Affinage

ABRAXAS2

BRISC complex subunit Abraxas 2 · UniProt Q15018

Length
415 aa
Mass
46.9 kDa
Annotated
2026-06-09
32 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ABRAXAS2 (ABRO1/KIAA0157/FAM175B) is a cytoplasmic scaffold protein that defines the BRISC deubiquitinase complex and directs Lys63-linked deubiquitination across innate immune, hematopoietic, telomeric, and cardiac contexts (PMID:20656690, PMID:20656689). It binds BRCC36 directly, and the minimal BRCC36-ABRO1 heterodimer retains K63-specific DUB activity; selectivity arises from the orientation of the substrate isopeptide bond in the active site rather than preferential chain binding (PMID:20032457). Structural work established that ABRO1 contacts switch BRCC36 into an active conformation, and that a higher-order 'super-dimer' (dimer of heterodimers) is required for catalysis and for engagement of targeting proteins such as SHMT2 and RAP80, with SHMT2 binding by ABRO1 acting as an inhibitory brake on chain cleavage (PMID:26344097, PMID:31253574). ABRO1 confers cytoplasmic localization to BRCC36, in contrast to the paralog Abraxas, which assembles the nuclear BRCA1-A complex; both complexes share BRE and NBA1/MERIT40, and loss of BRISC shifts the balance toward nuclear BRCA1-A activity at DNA double-strand breaks (PMID:20656690, PMID:20656689, PMID:21282113). Through this scaffolded DUB activity, BRISC/ABRO1 removes K63 chains from defined substrates: tankyrase 1 to control sister telomere resolution (PMID:27993934), JAK2 downstream of the LNK SH2 domain to restrain HSC expansion and thrombopoietin signaling (PMID:30755420), NLRP3 to license inflammasome activation in macrophages (PMID:37781816), PPM1B in a YAP-dependent phase-separated condensate during vascular stiffening (PMID:39742393), and β-catenin at K508 to limit its nuclear accumulation and prevent cardiac hypertrophy (PMID:41789465). Independently of its DUB scaffolding role, ABRO1 protects stalled and reversed replication forks from DNA2/WRN-mediated degradation, and its loss drives chromosome instability, cytosolic ssDNA accumulation, and cGAS-STING activation (PMID:28860160, PMID:35817959). ABRO1 also stabilizes p53 via USP7 and stabilizes BRCC3 itself by competing with the E3 ligase WWP2, while its own levels are subject to transcriptional control by YY1 and to pathogen-driven degradation by the bacterial effector NleG6 through TOLLIP-mediated autophagy (PMID:25283148, PMID:33107021, PMID:32845162, PMID:40013521).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 2009 High

    Established the minimal biochemical unit of cytoplasmic K63 deubiquitination by showing ABRO1 binds BRCC36 directly and the heterodimer is sufficient for activity, and defined how chain selectivity is achieved.

    Evidence in vitro reconstitution of the heterodimer with defined ubiquitin substrates and binding studies

    PMID:20032457

    Open questions at the time
    • Did not resolve the structural basis of the active-site geometry
    • Cellular substrates not yet identified
  2. 2010 High

    Defined ABRO1 as a cytoplasmic scaffold that segregates BRCC36 into a distinct complex (BRISC) from the nuclear BRCA1-A complex and as the sole subunit required to activate BRCC36 in the cytosol.

    Evidence co-immunoprecipitation, subcellular fractionation, siRNA knockdown, and functional DUB assays in two concurrent studies

    PMID:20656689 PMID:20656690

    Open questions at the time
    • Physiological cytoplasmic substrates not defined
    • Mechanism balancing BRISC vs BRCA1-A pools unresolved
  3. 2010 Medium

    Linked ABRO1 to stress-protective signaling beyond the DUB complex by identifying THAP5 interaction and a cardioprotective role in ischemia/reperfusion.

    Evidence co-IP, mouse MI/R model, knockdown and overexpression cell death assays

    PMID:21195082

    Open questions at the time
    • Specific K63 substrates in cardiomyocytes not identified
    • Single lab
  4. 2011 Medium

    Showed the two BRCC36 complexes share BRE and NBA1/MERIT40 and that NBA1-BRE contacts maintain complex integrity and IR resistance, framing the modular architecture.

