Affinage

APOBEC3B

DNA dC->dU-editing enzyme APOBEC-3B · UniProt Q9UH17

Length
382 aa
Mass
45.9 kDa
Annotated
2026-04-28
100 papers in source corpus 50 papers cited in narrative 50 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

APOBEC3B is a nuclear-localized, dual-domain DNA cytosine deaminase that functions as both an innate immune effector against retroviruses and retrotransposons and an endogenous source of somatic mutations in cancer, deaminating cytosines to uracils in single-stranded DNA—particularly within TC dinucleotide motifs on lagging-strand replication templates, R-loops, and DNA hairpin structures (PMID:23389445, PMID:26832400, PMID:37735199, PMID:38499542). Only the C-terminal deaminase domain (CD2) is catalytically active, while the N-terminal domain (CD1) mediates nuclear import through two distinct surfaces, attenuates catalytic activity through RNA-dependent sequestration into high-molecular-weight complexes, and contributes deamination-independent functions including LINE-1 restriction, HBV inhibition, and PRC2-mediated epigenetic repression of H3K27me3 (PMID:26195824, PMID:29787764, PMID:28575276, PMID:16648136, PMID:31154396). Catalytic output is governed by a closed-to-open active-site conformational switch controlled by loop 1, by PKA phosphorylation of Thr214 which abolishes ssDNA binding, and by viral countermeasures including EBV BORF2 which occludes the active site and relocalizes APOBEC3B from the nucleus (PMID:27163633, PMID:29234087, PMID:31165764, PMID:30420783, PMID:35476445). Transcription of APOBEC3B is activated by NF-κB (both canonical and non-canonical), the RB/E2F axis, and TEAD transcription factors, and repressed by the p53–p21–DREAM pathway, explaining its upregulation by HPV E6, polyomavirus large T antigen, and DNA-damaging chemotherapy (PMID:26420215, PMID:27577680, PMID:28977491, PMID:28077648, PMID:30723127, PMID:33323971).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2005 High

    Initial characterization established that APOBEC3B packages into HIV-1 virions via binding the Gag nucleocapsid domain and inhibits HIV-1 infectivity in a Vif-resistant manner, distinguishing it from APOBEC3G.

    Evidence Co-immunoprecipitation with HIV-1 Gag nucleocapsid, Vif-binding assays, and virion infectivity assays

    PMID:15993456

    Open questions at the time
    • Mechanism of Vif resistance not structurally resolved
    • Contribution of deamination vs. deamination-independent restriction not separated
  2. 2006 High

    APOBEC3B was shown to restrict both LINE-1 (deamination-independent) and LTR retrotransposons (deamination-dependent), revealing dual mechanisms of retroelement defense and establishing its role as a genomic guardian against endogenous mobile elements.

    Evidence L1 retrotransposition assays with catalytic-dead mutants; co-IP of A3B with IAP Gag and sequencing of edited IAP reverse transcripts

    PMID:16407327 PMID:16648136

    Open questions at the time
    • Identity of the deamination-independent mechanism blocking LINE-1 unknown
    • Physiological relevance in human tissues not established
  3. 2007 High

    Domain dissection revealed that only the C-terminal deaminase domain catalyzes cytidine deamination (shown for both HBV hypermutation and HIV restriction), while the N-terminal domain contributes a deamination-independent antiviral component; APOBEC3B was also found to interact with hnRNP K and suppress HBV transcription.

    Evidence Active-site mutagenesis of both domains with HIV infectivity and HBV hypermutation readouts; co-IP identifying hnRNP K, EMSA/ChIP at HBV enhancer

    PMID:17434555 PMID:17672864 PMID:18024895

    Open questions at the time
    • Structural basis for domain-specific catalysis unknown
    • Whether hnRNP K interaction occurs in physiological HBV infection not demonstrated
  4. 2011 High

    Nuclear localization determinants were mapped to specific N-terminal residues (aa 18–24), and endogenous APOBEC3B was identified as the primary LINE-1 restriction factor in HeLa and human embryonic stem cells, establishing its unique nuclear localization among APOBEC3 family members as functionally consequential.

    Evidence Systematic mutagenesis and chimera construction with localization imaging; shRNA knockdown of all seven APOBEC3 members with L1 retrotransposition readout

    PMID:21715505 PMID:21878639

    Open questions at the time
    • Nuclear import receptor/pathway not identified
    • Whether nuclear localization is required for LINE-1 restriction not formally tested
  5. 2013 High

    A landmark study demonstrated that APOBEC3B is the predominant source of C-to-U editing activity and C-to-T mutations in breast cancer, directly establishing it as an endogenous mutagen driving cancer genome evolution.

    Evidence Nuclear fractionation, biochemical deamination assays on breast cancer cell extracts, shRNA knockdown reducing genomic uracil and C-to-T mutations, overexpression causing DNA fragmentation and γ-H2AX

    PMID:23389445

    Open questions at the time
    • Relative contribution of APOBEC3A vs. APOBEC3B in patient tumors debated
    • Mechanism channeling uracils to fixed mutations not defined
  6. 2015 High

    Crystal structures of the APOBEC3B catalytic domain revealed a tightly closed active site, and biochemical studies confirmed only CD2 is catalytically active; structural analysis explained A3B's attenuated activity relative to A3A through specific CTD substitutions impairing ssDNA binding, and the N-terminal CD1 was shown to facilitate overall activity.

    Evidence X-ray crystallography with dCMP-bound co-crystal, active-site mutagenesis, A3A-A3B chimera analysis, kinetic assays on purified CTD

    PMID:26195824 PMID:26281709 PMID:26384561 PMID:26416889

    Open questions at the time
    • No structure of full-length A3B with ssDNA substrate
    • Mechanism of CD1 facilitation of CD2 activity unresolved
  7. 2015 High

    Transcriptional regulation of APOBEC3B was elucidated: non-canonical NF-κB (RELB) was shown to activate the A3B promoter upon PKC stimulation, HPV E6 was identified as sufficient for A3B upregulation, and A3B was found to catalyze deamination at estrogen receptor binding sites to drive ER-mediated transcription through BER-induced chromatin remodeling.

    Evidence ChIP of RELB at A3B promoter with PKC/NF-κB inhibition; HPV E6 gain/loss-of-function with deaminase activity assays; ChIP for A3B and BER factors at ER binding sites with RNA-seq

    PMID:25538195 PMID:26411678 PMID:26420215

    Open questions at the time
    • How ER-targeted deamination avoids deleterious mutagenesis not explained
    • Whether RELB and classical NF-κB act cooperatively or separately on A3B promoter unclear
  8. 2016 High

    APOBEC3B mutagenesis was shown to preferentially target lagging-strand replication templates, with replication stress amplifying the effect; classical NF-κB (p65/p50) binding sites were mapped on the A3B promoter, complementing the RELB pathway.

