Affinage

MAD2L1BP

MAD2L1-binding protein · UniProt Q15013

Length
274 aa
Mass
31.1 kDa
Annotated
2026-04-28
47 papers in source corpus 20 papers cited in narrative 20 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MAD2L1BP (p31comet) is the principal antagonist of the spindle assembly checkpoint (SAC), functioning as a conformational adaptor that selectively recognizes closed-Mad2 (C-Mad2) to promote timely mitotic exit and, outside mitosis, to regulate DNA repair pathway choice. It competes with open-Mad2 for the C-Mad2 dimerization surface to block SAC signal amplification at kinetochores, and it recruits the AAA-ATPase TRIP13 to catalyze ATP-dependent disassembly of the Mitotic Checkpoint Complex (MCC), releasing Mad2 and Cdc20 to restore APC/C activity (PMID:16525508, PMID:25092294, PMID:26324890). Its checkpoint-silencing function is held in check during active SAC signaling by PLK1-mediated phosphorylation of Ser-102, which weakens Mad2 binding, and is activated by HOIP-dependent linear ubiquitination that reduces PLK1 association (PMID:31118282, PMID:40462232). Beyond mitosis, p31comet promotes homologous recombination by recruiting TRIP13 to remodel the REV7–Shieldin complex (PMID:33051298), and biallelic loss-of-function mutations cause oocyte metaphase I arrest leading to female infertility as well as mosaic variegated aneuploidy with tumor predisposition (PMID:37334967, PMID:37796616).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2002 High

    Identification of MAD2L1BP as a MAD2-binding protein that forms a complex upon spindle attachment completion established it as a candidate SAC-silencing factor, answering the question of how Mad2 is extracted from Cdc20 at anaphase onset.

    Evidence Co-immunoprecipitation, overexpression/depletion in mammalian cells with securin destruction and mitotic timing readouts

    PMID:12456649

    Open questions at the time
    • Mechanism of Mad2 release from Cdc20 not resolved
    • No structural information on the p31comet–Mad2 interaction
    • Downstream ATPase requirement unknown
  2. 2004 High

    Demonstrating that p31comet binds selectively to the closed (C-Mad2) conformer and antagonizes Mad2-dependent APC/C inhibition in reconstituted systems established conformational selectivity as the basis of its checkpoint-silencing mechanism.

    Evidence Purified recombinant APC/C ubiquitination assay, Xenopus egg extract checkpoint assay, Co-IP from HeLa cells

    PMID:15257285

    Open questions at the time
    • How p31comet discriminates C-Mad2 from O-Mad2 at atomic level not known
    • Whether p31comet disrupts or merely caps Mad2-Cdc20 unclear
  3. 2006 High

    NMR-based evidence that p31comet competes with O-Mad2 for C-Mad2 binding resolved the molecular basis of SAC amplification blockade — it prevents the O-Mad2:C-Mad2 conformational dimer essential for checkpoint signal propagation.

    Evidence NMR chemical shift perturbation, Mad2 dimer-interface mutagenesis with SAC rescue in S. cerevisiae

    PMID:16525508

    Open questions at the time
    • Full atomic structure of p31comet–C-Mad2 complex not determined
    • In vivo dynamics of competition at kinetochores unresolved
  4. 2011 High

    Multiple studies converged to show that p31comet binds Mad2 within the intact MCC and promotes ATP-dependent extraction of Mad2 and Cdc20, establishing MCC disassembly as a discrete biochemical step in checkpoint silencing downstream of kinetochore satisfaction.

    Evidence Recombinant protein addition to checkpoint-arrested cell extracts, ATP analog experiments, live-cell imaging, kinetochore localization

    PMID:21300909 PMID:21965286 PMID:22100920

    Open questions at the time
    • Identity of the ATPase catalyzing disassembly unknown at this point
    • Whether p31comet acts catalytically or stoichiometrically unclear
  5. 2014 High

    Identification of TRIP13 as the AAA-ATPase that works jointly with p31comet to disassemble the MCC, together with the finding that Ser-102 phosphorylation regulates Mad2 binding affinity, defined both the catalytic engine and a key regulatory switch for checkpoint silencing.