    Evidence co-IP, domain-mapping pulldowns, siRNA knockdown, colony survival after IR

    PMID:21282113

    Open questions at the time
    • Role of shared subunits within BRISC specifically not dissected
    • Single lab
  5. 2012 Medium

    Connected ABRO1 to the oxidative stress response by showing nuclear translocation and ATF4/ATF5/JunD binding required for cytoprotection.

    Evidence co-IP, confocal co-localization, knockdown and viability assays

    PMID:22974638

    Open questions at the time
    • Whether this is DUB-dependent unclear
    • Single lab
  6. 2014 Medium

    Revealed a DUB-independent tumor-suppressive function: ABRO1 stabilizes p53 by bridging it to USP7 after DNA damage.

    Evidence co-IP, fractionation, knockdown/overexpression, tumor formation assays

    PMID:25283148

    Open questions at the time
    • Structural basis of ABRO1-USP7-p53 ternary complex unknown
    • Single lab
  7. 2015 High

    Provided the atomic mechanism of activation, showing ABRO1 contacts convert BRCC36 to an active conformation and that super-dimerization gates both catalysis and engagement of targeting proteins SHMT2 and RAP80.

    Evidence X-ray crystallography, mutagenesis, in vitro DUB assays, SEC, co-IP

    PMID:26344097

    Open questions at the time
    • In vivo regulation of super-dimer assembly not established
  8. 2016 High

    Identified the first defined physiological BRISC substrate, tankyrase 1, establishing cell-cycle-regulated K63 deubiquitination controlling telomere cohesion.

    Evidence reciprocal co-IP, ubiquitination assays, cell cycle synchronization, telomere FISH

    PMID:27993934

    Open questions at the time
    • How BRISC is recruited to tankyrase 1 in G1 not defined
  9. 2017 High

    Uncovered a replication fork protection role distinct from DUB scaffolding, with ABRO1 blocking DNA2/WRN-mediated degradation of reversed forks and suppressing genome instability and tumorigenesis.

    Evidence DNA fiber assays, RAD51 epistasis, Abro1-null mouse phenotype

    PMID:28860160

    Open questions at the time
    • Molecular mechanism of fork protection unknown
    • Relationship to BRISC activity at forks not clarified
  10. 2019 Medium

    Placed ABRO1 within a defined fork remodeling pathway protecting SMARCAL1/ZRANB3/HLTF-generated reversed forks, parallel to the FBH1 pathway.

    Evidence DNA fiber assay with epistasis across multiple remodelers

    PMID:33188024

    Open questions at the time
    • Direct biochemical role at forks not shown
    • Single lab
  11. 2019 High

    Defined a hematopoietic function: BRISC restrains TPO-induced JAK2 K63-ubiquitination via an LNK-bound phosphotyrosine on ABRO1, controlling HSC homeostasis.

    Evidence phosphopeptide pull-down, mouse KO, K63-Ub assays, flow cytometry

    PMID:30755420

    Open questions at the time
    • Kinase generating the ABRO1 phosphotyrosine not identified
  12. 2019 High

    Showed structurally how the two adaptors specialize BRCC36, with ABRO1-bound SHMT2α inhibiting chain cleavage while Abraxas integrates RAP80 in BRCA1-A.

    Evidence cryo-EM/crystal structures with binding and DUB inhibition assays

    PMID:31253574

    Open questions at the time
    • Signals controlling SHMT2-mediated inhibition in cells unknown
  13. 2019 Medium

    Extended ABRO1's role in protein stabilization to cancer, showing FAM175B blocks ubiquitin-dependent ATF4 degradation to drive CHOP-dependent apoptosis in esophageal carcinoma.

    Evidence co-IP, confocal, ubiquitination assay, luciferase reporter, knockdown

    PMID:30854784

    Open questions at the time
    • Whether stabilization requires DUB activity unclear
    • Single lab
  14. 2020 Medium

    Demonstrated ABRO1 stabilizes its own catalytic partner BRCC3 by competing with the E3 ligase WWP2 for binding.

    Evidence co-IP competition, ubiquitination assays, proteasome inhibitor experiments

    PMID:33107021

    Open questions at the time
    • Structural basis of competition not resolved
    • Single lab
  15. 2020 Medium

    Identified YY1 as a transcriptional activator of human ABRO1, providing a regulatory input controlling its expression.