    Evidence Yeast model with mutation reporters at defined chromosomal loci, whole-genome sequencing, genetic epistasis with replication mutants; EMSA and luciferase reporter mapping NF-κB sites

    PMID:26832400 PMID:27577680

    Open questions at the time
    • Replication strand bias demonstrated in yeast, not directly in human cancer cells
    • Integration of canonical and non-canonical NF-κB signaling at A3B promoter not resolved
  9. 2017 High

    Multiple mechanistic advances clarified A3B regulation and activity: loop 1 was identified as the conformational gatekeeper controlling substrate access; the N-terminal CD1 domain was shown to attenuate catalysis through RNA-dependent high-molecular-weight complex formation; the p53–p21–DREAM axis was established as a transcriptional repressor; TEAD4 was identified as an E6-induced activator; error-free lesion bypass (Ubc13/Mms2/Mph1) was shown to counteract A3B-induced uracils; and A3B tetramers were found unable to access transcription bubbles.

    Evidence NMR/crystal structures with loop-swap mutagenesis; SEC/RNase treatment of endogenous A3B complexes; ChIP of DREAM at A3B promoter; ChIP of TEAD4; yeast genetic epistasis; in vitro reconstitution with purified full-length A3B

    PMID:27163633 PMID:28077648 PMID:28334887 PMID:28575276 PMID:28977491 PMID:28981865 PMID:29234087

    Open questions at the time
    • How RNA-bound CD1 complexes are disassembled to activate A3B in vivo unknown
    • Full-length structure showing CD1-CD2 interdomain communication absent
    • Whether DREAM and TEAD regulation are independent or interconnected not tested
  10. 2018 High

    EBV BORF2 was discovered as a direct antagonist that stoichiometrically inhibits A3B deaminase activity and relocalizes it from the nucleus, and two distinct N-terminal surfaces required for nuclear import were precisely mapped, completing the nuclear localization model.

    Evidence Proteomics, co-IP, in vitro deaminase inhibition, immunofluorescence relocalization, BORF2-null virus genetics; systematic NTD mutagenesis and domain-grafting

    PMID:29787764 PMID:30420783

    Open questions at the time
    • Structural basis of BORF2–A3B interaction not yet resolved at this time
    • Identity of the nuclear import receptor(s) still unknown
  11. 2019 High

    PKA was identified as a direct kinase phosphorylating A3B at Thr214, abolishing deaminase activity while retaining antiviral/anti-retrotransposon functions; the RB/E2F axis was established as a major transcriptional driver via polyomavirus T antigen studies; and UNG-initiated BER was shown to be the primary error-free pathway counteracting A3B-induced uracils, with synthetic lethality between A3B and UNG loss.

    Evidence In vitro kinase assay, phosphomimetic mutagenesis, MD simulations; T antigen LXCXE mutagenesis with RB knockdown and CDK4/6 inhibition; UNG KO with MMR epistasis and cell viability assays

    PMID:30723127 PMID:31165764 PMID:31611371

    Open questions at the time
    • Whether PKA phosphorylation occurs physiologically in cancer cells not demonstrated
    • How RB/E2F and NF-κB pathways are integrated at the A3B promoter unclear
    • Whether synthetic lethality with UNG translates to in vivo tumor models unknown
  12. 2020 High

    Chemotherapy-induced APOBEC3B expression was shown to proceed through DNA-PKcs/ATM→NF-κB signaling independently of p53, providing a mechanism for therapy-driven mutagenesis; DHX9 was identified as a negative regulator of A3B anti-HBV activity.

    Evidence DNA-PKcs/ATM pharmacological inhibition and knockdown with NF-κB ChIP at A3B promoter; co-IP/MS identifying DHX9 with functional HBV readout

    PMID:32056513 PMID:33323971

    Open questions at the time
    • Whether chemotherapy-induced A3B contributes to therapy resistance mutations in patients not shown
    • DHX9–A3B interaction surface not mapped
  13. 2022 High

    Cryo-EM structure of the BORF2–APOBEC3B complex revealed the molecular mechanism of viral antagonism: a >1000-Ų interface occludes the A3B active site, and BORF2-specific insertions confer selectivity for A3B over other APOBEC3 family members; this antagonism was shown to be conserved among gamma-herpesviruses.

    Evidence Cryo-EM structure determination; mutagenesis mapping separable binding and inhibition surfaces; ancestral A3B reconstruction; cross-species functional testing

    PMID:35476445 PMID:36458685

    Open questions at the time
    • Whether therapeutic disruption of BORF2–A3B interaction can enhance antiviral defense untested
    • Whether other viral factors use similar occlusion mechanisms unknown
  14. 2023 High

    APOBEC3B was shown to directly bind and resolve R-loops, deaminating ssDNA within these structures to drive transcription-associated mutagenesis; it was also found to form complexes with PABPC1/G3BP1 to stimulate PKR and protect stress granules, revealing deamination-independent innate immune functions; in vivo mouse models confirmed that catalytic activity drives C-to-T mutations, accelerated carcinogenesis, and metastasis, and separately revealed A3B-mediated C-to-U RNA editing.

    Evidence DRIP-seq and A3B ChIP-seq in KO/overexpression cells; co-IP of PABPC1/G3BP1 with PKR activation assays; transgenic mouse WGS with catalytic-dead controls; RNA-seq vs. genomic DNA comparison in inducible mouse model

    PMID:36781883 PMID:37735199 PMID:37797615 PMID:38001542

    Open questions at the time
    • Relative contribution of R-loop vs. replication-fork substrates to tumor mutagenesis not quantified
    • Whether RNA editing by A3B is physiologically relevant or an overexpression artifact uncertain
    • Whether PABPC1/PKR function operates in cancer contexts unknown
  15. 2024 High

    High-throughput substrate profiling and genome-wide uracilome mapping established that APOBEC3B preferentially deaminates cytosines in 4-nucleotide DNA hairpin loops (distinct from A3A's 3-nt preference) and near transcription start sites, providing substrate-structure-level resolution to distinguish A3B from A3A contributions in tumor genomes.

