLC Transporters.
Molecular cloning and characterization of a transmembrane surface antigen in human cells.
Caspase mediated cleavage of BAP31
Loading of antigenic peptides on to class I MHC
Transport of MHC heterotrimer to ER exit site
Formation of peptide loading complex (PLC)
Dissociation of the Antigenic peptide:MHC:B2M peptide loading complex
Deep research report on BCAP31
Proteomics characterization of abundant Golgi membrane proteins.
Identification of differentially expressed genes in mouse spermatogenesis.
Bap29/31 influences the intracellular traffic of MHC class I molecules.
Bap31 enhances the endoplasmic reticulum export and quality control of human class I MHC molecules.
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BAP31 overexpression increases MHC-I cell-surface expression and export in the tested human-cell system.
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The tested BAP31 knockdown and deficient-fibroblast comparisons do not show reduced surface MHC-I, limiting claims of an obligatory mechanism.
Structural and biophysical characterization of the cytoplasmic domains of human BAP29 and BAP31.
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The isolated BAP31 variant death-effector domain forms a parallel coiled-coil dimer.
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The tested isolated cytoplasmic domains did not form a BAP29-BAP31 heteromer; this experiment does not settle full-length membrane association.
Export of cellubrevin from the endoplasmic reticulum is controlled by BAP31.
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Rat-liver clathrin-coated-vesicle fractions show cellubrevin enrichment with virtually no BAP31; BAP31 is enriched in ER-related fractions.
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BAP31 tail-mutant expression selectively retains cellubrevin in the tested system, while transferrin-receptor surface delivery is preserved.