    Evidence Biochemical fractionation/mass spectrometry from HeLa extracts, in vitro MCC disassembly and APC/C activity assays; phospho-mutagenesis with SAC readout

    PMID:24596092 PMID:25092294

    Open questions at the time
    • Kinase responsible for Ser-102 phosphorylation in vivo not identified in 2014
    • Structural basis of TRIP13–p31comet–MCC ternary complex unknown
  6. 2015 High

    Biochemical reconstitution showed p31comet and MCC mutually enhance each other's binding to TRIP13 oligomer, revealing a cooperative substrate-recognition mechanism for checkpoint complex disassembly; separately, IKK-β was identified as an activating kinase for p31comet in Xenopus extracts.

    Evidence Pulldown/binding assays with purified TRIP13, p31comet, and MCC; Xenopus egg extract checkpoint assay with kinase identification

    PMID:25892037 PMID:26324890

    Open questions at the time
    • Physiological relevance of IKK-β phosphorylation in somatic human cells untested
    • Cryo-EM structure of the ternary complex lacking
  7. 2019 High

    PLK1 was identified as the mitotic kinase that phosphorylates p31comet Ser-102 to suppress TRIP13-dependent MCC disassembly during active checkpoint, resolving how futile assembly/disassembly cycles are prevented.

    Evidence Selective PLK1 inhibitor (BI-2536) in checkpoint-arrested HeLa extracts, in vitro kinase assay, S102A mutagenesis, MCC disassembly assay

    PMID:31118282

    Open questions at the time
    • Phosphatase that reverses Ser-102 phosphorylation to trigger silencing not identified
    • Spatiotemporal dynamics of PLK1-p31comet interaction at kinetochores vs. cytosol unresolved
  8. 2020 Medium

    Discovery that p31comet promotes homologous recombination by recruiting TRIP13 to remodel the REV7–Shieldin complex extended its function beyond mitosis, establishing a shared HORMA-domain remodeling mechanism in DNA repair pathway choice.

    Evidence Co-immunoprecipitation, chromatin fractionation, HR/NHEJ repair assays, PARP inhibitor resistance assay

    PMID:33051298

    Open questions at the time
    • Single-lab finding; independent replication in other cell systems needed
    • Structural basis of p31comet–REV7 recognition vs. p31comet–Mad2 recognition not compared
  9. 2023 High

    Human genetic studies established that biallelic MAD2L1BP loss-of-function causes oocyte metaphase I arrest (female infertility) and mosaic variegated aneuploidy with microcephaly and tumor predisposition, providing direct in vivo proof that p31comet is essential for SAC silencing in meiosis and for genome stability.

    Evidence Whole-exome sequencing, cRNA rescue of patient oocytes, patient-derived cell aneuploidy analysis, recombinant protein binding/functional assays

    PMID:37334967 PMID:37796616

    Open questions at the time
    • Whether male infertility also results from MAD2L1BP deficiency not established
    • Genotype–phenotype correlation across different truncation positions incomplete
  10. 2025 Medium

    HOIP-mediated linear ubiquitination of p31comet was shown to activate it by reducing PLK1 binding, adding a non-degradative ubiquitin signal as a new regulatory layer; separately, a testis-specific splice variant (Variant 1) with reduced Mad2 binding was characterized, revealing tissue-specific tuning of checkpoint silencing.

    Evidence Ubiquitination assays, Co-IP of HOIP–p31comet and PLK1–p31comet, HOIP-KO cells, mitotic duration imaging; splice variant binding/stability/expression analysis

    PMID:40243841 PMID:40462232

    Open questions at the time
    • Deubiquitinase that removes linear ubiquitin chains from p31comet not identified
    • Functional significance of Variant 1 in spermatogenesis untested
    • Single-lab findings for both discoveries

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity of the phosphatase that dephosphorylates Ser-102 to trigger checkpoint silencing, the high-resolution structure of the TRIP13–p31comet–MCC ternary complex during active remodeling, and the relative contributions of p31comet's mitotic versus DNA-repair functions to the mosaic aneuploidy/tumor predisposition phenotype.
  • Ser-102 phosphatase identity unknown
  • No cryo-EM or crystal structure of TRIP13–p31comet–MCC catalytic intermediate
  • Relative contribution of SAC vs. HR defects to tumor predisposition in patients not dissected