    Evidence Oligo-seq in vitro profiling; Uracil-seq in E. coli expressing A3B; reanalysis of human tumor mutations for hairpin signatures

    PMID:38499542 PMID:38499553

    Open questions at the time
    • Whether hairpin preferences hold in chromatinized human genomic DNA not tested
    • Structural basis for 4-nt vs. 3-nt loop preference not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity of the nuclear import receptor(s) recognizing A3B's N-terminal surfaces, the structural basis of full-length A3B interdomain communication, how RNA-mediated inhibition is relieved in specific cellular contexts, and the quantitative apportionment of APOBEC3A versus APOBEC3B contributions to human tumor mutagenesis.
  • No full-length APOBEC3B structure with ssDNA substrate
  • Nuclear import receptor(s) not identified
  • Physiological triggers for releasing RNA-mediated inhibition unknown
  • A3A vs. A3B attribution in patient tumors remains contested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140097 catalytic activity, acting on DNA 10 GO:0003677 DNA binding 5 GO:0140098 catalytic activity, acting on RNA 1
Localization
GO:0005634 nucleus 3
Pathway
R-HSA-168256 Immune System 6 R-HSA-74160 Gene expression (Transcription) 6 R-HSA-1643685 Disease 4 R-HSA-73894 DNA Repair 3 R-HSA-4839726 Chromatin organization 1
Partners
BORF2DHX9EZH2G3BP1HNRNPKMSL2PABPC1PRKACA
Complex memberships
PABPC1/G3BP1 stress granule complexPRC2