    Evidence ChIP, EMSA, luciferase reporters, YY1 knockdown/overexpression

    PMID:32845162

    Open questions at the time
    • Physiological conditions driving YY1 regulation unknown
    • Single lab
  16. 2022 High

    Linked ABRO1-dependent fork protection to innate immunity, showing its loss produces cytosolic rDNA-containing ssDNA that activates cGAS-STING in a DNA2-dependent manner.

    Evidence DNA fiber assay, mouse KO, cytosolic ssDNA IF, cGAS-STING reporters, P-body quantification

    PMID:35817959

    Open questions at the time
    • How replication stress couples to P-body formation incompletely defined
  17. 2023 Medium

    Established ABRO1 as required for NLRP3 deubiquitylation and inflammasome activation, linking it to clonal-hematopoiesis-driven atherosclerosis.

    Evidence hematopoietic Abro1 KO, bone marrow transplant, inflammasome assays, atherosclerosis quantification

    PMID:37781816

    Open questions at the time
    • Direct NLRP3 ubiquitin site not mapped
    • Single lab
  18. 2023 Medium

    Revealed a DUB-independent role in cardiomyocyte proliferation through restriction of METTL3-mediated m6A methylation of Psph and downstream CDK2 activation.

    Evidence mouse KO/OE, m6A assays, CDK2 phosphorylation assays, proliferation quantification

    PMID:36639869

    Open questions at the time
    • Mechanism by which ABRO1 restricts METTL3 unclear
    • Single lab
  19. 2025 Medium

    Showed ABRO1 undergoes YAP-dependent phase separation with PPM1B and promotes its K63 deubiquitination, controlling TGF-β-Smad signaling and arterial stiffness.

    Evidence GST pull-down, co-IP, phase-separation imaging, SMC-specific KO mice, ubiquitination assays

    PMID:39742393

    Open questions at the time
    • Determinants of condensate formation not defined
    • Single lab
  20. 2025 Medium

    Identified ABRAXAS2 as a target of bacterial subversion, with effector NleG6 driving K27/K29 ubiquitination at K89/K114 and TOLLIP-mediated autophagic degradation to dampen NF-κB inflammation.

    Evidence co-IP, K89R/K114R mutagenesis, autophagy inhibitors, TOLLIP knockdown, NF-κB reporters

    PMID:40013521

    Open questions at the time
    • Whether host ligases use the same sites unknown
    • Single lab
  21. 2026 High

    Defined β-catenin as a BRISC substrate, with ABRO1-directed K63 deubiquitination at K508 restraining β-catenin nuclear signaling and preventing cardiac hypertrophy.

    Evidence IP-MS, ubiquitinome profiling, K508R mutagenesis, cardiomyocyte-specific KO/OE, CUT&TAG, ICG-001 rescue

    PMID:41789465

    Open questions at the time
    • Recruitment of BRISC to β-catenin not defined
  22. 2026 Medium

    Identified DPP9 as a regulator that disrupts the BRCC36-ABRO1 interaction, potentially compromising BRISC integrity.

