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
Molecular cloning and characterization of a novel human gene containing ankyrin repeat and double BTB/POZ domain.
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ABTB1/BPOZ encodes a 478 amino acid protein with ankyrin-repeat and BTB/POZ domains and was proposed to function through protein-protein interactions or complex formation.
"A novel human gene containing an ankyrin repeat and BTB/POZ domains (BPOZ) was isolated from a human leukocyte cDNA library"
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ABTB1/BPOZ is broadly expressed in fetal tissues and may have developmentally regulated roles.
"ubiquitously expressed in all fetal tissues examined"
Growth-suppressive effects of BPOZ and EGR2, two genes involved in the PTEN signaling pathway.
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BPOZ/ABTB1 was identified as a PTEN-responsive gene whose overexpression suppresses cancer-cell growth and G1/S progression in the assays described in the abstract.
"BPOZ were able to suppress growth of cancer cells"
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The cached publication text is abstract-only and does not expose the subcellular localization details that UniProt cites from this PMID.
"Growth-suppressive effects of BPOZ and EGR2, two genes involved in the PTEN signaling pathway."
Bood POZ containing gene type 2 is a human counterpart of yeast Btb3p and promotes the degradation of terminal deoxynucleotidyltransferase.
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ABTB1/BPOZ-2 binds CUL3 in vitro and in vivo and itself undergoes CUL3-dependent ubiquitination and proteasomal degradation.
"BPOZ-2 bound to E3 ligase CUL3 in vitro and in vivo. BPOZ-2 itself was ubiquitinated through the CUL3-based E3 ligase mainly within the nucleus and degraded by the 26S proteasome."
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ABTB1/BPOZ-2, CUL3, and TdT form a ternary complex, and BPOZ-2/CUL3 promotes TdT ubiquitination and degradation.
"TdT, BPOZ-2, and CUL3 formed a ternary complex in vivo. TdT was ubiquitinated only within the nucleus and degraded by the 26S proteasome."
BPOZ-2 directly binds to eEF1A1 to promote eEF1A1 ubiquitylation and degradation and prevent translation.
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ABTB1/BPOZ-2 directly binds eEF1A1 through its ankyrin repeats and BTB/POZ domains and promotes eEF1A1 ubiquitination and degradation.
"BPOZ-2 binds to eEF1A1 through the ankyrin repeats and both BTB/POZ domains in BPOZ-2 and Domains I and III in eEF1A1."
Ubiquitylation of terminal deoxynucleotidyltransferase inhibits its activity.
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The BPOZ-2/Cul3 system can ubiquitylate TdT in vitro, although TdT also has CUL3-independent ubiquitylation routes.
"We show here that TdT is ubiquitylated by the Cul3-based ubiquitylation system in vitro."
BPOZ-2 is a negative regulator of the NLPR3 inflammasome contributing to SARS-CoV-2-induced hyperinflammation.
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ABTB1/BPOZ-2 recruits CUL3 to NLRP3 and mediates NLRP3 degradation, and BPOZ-2 loss increases inflammatory output in NLRP3-stimulated macrophage and mouse models.
"BPOZ-2 interacted with NLRP3 and mediated its degradation by recruiting Cullin 3."
Dynamics of cullin-RING ubiquitin ligase network revealed by systematic quantitative proteomics.
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The CRL-network study provides the broader framework for cullins assembled with adaptor modules, consistent with treating ABTB1-CUL3 binding as cullin-binding and CRL3-complex context rather than catalytic E3 ligase activity.
"a large fraction of cullins are assembled with adaptor modules"
MicroRNA-125b transforms myeloid cell lines by repressing multiple mRNA.
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ABTB1 is identified as a direct target of miR-125b in myeloid cell models, with 3'UTR luciferase reporter validation, mRNA and protein down-regulation on miR-125b overexpression, and the report describing ABTB1 as an anti-proliferative factor. This is post-transcriptional regulation context and does not by itself establish a new GO molecular function or localization for ABTB1.
Adaptive and non-adaptive gene expression responses in prostate cancer during androgen deprivation.
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In prostate cancer, ABTB1 is an androgen-receptor-associated gene whose expression is retained under androgen-deprivation adaptation, and ABTB1 expression is a statistically significant marker of progression-free survival in TCGA prostate adenocarcinoma multivariable modeling. This is a correlative clinical association, not direct mechanistic or pathway evidence, and does not justify a new GO process annotation.
A proteome-scale map of the human interactome network.
Architecture of the human interactome defines protein communities and disease networks.
Extensive disruption of protein interactions by genetic variants across the allele frequency spectrum in human populations.
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.
Multimodal cell maps as a foundation for structural and functional genomics.
UniProtKB Q969K4 ABTB1 record
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UniProt curates ABTB1 as cytoplasmic and lists CUL3 among its interaction partners.
"Q969K4; Q13618: CUL3; NbExp=5"
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UniProt also lists EEF1A2 as a reproducible ABTB1 interaction partner, but this review treats elongation-factor binding as unresolved non-core context.
"Q969K4; Q05639: EEF1A2; NbExp=12"
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The UniProt flat file contains UniProt-only GO rows that were not present in the QuickGO GOA download used to seed this review.
"GO; GO:0003746; F:translation elongation factor activity"
ABTB1 review notes
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OpenScientist follow-up evidence supported adding ABTB1 substrate-adaptor activity and protein ubiquitination proposals while keeping downstream substrate-specific disease and stress processes conservative.
"Added `GO:1990756 ubiquitin-like ligase-substrate adaptor activity` and `GO:0016567 protein ubiquitination` as NEW IDA proposals for ABTB1."
Falcon deep research synthesis of ABTB1 function
OpenScientist report on ABTB1/BPOZ-2 as a CUL3 substrate adaptor.
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OpenScientist found direct ABTB1/BPOZ-2 substrate evidence and recommended updating the prior conservative boundary on GO:1990756.
"The gene review's current conservative position, which accepts CUL3 binding but withholds substrate adaptor annotation, can now be updated based on the evidence compiled here."