Evidence

Reading pass · 50 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2013 APOBEC3B is a nuclear-localized DNA cytosine deaminase (C-to-U) that is the predominant source of DNA C-to-U editing activity in breast cancer cell-line extracts; knockdown reduces genomic uracil and C-to-T mutations, while overexpression causes DNA fragmentation, γ-H2AX accumulation, and C-to-T mutations, establishing it as an endogenous mutagen. Nuclear fractionation, biochemical deamination assays on cell extracts, shRNA knockdown with genomic uracil quantification, and overexpression with mutational frequency analysis Nature High 23389445
2006 APOBEC3B inhibits LINE-1 retrotransposition by a deamination-independent mechanism; a catalytically inactive APOBEC3B mutant retains anti-L1 activity, and no cDNA C-to-T hypermutations were detected, indicating a pre-integration block. L1 retrotransposition cell assay, catalytic mutant expression, 3D-PCR hypermutation analysis The Journal of biological chemistry High 16648136
2006 APOBEC3B inhibits LTR-retrotransposon (IAP) replication via a DNA editing (deamination-dependent) mechanism; APOBEC3B specifically interacts with the IAP Gag protein and packages into IAP virus-like particles, inducing extensive editing of IAP reverse transcripts. Co-immunoprecipitation of APOBEC3B with IAP Gag, retrotransposition assay, sequencing of reverse transcripts for editing Nucleic acids research High 16407327
2005 APOBEC3B packages into HIV-1 virions by binding the nucleocapsid domain of HIV-1 Gag; it inhibits both Vif-deficient and wild-type HIV-1 infectivity because it cannot bind HIV-1 Vif, making it Vif-resistant. Co-immunoprecipitation of APOBEC3B with HIV-1 Gag nucleocapsid domain; Vif-binding assays; virion infectivity assays Virology High 15993456
2007 APOBEC3B contains two enzymatically active cytidine deaminase domains (unlike APOBEC3G, which has only one active C-terminal domain); catalytically inactive APOBEC3B retains partial (~8-fold) HIV-1 inhibitory activity, indicating a deamination-independent component. Active-site mutagenesis of both deaminase consensus sequences, HIV-1 infectivity assays Virology High 17434555
2015 Crystal structure of the APOBEC3B catalytic domain reveals a tightly closed active site regulated by adjacent flexible loops; dCMP-bound structure informs a multistep ssDNA binding model; active-site residues identified by mutagenesis as critical for catalysis. X-ray crystallography (multiple crystal forms), active-site mutagenesis, dCMP-bound co-crystal structure The Journal of biological chemistry High 26416889
2016 NMR solution structure of the APOBEC3B catalytic domain shows that loop 1 controls substrate access to the active site; substituting APOBEC3A loop 1 into APOBEC3B greatly increases deaminase activity, and H29R in APOBEC3A loop 1 reduces A3A activity to A3B levels, establishing loop 1 as the primary activity determinant. NMR structure determination, loop-swap mutagenesis, in vitro deaminase activity assays Biochemistry High 27163633
2017 Crystal structures of APOBEC3B catalytic domain in alternative closed conformations, combined with MD simulations, show dynamic equilibrium of active-site loops; loop 1 mimicry of APOBEC3A elevates ssDNA deaminase activity, indicating that a closed-to-open conformational switch controls substrate binding. X-ray crystallography, all-atom MD simulations, loop-swap mutagenesis with in vitro deaminase assays Scientific reports High 29234087
2016 APOBEC3B and APOBEC3A preferentially deaminate the lagging strand template during DNA replication; replication fork-stabilizing protein deficiencies and replication stress strongly augment APOBEC3B mutagenesis, identifying ssDNA formed during lagging-strand synthesis as a major APOBEC3B substrate. Yeast model system with mutation reporters at defined chromosomal locations, whole-genome sequencing of APOBEC3A/3B-expressing yeast, genetic epistasis with replication mutants Cell reports High 26832400
2015 PKC activation (via phorbol ester) induces APOBEC3B expression and activity through non-canonical NF-κB signaling involving RELB (not RELA) recruitment to the APOBEC3B promoter; PKC or NF-κB inhibition suppresses this induction. PKC agonist treatment, pharmacological inhibition of PKC/NF-κB, chromatin immunoprecipitation of RELB at the A3B promoter, deaminase activity assays Cancer research High 26420215
2014 HPV E6 oncoprotein (high-risk but not low-risk types) is sufficient to upregulate APOBEC3B mRNA expression and enzymatic activity; endogenous E6 is required for A3B upregulation in HPV-positive cell lines; the mechanism likely involves E6-mediated TP53 functional inactivation causing derepression of A3B transcription. HPV genome transfection, E6 transduction, E6-inactivation mutagenesis, shRNA knockdown of E6, deaminase activity assays mBio High 25538195
2018 EBV ribonucleotide reductase large subunit BORF2 binds the APOBEC3B catalytic domain, stoichiometrically inhibits its DNA cytosine deaminase activity, and causes dramatic relocalization of nuclear APOBEC3B to perinuclear bodies; BORF2-null virus shows lower titers and APOBEC3B-dependent hypermutation. Proteomics, co-immunoprecipitation, mutagenesis mapping of interaction surface, in vitro deaminase inhibition assay, immunofluorescence relocalization, BORF2-null virus experiments Nature microbiology High 30420783
2022 Cryo-EM structure of the EBV BORF2–APOBEC3B complex reveals a >1000-Ų binding interface that blocks the APOBEC3B active site from accessing ssDNA; unique BORF2 insertions absent from other ribonucleotide reductases mediate preferential binding to APOBEC3B over APOBEC3A and APOBEC3G. Cryo-EM structure determination of the BORF2–APOBEC3B complex Science advances High 35476445
2018 APOBEC3B nuclear localization requires two distinct N-terminal domain surfaces (import surface 1: first 30 amino acids; import surface 2: loop 5/α-helix 3); disruption of either surface completely abolishes nuclear localization, and these surfaces graft nuclear import into related cytoplasmic APOBEC3 family members. Mutagenesis of N-terminal domain residues, subcellular localization assays (fluorescence microscopy), domain-swap experiments into related APOBEC3 members Journal of molecular biology High 29787764
2011 Amino acids 18, 19, 22, and 24 in the N-terminal domain of APOBEC3B are major determinants for nuclear localization; replacing the first 60 amino acids of A3B with A3G retargets the chimeric protein to the cytoplasm and enhances HIV restriction while retaining LINE-1 inhibition. Mutagenesis, chimeric protein construction, subcellular localization imaging, HIV infectivity assays, LINE-1 retrotransposition assay Journal of virology High 21715505
2011 Endogenous APOBEC3B (not other APOBEC3 members) is the primary restriction factor for engineered LINE-1 retrotransposition in HeLa cells and human embryonic stem cells; shRNA knockdown of A3B specifically increases L1 retrotransposition 2–3.7-fold. shRNA knockdown of individual endogenous APOBEC3 proteins, L1 retrotransposition cell assay The Journal of biological chemistry High 21878639
2007 APOBEC3B interacts with heterogeneous nuclear ribonucleoprotein K (hnRNP K) and inhibits hnRNP K binding to the HBV enhancer II, suppressing HBV S gene transcription and HBV core-associated DNA synthesis; A3B also directly suppresses HBV S gene promoter activity. Co-immunoprecipitation identifying hnRNP K as major interaction partner, EMSA/ChIP for hnRNP K binding to HBV enhancer, luciferase promoter assays, HBsAg/HBeAg expression assays Cellular microbiology High 17672864
2015 APOBEC3B-catalyzed C-to-U deamination at estrogen receptor (ERα) binding regions generates DNA strand breaks via base excision repair (BER) activation; these breaks are repaired by NHEJ and promote chromatin remodeling at ER target gene regulatory regions, thereby driving ERα-mediated transcription. A3B is required for ER-regulated gene expression. A3B knockdown and overexpression, ChIP for A3B and BER factors at ER binding sites, NHEJ reporter assays, RNA-seq of ER target genes Cell reports High 26411678