    Evidence TurboID proximity labeling, NanoBRET in living cells, co-IP validation

    PMID:41636814

    Open questions at the time
    • Functional consequence of disruption on substrate processing not shown
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ABRO1 selects among its many K63 substrates in different tissues, and how its DUB-scaffolding role is mechanistically separated from its DUB-independent functions (fork protection, p53/ATF4 stabilization, m6A regulation), remain open.
  • No unified model for substrate/context selection
  • Switch between scaffolding and DUB-independent activities undefined
  • In vivo regulation of super-dimerization and SHMT2 inhibition unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 4 GO:0140096 catalytic activity, acting on a protein 4
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 2
Pathway
R-HSA-168256 Immune System 4 R-HSA-73894 DNA Repair 4 R-HSA-162582 Signal Transduction 3
Partners
ATF4BRCC36/BRCC3BRELNKMERIT40/NBA1SHMT2USP7YAP
Complex memberships
BRCA1-A complex (paralog-related)BRISC complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 ABRAXAS2 (KIAA0157/ABRO1) is a cytoplasmic scaffold protein that forms a distinct complex with BRCC36 (separate from the nuclear BRCA1-A complex). KIAA0157 localizes mainly in the cytosol and activates BRCC36 DUB activity in the cytoplasm. Reduction of KIAA0157 expression led to an increase of the BRCA1-A complex in the nucleus, indicating fine balance between the two complexes in vivo. Co-immunoprecipitation, subcellular fractionation, siRNA knockdown, functional DUB assays The Journal of biological chemistry High 20656690
2010 Within the BRISC complex, KIAA0157 (ABRO1/ABRAXAS2) is the only interaction required for BRCC36 DUB activity; BRISC deficiency enhanced formation of the BRCA1-RAP80 complex in vivo, increasing BRCA1 levels at DNA double-strand breaks. In vitro DUB activity assays with purified complexes, Co-IP, siRNA knockdown, laser-induced DSB recruitment assays The Journal of biological chemistry High 20656689
2009 ABRO1 binds directly to BRCC36 and the BRCC36-ABRO1 heterodimer constitutes a minimal complex retaining Lys63-specific DUB activity. BRISC selectivity for K63-linked chains is not due to preferential binding to K63 polyubiquitin but is dictated by orientation of the substrate isopeptide bond within the active site. Biochemical reconstitution of heterodimer, in vitro DUB assays with defined ubiquitin substrates, binding studies The Journal of biological chemistry High 20032457
2015 Crystal structure of the active BRCC36-KIAA0157 (ABRAXAS2) heterodimer and an inactive BRCC36 homodimer was solved. KIAA0157 contacts switch BRCC36 to an active conformation. Higher-order 'super-dimer' assembly (dimer of heterodimers) is required for DUB activity and for interaction with targeting proteins SHMT2 and RAP80, implicating super-dimerization as a regulatory mechanism controlling subcellular localization and biological function. X-ray crystallography, in vitro DUB activity assays, mutagenesis, co-immunoprecipitation, size-exclusion chromatography Molecular cell High 26344097
2019 Cryo-EM/crystal structures of BRISC and BRCA1-A complexes revealed that ABRO1 (in BRISC) binds SHMT2α (a metabolic enzyme), and this interaction prevents BRCC36 from binding and cleaving ubiquitin chains, establishing a regulatory inhibitory mechanism. In BRCA1-A, the paralog ABRAXAS integrates RAP80 and sequesters BRCA1 away from DSB sites. The two adaptor subunits confer distinct targeting and regulatory functions to BRCC36. Cryo-EM structure determination, biochemical binding assays, in vitro DUB inhibition assays Molecular cell High 31253574
2011 Both BRCC36-containing complexes (nuclear BRCA1-A with Abraxas; cytoplasmic BRISC with ABRO1) share BRE and NBA1/MERIT40 subunits. NBA1 interacts with BRE through a C-terminal conserved motif of NBA1 and the C-terminal UEV domain of BRE, and this interaction is critical for maintaining the integrity of both complexes and for cellular resistance to ionizing radiation. Co-immunoprecipitation, siRNA knockdown, domain-mapping pulldown assays, colony survival after IR The Journal of biological chemistry Medium 21282113