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 7 GO:0060090 molecular adaptor activity 3
Localization
GO:0005694 chromosome 1 GO:0005829 cytosol 1
Pathway
R-HSA-1640170 Cell Cycle 10 R-HSA-73894 DNA Repair 2
Partners
BUBR1CDC20HOIPMAD2L1MAD2L2PLK1TRIP13
Complex memberships
MCC (as transient interactor via C-Mad2)

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 MAD2L1BP (CMT2/p31comet) was identified as a novel MAD2-binding protein; upon completion of spindle attachment, the CMT2-MAD2 complex forms coincident with dissociation of the p55CDC-MAD2 complex. Overexpression causes premature securin destruction and mitotic exit without chromosome segregation; depletion induces cell death after a transient anaphase delay. Co-immunoprecipitation, overexpression and depletion (RNAi) in mammalian cells with securin degradation and mitotic timing readouts The EMBO journal High 12456649
2004 p31comet binds selectively to the Cdc20-bound (closed) conformation of Mad2, antagonizes Mad2-dependent APC/C(Cdc20) inhibition in vitro and in Xenopus egg extracts, and forms a transient complex with APC/C(Cdc20)-bound Mad2 during checkpoint inactivation in HeLa cells, enhancing APC/C activity without disrupting the Mad2-Cdc20 interaction. Purified recombinant protein APC/C ubiquitination assay, Xenopus egg extract checkpoint assay, Co-immunoprecipitation from HeLa cells, RNAi depletion The EMBO journal High 15257285
2006 p31comet competes with O-Mad2 for binding to the C-Mad2 conformer, thereby blocking the O-Mad2:C-Mad2 conformational dimer that is required for SAC amplification. NMR chemical shift perturbations showed O-Mad2 undergoes a major conformational rearrangement upon C-Mad2 binding, and p31comet's negative effect on the SAC is based on this competition. NMR chemical shift perturbation, mutagenesis of Mad2 dimer interface with SAC rescue assay in S. cerevisiae, in vitro binding assays The EMBO journal High 16525508
2011 p31comet binds Mad2 when Mad2 is incorporated in the Mitotic Checkpoint Complex (MCC) together with BubR1 and Cdc20, and promotes extraction of Mad2 from the MCC to silence the checkpoint downstream of kinetochores. RNAi of p31comet increased Mad2 bound to BubR1-Cdc20; addition of recombinant p31comet to checkpoint-arrested extracts removes Mad2 from MCC; a p31comet mutant unable to bind Mad2 is inactive. RNAi, Co-immunoprecipitation, recombinant protein addition to checkpoint-arrested cell extracts, live-cell imaging of mitotic timing Journal of cell science High 22100920
2011 p31comet promotes disassembly of the Mitotic Checkpoint Complex (MCC) causing dissociation of Cdc20 from BubR1, and this process requires hydrolyzable ATP (β,γ-hydrolyzable ATP), linking p31comet action to an ATPase activity. In vitro MCC disassembly assay using isolated MCC from checkpoint-arrested HeLa cells, ATP analog experiments Proceedings of the National Academy of Sciences of the United States of America High 21300909
2011 p31comet localizes to kinetochores and cytosol during mitosis, traffics on and off kinetochores like Mad2, and is required for timely mitotic exit even when kinetochore-microtubule attachments are mature; cells depleted of p31comet arrest in metaphase with high cyclin B and satisfied checkpoint. Live-cell fluorescence imaging, RNAi depletion, kinetochore tracking, cyclin B level measurement Molecular biology of the cell High 21965286
2014 TRIP13 AAA-ATPase, working jointly with p31comet, disassembles the MCC by promoting release of Mad2 and Cdc20 from the complex, abrogating APC/C inhibition. TRIP13 was identified in HeLa cell extracts as the ATP-hydrolyzing factor required for p31comet-dependent MCC disassembly. Biochemical fractionation and identification of HeLa extract factor by mass spectrometry, in vitro MCC disassembly assay, APC/C activity assay Proceedings of the National Academy of Sciences of the United States of America High 25092294
2015 Oligomeric TRIP13 binds both p31comet and MCC simultaneously; p31comet and checkpoint complexes mutually promote each other's binding to TRIP13. The substrate-binding site of TRIP13 contains subsites specific for p31comet and for C-Mad2-containing complex, and simultaneous occupancy of both subsites is required for high-affinity binding. Pulldown/binding assays with purified recombinant TRIP13, p31comet, and MCC; competition experiments; mutagenesis Proceedings of the National Academy of Sciences of the United States of America High 26324890
2014 Phosphorylation of p31comet on Ser-102 weakens its binding to Mad2, thereby paradoxically promoting SAC activity in mitosis. Attenuating p31comet-Mad2 affinity by this phosphorylation enhances p31comet-mediated bypass of the SAC. Phospho-mutagenesis (S102A/S102D), Co-immunoprecipitation, cell-based SAC activity assay The Journal of biological chemistry Medium 24596092