2017 Full-length APOBEC3B purified from cells cycles rapidly between DNA substrates and can deaminate RPA-bound ssDNA; APOBEC3B tetramers are inhibited from deaminating during transcription due to size limitations, whereas APOBEC3A monomers are not so restricted. Purification of full-length APOBEC3B, in vitro deamination assays on replication-mimicking ssDNA substrates and RPA-coated ssDNA, biochemical comparison with APOBEC3A and APOBEC3H Nucleic acids research High 28981865
2017 APOBEC3B catalytic domain crystal structure reveals that N-terminal non-catalytic CD1 regulates catalytic activity; A3B expressed in human cells exists in hypoactive high-molecular-weight complexes; RNase A treatment activates these complexes. CD1 hydrophobic surface residue W127 and positively-charged surfaces mediate RNA-dependent attenuation of A3B catalysis; hnRNPs bind A3B via CD1 surface hydrophobic residues. Crystal structure of A3B-CD1 variant, size-exclusion chromatography, RNase A treatment, mutagenesis, hnRNP co-immunoprecipitation Nucleic acids research High 28575276
2019 APOBEC3B-expressing cells are selectively killed by inhibiting uracil DNA glycosylase (UNG); this synthetic lethality requires mismatch repair proteins (MSH2, MLH1) and p53, indicating that UNG-initiated BER is the major error-free counteraction of A3B-induced genomic uracil. UNG knockout in 293 and MCF10A cells expressing A3B, shRNA of MMR genes, cell viability assays, genomic uracil quantification, UNG complementation rescue Proceedings of the National Academy of Sciences of the United States of America High 31611371
2017 p53 directly represses APOBEC3B expression by inducing p21 (CDKN1A), which recruits the DREAM repressor complex to the A3B gene promoter; loss of p53 (by mutation or HPV-mediated inhibition) prevents DREAM recruitment, causing elevated A3B expression and deaminase activity. p53 knockdown/overexpression, ChIP for DREAM complex at A3B promoter, p21 knockdown, deaminase activity assays Nucleic acids research High 28977491
2016 The classical NF-κB pathway (p65/p50 and p65/c-Rel heterodimers) activates APOBEC3B transcription; three NF-κB binding sites in the A3B promoter were identified and validated by luciferase reporter and EMSA assays; PKC activates this pathway leading to A3B expression. NF-κB binding site identification by luciferase reporter assay and EMSA, PKC/IKK pharmacological inhibition, shRNA knockdown Biochemical and biophysical research communications High 27577680
2017 HPV16 E6 upregulates APOBEC3B via the TEAD family transcription factors; E6-mediated p53 degradation increases TEAD1/4 protein levels, TEAD4 binds the A3B promoter (validated by ChIP), and TEAD4 knockdown reduces A3B mRNA in E6-expressing cells. Luciferase reporter assay mapping TEAD-binding sites, ChIP of TEAD4 at A3B promoter, TEAD knockdown, ectopic TEAD4 expression, E6 mutant analysis Journal of virology High 28077648
2019 Polyomavirus large T antigen upregulates APOBEC3B through its LXCXE RB-interacting motif (not through p53-binding domain); the upregulated enzyme localizes strongly to the nucleus and partially to viral replication centers; global gene expression analyses implicate the RB/E2F axis in promoting APOBEC3B transcription. Truncated T antigen expression, LXCXE motif mutagenesis, RB1/RBL1/RBL2 genetic knockdown, CDK4/6 inhibition, RNA-seq, subcellular localization imaging mBio High 30723127
2023 APOBEC3B physically interacts with R-loop-associated factors and directly binds R-loops both in cells and in vitro; A3B overexpression decreases R-loops genome-wide and A3B knockout increases R-loops; A3B preferentially deaminates ssDNA within R-loop structures, contributing to transcription-associated mutagenesis. APOBEC3B proteomics identifying R-loop factors, biochemical R-loop binding assays in vitro and in vivo (DRIP-seq), genome-wide R-loop mapping in A3B KO and overexpression cells, APOBEC3B ChIP-seq Nature genetics High 37735199
2023 APOBEC3B forms a complex with PABPC1 to stimulate PKR (protein kinase R) and counterbalance ADAR1's PKR-suppressing activity during viral infection, promoting translational shutdown; APOBEC3B also localizes to stress granules through PABPC1 interaction and protects stress granule-associated mRNA from RNase L-induced cleavage by interacting with G3BP1. Co-immunoprecipitation identifying PABPC1 and G3BP1 as APOBEC3B interactors, PKR activation assays, stress granule imaging, RNase L activity assays, APOBEC3B KO viral infection experiments Nature communications High 36781883
2019 Protein kinase A (PKA) physically binds APOBEC3B and phosphorylates Thr214; phosphomimetic mutants T214D and T214E completely lose deaminase activity in vitro and in cell-based foreign DNA editing assays; MD simulations show Thr214 phosphorylation disrupts ssDNA binding at the catalytic core; anti-retroviral and anti-retrotransposition activities are retained despite loss of deaminase activity. Co-immunoprecipitation of PKA with A3B, in vitro kinase assay, phosphomimetic mutagenesis, in vitro deaminase assays, cell-based DNA editing assays, MD simulations Scientific reports High 31165764
2015 Only the C-terminal deaminase domain (CD2) of APOBEC3B is catalytically active for cytosine deamination; both A3B and A3B-CD2 can also deaminate methylcytosine (mC); engineered A3B-CD2 variants achieve >100-fold enhanced mC deamination activity through structural/functional analysis-guided mutagenesis. In vitro deaminase assays with domain mutants, engineering of active-site variants, biochemical comparison of CD1 and CD2 The Biochemical journal High 26195824
2007 Only the carboxy-terminal deaminase domain of APOBEC3B catalyzes cytidine deamination leading to HBV hypermutation; the amino-terminal domain contributes to full HBV replication inhibition through a deamination-independent mechanism; both domains must be intact for maximum anti-HBV effect. Mutagenesis of both deaminase active sites (C97S, H66R, carboxy-terminal mutations), HBV hypermutation assay (3D-PCR), HBV replication inhibition assay The Journal of general virology High 18024895
2017 APOBEC3B interacts with PRC2 (Polycomb Repressor Complex 2) in a deaminase-independent manner, suppressing global H3K27me3 and reducing H3K27me3 occupancy at the CCL2 chemokine promoter, thereby promoting CCL2 expression and recruitment of myeloid-derived suppressor cells and tumor-associated macrophages. Co-immunoprecipitation of A3B with PRC2, ChIP for H3K27me3 at CCL2 promoter in A3B-expressing cells, deaminase dead mutant (E68Q/E255Q) showing same effect, RNA-seq, flow cytometry for immune cell infiltration Gut High 31154396
2015 The APOBEC3B catalytic domain is in equilibrium between monomer and dimer; the M-junction methionine between NTD and CTD is essential for structural stability and high mutagenic activity; APOBEC3B-CTD is at least 10-fold less efficient at deaminating 5-methylcytosine compared to cytosine, and 10-fold less efficient than APOBEC3A at mutating 5mC. In vitro deaminase kinetic assays on purified CTD, size-exclusion chromatography, MALDI-TOF, mutagenesis of junction methionine, bacterial mutagenesis assay Journal of molecular biology High 26281709
2015 The molecular basis for APOBEC3B's attenuated activity relative to APOBEC3A maps to a few substitutions in the CTD that impair ssDNA binding, while the NTD facilitates A3B activity; A3A-A3B chimeras and mutant analysis revealed these determinants; APOBEC3B cannot induce DNA double-strand breaks unlike APOBEC3A. A3A-A3B chimera construction and mutagenesis, in vitro deamination assays, DNA strand break assays, comparison with rhesus macaque orthologs Nucleic acids research High 26384561