2017 ABRO1 protects stalled replication fork stability by inhibiting DNA2 nuclease/WRN helicase-mediated degradation of reversed forks. Depletion of RAD51 prevented DNA2/WRN-dependent fork degradation in Abro1-deficient cells, placing ABRO1 in a fork protection pathway distinct from BRCA2 (which blocks MRE11-dependent degradation). Abro1-null mice display increased chromosome instability and are tumor-prone. DNA fiber assay, siRNA/genetic knockdown, mouse knockout, genetic epistasis (RAD51 depletion) Genes & development High 28860160
2020 In fork reversal, ABRO1 (along with BRCA2 and FANCD2) protects reversed forks generated by SMARCAL1, ZRANB3, and HLTF from degradation, a pathway distinct from the FBH1-mediated fork remodeling pathway protected by 53BP1/FANCA/FANCC/FANCG/BOD1L/VHL. DNA fiber assay, siRNA knockdown, genetic epistasis with multiple fork remodeling factors Science advances Medium 33188024
2022 Abro1 (and FANCD2) protect stalled replication forks, and their deficiency leads to accumulation of cytosolic single-stranded DNA (containing ribosomal DNA) that activates cGAS-STING-dependent innate immune signaling in a DNA2-dependent manner. Abro1 and FANCD2 also limit the formation of replication stress-induced P-bodies, which can modulate innate immune activation. DNA fiber assay, mouse knockout, immunofluorescence for cytosolic ssDNA, cGAS-STING pathway reporters, P-body quantification Nature cell biology High 35817959
2014 ABRO1 stabilizes p53 by facilitating the interaction of p53 with the deubiquitinase USP7. DNA damage induces accumulation of endogenous ABRO1 and its translocation to the nucleus; p53 induction by DNA damage is almost completely attenuated by ABRO1 depletion. Co-immunoprecipitation, subcellular fractionation, siRNA knockdown, overexpression, tumor formation assays Nature communications Medium 25283148
2012 ABRO1 interacts directly with ATF4, ATF5, and JunD (AP-1 family transcription factors). Under cellular stress, ABRO1 translocates from the cytoplasm to the nucleus and co-localizes with ATF4; this ATF4-ABRO1 interaction is required for the cytoprotective function of ABRO1 following oxidative stress. Co-immunoprecipitation, confocal microscopy co-localization, siRNA knockdown, cell viability assays Biochimica et biophysica acta Medium 22974638
2010 ABRO1/KIAA0157 interacts with THAP5, a zinc finger transcription factor involved in G2/M control and apoptosis. ABRO1 protein levels increase in myocardial ischemia/reperfusion injury; reducing ABRO1 exacerbated cardiomyocyte death while overexpression provided protection against oxidative stress-induced apoptosis, linked to decreased Lys63-linked ubiquitination of specific substrates. Co-immunoprecipitation (ABRO1-THAP5 interaction), in vivo mouse MI/R model, siRNA knockdown, overexpression, cell death assays Journal of molecular and cellular cardiology Medium 21195082
2016 ABRO1/BRCC36 (BRISC complex) removes K63-linked ubiquitin chains from tankyrase 1 during G1 phase, countering the action of E3 ligase RNF8 that adds K63-linked chains in late S/G2. This cell cycle-regulated ubiquitination/deubiquitination controls tankyrase 1 stabilization, its association with telomeres, and timely sister telomere resolution. Co-immunoprecipitation, ubiquitination assays, siRNA knockdown, telomere FISH, cell cycle synchronization The EMBO journal High 27993934
2019 The LNK SH2 domain directly interacts with a phosphorylated tyrosine residue in KIAA0157 (ABRAXAS2). KIAA0157 deficiency in mice leads to expansion of phenotypic and functional HSCs. BRISC (via KIAA0157) attenuates TPO-induced JAK2 K63-ubiquitination; BRISC depletion increases JAK2 K63-ubiquitination, JAK2 activation, MPL receptor surface levels, and membrane-proximal JAK2/MPL association. Co-immunoprecipitation, phosphopeptide pull-down, mouse knockout, K63-ubiquitination assays, flow cytometry for HSC phenotyping and MPL surface levels Blood High 30755420
