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 UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Abr and Bcr are multifunctional regulators of the Rho GTP-binding protein family.
The human active breakpoint cluster region-related gene encodes a brain protein with homology to guanine nucleotide exchange proteins and GTPase-activating proteins.
Human ABR encodes a protein with GAPrac activity and homology to the DBL nucleotide exchange factor domain.
Abnormal function of astroglia lacking Abr and Bcr RacGAPs.
Abr and Bcr, two homologous Rac GTPase-activating proteins, control multiple cellular functions of murine macrophages.
Bcr and Abr cooperate in negatively regulating acute inflammatory responses.
Defining the membrane proteome of NK cells.
Regulation of synaptic Rac1 activity, long-term potentiation maintenance, and learning and memory by BCR and ABR Rac GTPase-activating proteins.
Control of local Rho GTPase crosstalk by Abr.
Abr, a negative regulator of Rac, attenuates cockroach allergen-induced asthma in a mouse model.
Deciphering the Molecular and Functional Basis of RHOGAP Family Proteins: A SYSTEMATIC APPROACH TOWARD SELECTIVE INACTIVATION OF RHO FAMILY PROTEINS.
Mapping the proximity interaction network of the Rho-family GTPases reveals signalling pathways and regulatory mechanisms.
EspH interacts with the host active Bcr related (ABR) protein to suppress RhoGTPases.
p75NTR indirectly activates RAC and Cdc42 via a guanyl-nucleotide exchange factor
RHOB GAPs stimulate RHOB GTPase activity
UniProtKB entry Q12979 (ABR_HUMAN)
Affinage mechanistic annotation for ABR (human)
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Provider record reports self_evaluation_pairwise win, faith_pct 100.0, 15 citations, all numeric PubMed ids (no bioRxiv DOIs in PMID-shaped fields). Its corpus-level conclusion that ABR acts in vivo predominantly as a negative regulator of Rac matches the primary literature.
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The record does NOT cite Amin et al. 2016 (PMID:27481945), the systematic RHOGAP specificity survey that reconciles the conflicting substrate claims and that Reactome relies on for ABR's RHOB assignment. That gap was found independently via the Reactome entry, not from the provider narrative.
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Five findings in its table (PMID:23152932 hypoxic pulmonary remodelling, PMID:28579391 hESC mitotic fidelity, PMID:31516309 trabecular-meshwork phagocytosis, PMID:37507586 osteoclast differentiation, PMID:38776074 GDM/hyperglycaemia RhoA activation) were deliberately not annotated: each is a single report, downstream of the Rac/Rho activity change, and the phagocytosis reports have opposite signs.
ABR WITH/FROM resolution and donor-evidence audit
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All 21 distinct WITH/FROM identifiers in ABR-goa.tsv resolve. Nine are not protein sequences (two PANTHER tree nodes, four InterPro signatures, two ARBA rules, three UniProt subcellular-location keywords); the rest resolve to reviewed Swiss-Prot entries except CGD:CAL0000181133, which is the unreviewed TrEMBL entry Q5AGW7 for Candida albicans BEM2.
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20 of 22 protein donor/row pairs carry their own experimental evidence at the donated term itself. The two exceptions are rat Abr and rat Bcr on GO:0014069, which hold that term only by IBA/ISO/ISS but carry IDA at the more specific GO:0099092. No donor is without experimental grounding at or below the donated term, so no row can be argued down on donor weakness.
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GO:0035023 is the only row whose sole protein donor is a paralog (UniProtKB:P11274, human BCR), with no ABR ortholog among its donors.