2017 APOBEC3B-induced mutations in ssDNA during replication are primarily avoided by error-free lesion bypass (template switching) mediated by Ubc13, Mms2, and Mph1; abasic sites (not the uracils themselves) are the mutagenic intermediates channeled through Rev1 when error-free bypass fails. Yeast genetic epistasis: APOBEC3B expression combined with BER endonuclease and DNA damage tolerance gene deletions, CAN1 forward mutation assay Nucleic acids research High 28334887
2016 BK polyomavirus large T antigen alone upregulates APOBEC3B expression and activity in primary kidney cells; APOBEC3B target motifs are depleted in BKPyV genomes and this depletion is enriched on the nontranscribed (lagging) strand, suggesting evolutionary pressure from APOBEC3B activity. BKPyV infection of primary cells, large T antigen transduction, APOBEC3B knockdown, deaminase activity assays, bioinformatic analysis of viral genome sequence composition Journal of virology Medium 27147740
2012 APOBEC3B can induce C-to-T base substitutions directly in human genomic DNA (including the cMYC oncogene) when transfected into lymphoma cells that highly express endogenous A3B; this establishes A3B as capable of directly mutating human chromosomal DNA. A3B transfection in lymphoma cells, sequencing of cMYC locus for base substitutions Scientific reports Medium 23150777
2017 APOBEC3B interacts with HBV core protein in an RNA-dependent manner (co-immunoprecipitation); APOBEC3B deaminates HBV minus- and plus-strand DNAs but not pregenomic RNA within core particles; inhibition of HBV replication primarily depends on the C-terminal active site. Co-immunoprecipitation of A3B with HBV core protein ± RNase, use of HBV polymerase mutants, 3D-PCR strand-specific editing analysis Antiviral research Medium 29129707
2020 DHX9 (DExD/H-box helicase 9) interacts with APOBEC3B and attenuates its anti-HBV activity by inhibiting A3B binding to HBV pregenomic RNA without affecting A3B intrinsic deaminase activity. Co-immunoprecipitation and mass spectrometry identifying DHX9, in vitro deaminase assay, pgRNA binding assay, DHX9 knockdown with HBV replication readout Emerging microbes & infections Medium 32056513
2016 The APOBEC3B tamoxifen-resistance promoting activity in ER+ breast cancer requires the enzyme's catalytic activity (deaminase function); APOBEC3B depletion prolongs tamoxifen responses in murine xenograft experiments. APOBEC3B overexpression (WT vs. catalytic mutant) and knockdown in ER+ breast cancer xenograft experiments with tamoxifen treatment Science advances High 27730215
2023 Human APOBEC3B expressed at tumor-like levels in a mouse model causes C-to-T mutations preferentially in TC dinucleotide motifs consistent with its biochemical activity; catalytic activity is required for all mutagenic and carcinogenic phenotypes (accelerated carcinogenesis, metastasis, tumor heterogeneity) observed in vivo. Transgenic mouse model expressing human APOBEC3B (WT vs. catalytic mutant), whole-genome sequencing of tumors for mutation signatures, tumor histology and metastasis quantification Cell reports. Medicine High 37797615
2023 At high acute expression levels, APOBEC3B causes C-to-U RNA editing events (UCC-to-UUC) in mouse tissues that are deaminase-dependent and not evident in corresponding genomic DNA, identifying a novel RNA editing activity of APOBEC3B. Doxycycline-inducible mouse model of APOBEC3B overexpression, RNA-sequencing vs. matched genomic DNA sequencing to detect C-to-U RNA edits Genome biology High 38001542
2024 APOBEC3B preferentially deaminates cytosines in DNA stem-loop (hairpin) structures, with distinct loop-length preferences (4-nt loops) compared to APOBEC3A (3-nt loops); specific flanking sequences strongly regulate APOBEC3B deaminase activity; structural features of APOBEC3B responsible for substrate preferences were identified. Oligo-seq (in vitro sequencing-based deamination assay), biochemical deamination assays on defined substrates, comparison with APOBEC3A, tumor genome analysis for hairpin-associated mutations Nature communications High 38499542
2024 Genome-wide uracilome mapping shows APOBEC3B prefers 4-nt hairpin loops while APOBEC3A prefers 3-nt hairpin loops; both enzymes preferentially deaminate cytosines near transcription start sites and on lagging-strand replication templates; these distinct substrate preferences produce different hairpin mutation signatures in human tumors. Uracil-seq in E. coli expressing A3B or A3B-CTD, whole-genome analysis, comparison with APOBEC3A uracilome, reanalysis of human tumor mutation data Nature communications High 38499553
2020 Induction of APOBEC3B expression by chemotherapy drugs (5-FU, etoposide, cisplatin) is mediated by DNA-PKcs and ATM activation leading to NF-κB recruitment to the A3B promoter; this induction is p53-independent; A3B knockdown re-sensitizes resistant cells to cisplatin. Pharmacological inhibition and gene knockdown of DNA-PKcs/ATM/ATR, NF-κB ChIP at A3B promoter, A3B KO in chemotherapy resistance assays Oncogene High 33323971
2022 Gamma-herpesvirus RNRs engage APOBEC3B via largely distinct surfaces; RNR-mediated enzymatic inhibition and relocalization of A3B depend on binding to different regions of the A3B catalytic domain; this antagonism is conserved only among gamma-herpesviruses infecting primates that encode A3B, and the reconstructed ancestral primate A3B is similarly engaged. Mutagenesis mapping of interaction surfaces, biochemical inhibition and relocalization assays, ancestral A3B reconstruction and functional testing, comparative virology across primate herpesviruses eLife High 36458685
2015 SIV Vif proteins (especially SIVmac239 Vif) can promote APOBEC3B degradation via the canonical polyubiquitination/proteasomal pathway; APOBEC3B protein levels are rescued by MG132 and by mutation of the E3 ligase-binding motif in Vif. Expression of SIV Vif proteins in human cells, proteasome inhibitor MG132 rescue, E3 ligase motif mutagenesis, endogenous APOBEC3B degradation in cancer cell lines Oncotarget Medium 26544511
2017 MSL2 (male-specific lethal 2) promotes HBV cccDNA stability by ubiquitylating and degrading APOBEC3B in hepatoma cells; HBx upregulates MSL2 through the YAP/FoxA1 signaling axis. MSL2 overexpression and knockdown, co-immunoprecipitation of MSL2 with A3B, ubiquitylation assay showing A3B degradation, cccDNA quantification, ChIP of FoxA1 at MSL2 promoter Hepatology (Baltimore, Md.) Medium 28608964
2021 APOBEC3B is preferentially expressed at the G2/M phase of the cell cycle in myeloma cells and normal bone marrow cells, as established by single-cell RNA-sequencing and cell sorting/protein quantification. Single-cell RNA-sequencing of 1276 primary myeloma cells, cell cycle sorting followed by APOBEC3B protein quantification Biochemical and biophysical research communications Medium 33592502
2018 Molecular dynamics simulations and mutational analysis identify Arg211 in loop 1 of A3B-CTD as a gatekeeper residue coordinating DNA in the active site and critical for nucleotide specificity; a unique autoinhibited conformation in A3B-CTD restricts DNA access to the active site. Advanced molecular modeling, experimental mutagenesis, MD simulations validated against known structures Journal of chemical theory and computation Medium 30457868
2019 APOBEC3B promotes HCC proliferation, migration, invasion, and metastasis through a deaminase-independent mechanism; overexpression of the deaminase-dead double mutant (E68A/E255Q) produces similar pro-tumorigenic effects as wild-type A3B, including enhanced cell cycle progression. Overexpression of WT vs. deaminase-dead A3B, A3B knockdown in high-expressing HCC cells, in vitro proliferation/invasion assays, in vivo xenograft and metastasis models Molecular carcinogenesis Medium 30575099