2023 ABRO1, as a scaffolding component of the BRISC-BRCC3 complex, is required for NLRP3 deubiquitylation and inflammasome activation in macrophages. Hematopoietic Abro1 deficiency reversed accelerated atherosclerosis and NETosis in Tet2 clonal hematopoiesis mice. Mouse knockout (hematopoietic Abro1 KO), bone marrow transplantation, NLRP3 inflammasome activation assays (IL-1β, caspase-1), atherosclerosis quantification Circulation Medium 37781816
2020 ABRO1 stabilizes BRCC3 protein by competing with the HECT-type E3 ubiquitin ligase WWP2 for binding to BRCC3, thereby preventing WWP2-mediated ubiquitination and proteasomal degradation of BRCC3. Co-immunoprecipitation, ubiquitination assays, siRNA knockdown, overexpression, proteasome inhibitor experiments FEBS letters Medium 33107021
2019 FAM175B (ABRAXAS2/ABRO1) interacts with ATF4 as shown by co-localization (confocal microscopy) and co-immunoprecipitation. FAM175B inhibits ubiquitin-dependent ATF4 degradation, elevating ATF4 protein levels, and promotes ATF4-dependent CHOP expression to drive apoptosis in esophageal squamous cell carcinoma cells. Co-immunoprecipitation, confocal co-localization, ubiquitination assay, luciferase reporter, siRNA knockdown Molecular oncology Medium 30854784
2023 ABRO1 regulates cardiomyocyte proliferation by targeting METTL3-mediated m6A methylation of Psph mRNA. ABRO1 restricts METTL3 activity, reducing PSPH expression; PSPH dephosphorylates CDK2 at Thr14/Tyr15 to activate it. ABRO1 deletion increased cardiomyocyte proliferation and restored heart function after myocardial injury. Mouse knockout and overexpression models, m6A methylation assays, CDK2 phosphorylation assays, cardiomyocyte proliferation quantification Molecular therapy Medium 36639869
2025 The bacterial T3SS effector NleG6 mediates K27- and K29-linked polyubiquitination at residues K89 and K114 of ABRAXAS2/FAM175B, leading to its degradation through TOLLIP-mediated selective autophagy. ABRAXAS2 degradation triggers subsequent degradation of BRCC3, which in turn prevents TNIP1/ABIN1 degradation and inhibits NF-κB-mediated inflammatory responses. Co-immunoprecipitation, ubiquitination site mutagenesis (K89R/K114R), autophagy inhibitor experiments, TOLLIP knockdown, NF-κB reporter assays Autophagy Medium 40013521
2025 ABRO1 directly binds YAP and undergoes liquid-liquid phase separation with YAP and PPM1B in a YAP-dependent manner, promoting PPM1B deubiquitination (K63-linked chains at K326) by BRCC36/BRCC3. Smooth muscle cell-specific Abro1-KO mice showed attenuated HFHSD-induced arterial stiffness and TGF-β-Smad signaling. GST pull-down, co-immunoprecipitation, immunofluorescence (phase separation), mouse SMC-specific KO, ubiquitination assays, Doppler ultrasound Circulation research Medium 39742393
2026 ABRO1 directly interacts with β-catenin and, as part of BRISC, cleaves K63-linked polyubiquitin chains at β-catenin lysine 508, thereby restraining β-catenin nuclear accumulation and transcriptional activation. Cardiomyocyte-specific Abro1 deletion causes spontaneous cardiac hypertrophy and contractile dysfunction reversible by β-catenin inhibitor ICG-001. Co-immunoprecipitation, immunoprecipitation-mass spectrometry, ubiquitinome profiling, site-specific mutagenesis (K508R), cardiomyocyte-specific KO/OE mice, CUT&TAG, pharmacological rescue Hypertension High 41789465
2026 DPP9 interacts with BRCC36/BRCC3 and ABRO1/ABRAXAS2 (BRISC complex components) as novel binding partners. NanoBRET assays in living cells showed that DPP9 disrupts the binding between BRCC36/BRCC3 and ABRO1/ABRAXAS2, potentially compromising BRISC integrity. TurboID proximity labeling, NanoBRET assay in living cells, validation by co-immunoprecipitation Cellular and molecular life sciences Medium 41636814
2020 The transcription factor YY1 positively regulates human ABRO1 expression by binding to cis-acting elements located -89 to -59 bp upstream of the ABRO1 transcriptional start site, as demonstrated by ChIP, EMSA, and luciferase reporter assays. Reporter gene assays, ChIP, EMSA, YY1 siRNA knockdown and overexpression Biochemistry and cell biology Medium 32845162