2019 Polo-like kinase 1 (Plk1) binds p31comet, phosphorylates it on S102, and thereby suppresses the ability of p31comet (together with TRIP13) to disassemble MCC during active checkpoint, preventing futile MCC assembly/disassembly cycles. Selective Plk1 inhibitor (BI-2536) experiments in checkpoint-arrested HeLa extracts, in vitro kinase assay with purified Plk1, S102A mutagenesis, MCC disassembly assay Proceedings of the National Academy of Sciences of the United States of America High 31118282
2015 In Xenopus egg extracts, p31comet is phosphorylated by IKK-β during mitosis, and this phosphorylation enhances p31comet's ability to antagonize the SAC and promote M-phase exit. Xenopus egg extract checkpoint assay, identification of IKK-β as p31comet kinase, phosphomutant analysis Cell cycle (Georgetown, Tex.) Medium 25892037
2020 p31comet-mediated suppression of Mad2 activation controls the timing of mitotic slippage; reduction of kinetochore-associated MAD2 (dependent on APC/CCDC20) leads to progressive SAC weakening during prolonged arrest, enabling cyclin B1 degradation and mitotic exit by slippage. RNAi depletion, live-cell imaging, kinetochore Mad2 quantification, APC/C activity assays Oncogene Medium 32029899
2020 p31comet binds to the REV7-Shieldin complex in cells, promotes TRIP13-dependent inactivation and extraction of REV7 from chromatin, thereby promoting homologous recombination over NHEJ. p31comet also counteracts REV7 function in translesion synthesis by releasing it from REV3 in the Pol ζ complex. Co-immunoprecipitation, chromatin fractionation, HR/NHEJ repair assays, PARP inhibitor resistance assay Proceedings of the National Academy of Sciences of the United States of America Medium 33051298
2009 p31comet overexpression induces cellular senescence dependent on Mad2 binding; a p31comet mutant lacking the Mad2-binding region does not cause senescence, and depletion of Mad2 by siRNA phenocopies p31comet-induced senescence. Senescence requires p21(Waf1/Cip1) accumulation downstream of p31comet-Mad2 interaction. Overexpression with Mad2-binding domain deletion mutant, siRNA knockdown, senescence assays, p21 knockdown rescue Molecular cancer research : MCR Medium 19276188
2023 Biallelic loss-of-function variants in MAD2L1BP cause female infertility due to oocyte metaphase I arrest. Truncating variants abolish MAD2 binding; microinjection of full-length MAD2L1BP cRNA rescues polar body extrusion in patient oocytes, while truncated variants cannot. Whole-exome sequencing, recombinant protein binding assay, mouse oocyte cRNA microinjection rescue, patient oocyte rescue eLife High 37334967
2023 Homozygous MAD2L1BP nonsense variant (R253*) causes mosaic variegated aneuploidy, microcephaly, epileptic encephalopathy, and juvenile granulosa cell tumors. Recombinant truncated p31comet was defective in TRIP13, Mad2, and Rev7 binding, unable to support SAC silencing or homology-directed repair, and failed to interact with tp53. Patient-derived cell aneuploidy analysis, recombinant protein binding assays, SAC silencing assay, HDR assay JCI insight High 37796616
2012 p31comet levels are closely linked to susceptibility to mitotic slippage; depletion of p31comet increases MCC levels, prolongs mitotic block, sensitizes cells to spindle poisons, and increases mitotic cell death upon challenge with nocodazole, vincristine, or taxol. RNAi knockdown, flow cytometry, drug sensitivity assays, time-lapse microscopy The Journal of biological chemistry Medium 22544748
2013 The Rb-E2F pathway regulates p31comet expression, and a narrow ratio of p31comet:Mad2 is required for cellular viability; coordinate regulation of this antagonist-effector pair is important for oncogenic cell outgrowth. Rb-E2F pathway manipulation, expression analysis, cell viability assays with titrated expression ratios Cell cycle (Georgetown, Tex.) Low 24131926
2025 HOIP E3 ubiquitin ligase modifies p31comet by linear (M1-linked) polyubiquitination on C-terminal lysine residues after cytokine stimulation; ubiquitinated p31comet shows reduced PLK1 binding, allowing p31comet activation. HOIP-deficient cells phenocopy p31comet-knockout with prolonged mitotic duration; ubiquitination-deficient p31comet mutant extends M-phase. Ubiquitination assays, Co-immunoprecipitation of HOIP-p31comet and PLK1-p31comet, HOIP knockout cells, mitotic duration live imaging, ubiquitination-site mutant analysis Cell & bioscience Medium 40462232
2025 p31comet is expressed as two splice variants: Variant 1 (with additional 32 N-terminal residues) and Variant 2. Variant 1 exhibits reduced MAD2 binding affinity and reduced ability to promote mitotic progression compared to Variant 2; Variant 1 also shows reduced protein stability. Variant 1 is uniquely expressed in the testes. Binding assays, mitotic progression assays, protein stability measurements, tissue expression analysis International journal of molecular sciences Medium 40243841