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 APOBEC3B is an enzymatic source of mutation in breast cancer. Nature 705 23389445
2013 Evidence for APOBEC3B mutagenesis in multiple human cancers. Nature genetics 628 23852168
2015 An APOBEC3A hypermutation signature is distinguishable from the signature of background mutagenesis by APOBEC3B in human cancers. Nature genetics 347 26258849
2014 Association of a germline copy number polymorphism of APOBEC3A and APOBEC3B with burden of putative APOBEC-dependent mutations in breast cancer. Nature genetics 234 24728294
2006 APOBEC3B and APOBEC3F inhibit L1 retrotransposition by a DNA deamination-independent mechanism. The Journal of biological chemistry 234 16648136
2006 APOBEC3A and APOBEC3B are potent inhibitors of LTR-retrotransposon function in human cells. Nucleic acids research 232 16407327
2018 APOBEC3B and APOBEC mutational signature as potential predictive markers for immunotherapy response in non-small cell lung cancer. Oncogene 207 29695832
2005 Human APOBEC3B is a potent inhibitor of HIV-1 infectivity and is resistant to HIV-1 Vif. Virology 191 15993456
2016 The DNA cytosine deaminase APOBEC3B promotes tamoxifen resistance in ER-positive breast cancer. Science advances 186 27730215
2016 APOBEC3A and APOBEC3B Preferentially Deaminate the Lagging Strand Template during DNA Replication. Cell reports 183 26832400
2014 Human papillomavirus E6 triggers upregulation of the antiviral and cancer genomic DNA deaminase APOBEC3B. mBio 170 25538195
2013 APOBEC3B upregulation and genomic mutation patterns in serous ovarian carcinoma. Cancer research 145 24154874
2014 Elevated APOBEC3B correlates with poor outcomes for estrogen-receptor-positive breast cancers. Hormones & cancer 132 25123150
2015 The PKC/NF-κB signaling pathway induces APOBEC3B expression in multiple human cancers. Cancer research 119 26420215
2018 Epstein-Barr virus BORF2 inhibits cellular APOBEC3B to preserve viral genome integrity. Nature microbiology 114 30420783
2017 APOBEC3A and APOBEC3B Activities Render Cancer Cells Susceptible to ATR Inhibition. Cancer research 113 28698210
2020 Rationally Designed APOBEC3B Cytosine Base Editors with Improved Specificity. Molecular cell 109 32721385
2014 A prevalent cancer susceptibility APOBEC3A hybrid allele bearing APOBEC3B 3'UTR enhances chromosomal DNA damage. Nature communications 107 25298230
2015 APOBEC3B-Mediated Cytidine Deamination Is Required for Estrogen Receptor Action in Breast Cancer. Cell reports 92 26411678
2012 APOBEC3B can impair genomic stability by inducing base substitutions in genomic DNA in human cells. Scientific reports 88 23150777
2017 Roles of APOBEC3A and APOBEC3B in Human Papillomavirus Infection and Disease Progression. Viruses 86 28825669
2015 Molecular mechanism and clinical impact of APOBEC3B-catalyzed mutagenesis in breast cancer. Breast cancer research : BCR 84 25848704
2012 APOBEC3A, APOBEC3B, and APOBEC3H haplotype 2 restrict human T-lymphotropic virus type 1. Journal of virology 83 22457529
2011 Endogenous APOBEC3B restricts LINE-1 retrotransposition in transformed cells and human embryonic stem cells. The Journal of biological chemistry 82 21878639
2015 Crystal Structure of the DNA Deaminase APOBEC3B Catalytic Domain. The Journal of biological chemistry 81 26416889
2016 Functional Upregulation of the DNA Cytosine Deaminase APOBEC3B by Polyomaviruses. Journal of virology 79 27147740
2017 Elevated APOBEC3B expression drives a kataegic-like mutation signature and replication stress-related therapeutic vulnerabilities in p53-defective cells. British journal of cancer 78 28535155
2014 In vivo and in vitro studies suggest a possible involvement of HPV infection in the early stage of breast carcinogenesis via APOBEC3B induction. PloS one 74 24858917
2019 Long non-coding RNA HULC activates HBV by modulating HBx/STAT3/miR-539/APOBEC3B signaling in HBV-related hepatocellular carcinoma. Cancer letters 73 30981758
2017 p53 controls expression of the DNA deaminase APOBEC3B to limit its potential mutagenic activity in cancer cells. Nucleic acids research 69 28977491
2019 APOBEC3B interaction with PRC2 modulates microenvironment to promote HCC progression. Gut 67 31154396
2017 APOBEC3B, a molecular driver of mutagenesis in human cancers. Cell & bioscience 65 28572915
2017 Hepatitis B virus X protein-elevated MSL2 modulates hepatitis B virus covalently closed circular DNA by inducing degradation of APOBEC3B to enhance hepatocarcinogenesis. Hepatology (Baltimore, Md.) 64 28608964
2020 APOBEC3B-mediated corruption of the tumor cell immunopeptidome induces heteroclitic neoepitopes for cancer immunotherapy. Nature communications 63 32034147
2007 Cytidine deaminase APOBEC3B interacts with heterogeneous nuclear ribonucleoprotein K and suppresses hepatitis B virus expression. Cellular microbiology 63 17672864
2023 APOBEC3B regulates R-loops and promotes transcription-associated mutagenesis in cancer. Nature genetics 62 37735199
2023 The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance. Nature genetics 61 38049664
2007 The intrinsic antiretroviral factor APOBEC3B contains two enzymatically active cytidine deaminase domains. Virology 60 17434555
2017 Human Papillomavirus 16 E6 Upregulates APOBEC3B via the TEAD Transcription Factor. Journal of virology 59 28077648
2020 The DNA Cytosine Deaminase APOBEC3B is a Molecular Determinant of Platinum Responsiveness in Clear Cell Ovarian Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 55 32060098
2011 The role of amino-terminal sequences in cellular localization and antiviral activity of APOBEC3B. Journal of virology 54 21715505
2012 Evidence of associations of APOBEC3B gene deletion with susceptibility to persistent HBV infection and hepatocellular carcinoma. Human molecular genetics 53 23213177
2005 Regulated production and anti-HIV type 1 activities of cytidine deaminases APOBEC3B, 3F, and 3G. AIDS research and human retroviruses 53 16060832
2016 Nuclear Magnetic Resonance Structure of the APOBEC3B Catalytic Domain: Structural Basis for Substrate Binding and DNA Deaminase Activity. Biochemistry 51 27163633
2016 Classical NF-κB pathway is responsible for APOBEC3B expression in cancer cells. Biochemical and biophysical research communications 51 27577680
2017 Enzyme cycling contributes to efficient induction of genome mutagenesis by the cytidine deaminase APOBEC3B. Nucleic acids research 49 28981865
2023 Human APOBEC3B promotes tumor development in vivo including signature mutations and metastases. Cell reports. Medicine 48 37797615
2015 Identification of APOBEC3B promoter elements responsible for activation by human papillomavirus type 16 E6. Biochemical and biophysical research communications 48 25800874
2015 APOBEC3B: pathological consequences of an innate immune DNA mutator. Biomedical journal 46 25566802
2015 DNA cytosine and methylcytosine deamination by APOBEC3B: enhancing methylcytosine deamination by engineering APOBEC3B. The Biochemical journal 46 26195824