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 The Lys63-specific deubiquitinating enzyme BRCC36 is regulated by two scaffold proteins localizing in different subcellular compartments. The Journal of biological chemistry 103 20656690
2020 Two replication fork remodeling pathways generate nuclease substrates for distinct fork protection factors. Science advances 87 33188024
2010 Differential regulation of JAMM domain deubiquitinating enzyme activity within the RAP80 complex. The Journal of biological chemistry 72 20656689
2023 BRCC3-Mediated NLRP3 Deubiquitylation Promotes Inflammasome Activation and Atherosclerosis in Tet2 Clonal Hematopoiesis. Circulation 70 37781816
2019 Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation. Molecular cell 65 31253574
2011 NBA1/MERIT40 and BRE interaction is required for the integrity of two distinct deubiquitinating enzyme BRCC36-containing complexes. The Journal of biological chemistry 62 21282113
2017 Abro1 maintains genome stability and limits replication stress by protecting replication fork stability. Genes & development 57 28860160
2009 Specificity of the BRISC deubiquitinating enzyme is not due to selective binding to Lys63-linked polyubiquitin. The Journal of biological chemistry 55 20032457
2015 Higher-Order Assembly of BRCC36-KIAA0157 Is Required for DUB Activity and Biological Function. Molecular cell 53 26344097
2014 ABRO1 suppresses tumourigenesis and regulates the DNA damage response by stabilizing p53. Nature communications 52 25283148
2022 Stalled replication fork protection limits cGAS-STING and P-body-dependent innate immune signalling. Nature cell biology 44 35817959
2016 Cell cycle-regulated ubiquitination of tankyrase 1 by RNF8 and ABRO1/BRCC36 controls the timing of sister telomere resolution. The EMBO journal 33 27993934
2019 The BRISC deubiquitinating enzyme complex limits hematopoietic stem cell expansion by regulating JAK2 K63-ubiquitination. Blood 31 30755420
2010 Regulation of Abro1/KIAA0157 during myocardial infarction and cell death reveals a novel cardioprotective mechanism for Lys63-specific deubiquitination. Journal of molecular and cellular cardiology 28 21195082
2024 Cholesterol trafficking to the ER leads to the activation of CaMKII/JNK/NLRP3 and promotes atherosclerosis. Journal of lipid research 27 38522750
2023 BRISC is required for optimal activation of NF-κB in Kupffer cells induced by LPS and contributes to acute liver injury. Cell death & disease 27 37968261
2019 Genetic variants affecting bone mineral density and bone mineral content at multiple skeletal sites in Hispanic children. Bone 21 31790847
2023 ABRO1 arrests cardiomyocyte proliferation and myocardial repair by suppressing PSPH. Molecular therapy : the journal of the American Society of Gene Therapy 19 36639869
2019 FAM175B promotes apoptosis by inhibiting ATF4 ubiquitination in esophageal squamous cell carcinoma. Molecular oncology 19 30854784
2021 Identification of serum exosomal miR-98-5p, miR-183-5p, miR-323-3p and miR-19b-3p as potential biomarkers for glioblastoma patients and investigation of their mechanisms. Current research in translational medicine 18 34837760
2020 ABRO1 stabilizes the deubiquitinase BRCC3 through inhibiting its degradation mediated by the E3 ubiquitin ligase WWP2. FEBS letters 18 33107021
2019 Connecting the Dots in the Neuroglobin-Protein Interaction Network of an Unstressed and Ferroptotic Cell Death Neuroblastoma Model. Cells 16 31405213
2012 ATF4 interacts with Abro1/KIAA0157 scaffold protein and participates in a cytoprotective pathway. Biochimica et biophysica acta 14 22974638
2025 A bacterial RING ubiquitin ligase triggering stepwise degradation of BRISC via TOLLIP-mediated selective autophagy manipulates host inflammatory response. Autophagy 5 40013521
2025 BRISC-Mediated PPM1B-K63 Deubiquitination and Subsequent TGF-β Pathway Activation Promote High-Fat/High-Sucrose Diet-Induced Arterial Stiffness. Circulation research 4 39742393
2025 CD4+ T Cell Subsets and PTPN22 as Novel Biomarkers of Immune Dysregulation in Dilated Cardiomyopathy. International journal of molecular sciences 2 40869128
2025 BRISC inactivation alleviates alcohol-induced liver injury in mice. Scientific reports 1 39934386
2026 Proximity labeling reveals non-catalytic interactions between DPP9 and ubiquitin signaling complexes. Cellular and molecular life sciences : CMLS 0 41636814
2026 BRISC Deficiency Drives Heart Failure by Regulating β-Catenin K63 Ubiquitination. Hypertension (Dallas, Tex. : 1979) 0 41789465
2026 Integrated data-independent acquisition and thermal proteome profiling for proteomic characterization of lamotrigine-treated MCF-7 cells. Analytical and bioanalytical chemistry 0 42159682
2025 Mesenchymal stromal cells secretory pattern contributes to oncoinflammatory bone marrow microenvironment in polycythemia vera. Hematology, transfusion and cell therapy 0 41317544
2020 Transcriptional regulation of human abraxas brother protein 1 expression by yin yang 1. Biochemistry and cell biology = Biochimie et biologie cellulaire 0 32845162

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