2016 Germline APOBEC3B deletion is associated with breast cancer risk in an Asian multi-ethnic cohort and with immune cell presentation. Breast cancer research : BCR 45 27233495
2018 APOBEC3B Nuclear Localization Requires Two Distinct N-Terminal Domain Surfaces. Journal of molecular biology 44 29787764
2018 BE-FLARE: a fluorescent reporter of base editing activity reveals editing characteristics of APOBEC3A and APOBEC3B. BMC biology 44 30593278
2023 Mutational impact of APOBEC3A and APOBEC3B in a human cell line and comparisons to breast cancer. PLoS genetics 42 38033156
2017 Structural determinants of APOBEC3B non-catalytic domain for molecular assembly and catalytic regulation. Nucleic acids research 41 28575276
2017 APOBEC3B edits HBV DNA and inhibits HBV replication during reverse transcription. Antiviral research 38 29129707
2019 The deaminase APOBEC3B triggers the death of cells lacking uracil DNA glycosylase. Proceedings of the National Academy of Sciences of the United States of America 37 31611371
2020 Endogenous APOBEC3B overexpression characterizes HPV-positive and HPV-negative oral epithelial dysplasias and head and neck cancers. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 35 32632179
2023 APOBEC3B drives PKR-mediated translation shutdown and protects stress granules in response to viral infection. Nature communications 33 36781883
2019 Polyomavirus T Antigen Induces APOBEC3B Expression Using an LXCXE-Dependent and TP53-Independent Mechanism. mBio 33 30723127
2017 Conformational Switch Regulates the DNA Cytosine Deaminase Activity of Human APOBEC3B. Scientific reports 31 29234087
2024 Mesoscale DNA features impact APOBEC3A and APOBEC3B deaminase activity and shape tumor mutational landscapes. Nature communications 30 38499542
2021 Hypoxia-Inducible Factor 1 Alpha-Mediated RelB/APOBEC3B Down-regulation Allows Hepatitis B Virus Persistence. Hepatology (Baltimore, Md.) 30 33991110
2019 Endogenous APOBEC3B Overexpression Constitutively Generates DNA Substitutions and Deletions in Myeloma Cells. Scientific reports 29 31073151
2017 Avoidance of APOBEC3B-induced mutation by error-free lesion bypass. Nucleic acids research 29 28334887
2015 Characterization of the Catalytic Domain of Human APOBEC3B and the Critical Structural Role for a Conserved Methionine. Journal of molecular biology 29 26281709
2007 Effects of point mutations in the cytidine deaminase domains of APOBEC3B on replication and hypermutation of hepatitis B virus in vitro. The Journal of general virology 29 18024895
2015 Molecular basis of the attenuated phenotype of human APOBEC3B DNA mutator enzyme. Nucleic acids research 28 26384561
2022 Cryo-EM structure of the EBV ribonucleotide reductase BORF2 and mechanism of APOBEC3B inhibition. Science advances 27 35476445
2019 Genetic Polymorphisms Predisposing the Interleukin 6-Induced APOBEC3B-UNG Imbalance Increase HCC Risk via Promoting the Generation of APOBEC-Signature HBV Mutations. Clinical cancer research : an official journal of the American Association for Cancer Research 27 31152021
2017 B-Myb Induces APOBEC3B Expression Leading to Somatic Mutation in Multiple Cancers. Scientific reports 27 28276478
2016 Mutation Processes in 293-Based Clones Overexpressing the DNA Cytosine Deaminase APOBEC3B. PloS one 27 27163364
2016 Association of Hepatitis B Virus Covalently Closed Circular DNA and Human APOBEC3B in Hepatitis B Virus-Related Hepatocellular Carcinoma. PloS one 27 27310677
2014 APOBEC3B gene overexpression in non-small-cell lung cancer. Biomedical reports 27 24748981
2009 Effects of structural variations of APOBEC3A and APOBEC3B genes in chronic hepatitis B virus infection. Hepatology research : the official journal of the Japan Society of Hepatology 27 19788695
2019 APOBEC3B promotes hepatocarcinogenesis and metastasis through novel deaminase-independent activity. Molecular carcinogenesis 26 30575099
2017 Progressive APOBEC3B mRNA expression in distant breast cancer metastases. PloS one 26 28141868
2011 Deletion of the APOBEC3B gene strongly impacts susceptibility to falciparum malaria. Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases 26 22108670
2021 Replication catastrophe induced by cyclic hypoxia leads to increased APOBEC3B activity. Nucleic acids research 24 34197599
2022 m6A demethylation of cytidine deaminase APOBEC3B mRNA orchestrates arsenic-induced mutagenesis. The Journal of biological chemistry 23 34998823
2021 Structure-Based Design of First-Generation Small Molecule Inhibitors Targeting the Catalytic Pockets of AID, APOBEC3A, and APOBEC3B. ACS pharmacology & translational science 22 34423273
2021 Immune inactivation by APOBEC3B enrichment predicts response to chemotherapy and survival in gastric cancer. Oncoimmunology 22 34552824
2016 APOBEC3B is an enzymatic source of molecular alterations in esophageal squamous cell carcinoma. Medical oncology (Northwood, London, England) 22 26880326
2021 Control of APOBEC3B induction and cccDNA decay by NF-κB and miR-138-5p. JHEP reports : innovation in hepatology 21 34704004
2020 Induction of APOBEC3B expression by chemotherapy drugs is mediated by DNA-PK-directed activation of NF-κB. Oncogene 21 33323971
2018 Structural Analysis of the Active Site and DNA Binding of Human Cytidine Deaminase APOBEC3B. Journal of chemical theory and computation 21 30457868
2014 Lack of association between intact/deletion polymorphisms of the APOBEC3B gene and HIV-1 risk. PloS one 21 24667791
2015 The roles of APOBEC3B in gastric cancer. International journal of clinical and experimental pathology 20 26191203
2024 Distinguishing preferences of human APOBEC3A and APOBEC3B for cytosines in hairpin loops, and reflection of these preferences in APOBEC-signature cancer genome mutations. Nature communications 19 38499553
2021 HPV-16/18 E6-induced APOBEC3B expression associates with proliferation of cervical cancer cells and hypomethylation of Cyclin D1. Molecular carcinogenesis 19 33631046
2019 Protein kinase A inhibits tumor mutator APOBEC3B through phosphorylation. Scientific reports 19 31165764
2023 APOBEC3B coordinates R-loop to promote replication stress and sensitize cancer cells to ATR/Chk1 inhibitors. Cell death & disease 18 37270643
2021 APOBEC3B is preferentially expressed at the G2/M phase of cell cycle. Biochemical and biophysical research communications 18 33592502
2020 DHX9 interacts with APOBEC3B and attenuates the anti-HBV effect of APOBEC3B. Emerging microbes & infections 18 32056513
2015 Degradation of the cancer genomic DNA deaminase APOBEC3B by SIV Vif. Oncotarget 18 26544511
2016 Expression of APOBEC3B mRNA in Primary Breast Cancer of Japanese Women. PloS one 17 27977754
2022 Evidence linking APOBEC3B genesis and evolution of innate immune antagonism by gamma-herpesvirus ribonucleotide reductases. eLife 16 36458685
2021 Correlation Between APOBEC3B Expression and Clinical Characterization in Lower-Grade Gliomas. Frontiers in oncology 16 33842328
2023 Acute expression of human APOBEC3B in mice results in RNA editing and lethality. Genome biology 15 38001542
2014 The role of APOBEC3B in chondrosarcoma. Oncology reports 14 25176183