Source papers

Stage 0 corpus · 47 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Conformation-specific binding of p31(comet) antagonizes the function of Mad2 in the spindle checkpoint. The EMBO journal 169 15257285
2002 Identification of a MAD2-binding protein, CMT2, and its role in mitosis. The EMBO journal 138 12456649
2006 Determinants of conformational dimerization of Mad2 and its inhibition by p31comet. The EMBO journal 117 16525508
2011 p31comet-mediated extraction of Mad2 from the MCC promotes efficient mitotic exit. Journal of cell science 115 22100920
2014 Disassembly of mitotic checkpoint complexes by the joint action of the AAA-ATPase TRIP13 and p31(comet). Proceedings of the National Academy of Sciences of the United States of America 108 25092294
2011 p31comet Promotes disassembly of the mitotic checkpoint complex in an ATP-dependent process. Proceedings of the National Academy of Sciences of the United States of America 82 21300909
2002 A novel NF-L mutation Pro22Ser is associated with CMT2 in a large Slovenian family. Neurogenetics 77 12481988
2015 Mode of interaction of TRIP13 AAA-ATPase with the Mad2-binding protein p31comet and with mitotic checkpoint complexes. Proceedings of the National Academy of Sciences of the United States of America 64 26324890
2007 Further evidence for genetic heterogeneity of distal HMN type V, CMT2 with predominant hand involvement and Silver syndrome. Journal of the neurological sciences 57 17663003
2003 Identification and functional analysis of six mycolyltransferase genes of Corynebacterium glutamicum ATCC 13032: the genes cop1, cmt1, and cmt2 can replace each other in the synthesis of trehalose dicorynomycolate, a component of the mycolic acid layer of the cell envelope. Archives of microbiology 56 12740729
2011 HSPB1 and HSPB8 in inherited neuropathies: study of an Italian cohort of dHMN and CMT2 patients. Journal of the peripheral nervous system : JPNS 53 22176143
2011 p31(comet) acts to ensure timely spindle checkpoint silencing subsequent to kinetochore attachment. Molecular biology of the cell 52 21965286
2019 Common alleles of CMT2 and NRPE1 are major determinants of CHH methylation variation in Arabidopsis thaliana. PLoS genetics 50 31887137
2016 P31comet, a member of the synaptonemal complex, participates in meiotic DSB formation in rice. Proceedings of the National Academy of Sciences of the United States of America 43 27601671
2020 Mitotic slippage is determined by p31comet and the weakening of the spindle-assembly checkpoint. Oncogene 42 32029899
2010 A novel HSPB1 mutation in an Italian patient with CMT2/dHMN phenotype. Journal of the neurological sciences 36 20870250
2020 p31comet promotes homologous recombination by inactivating REV7 through the TRIP13 ATPase. Proceedings of the National Academy of Sciences of the United States of America 30 33051298
2012 Depletion of p31comet protein promotes sensitivity to antimitotic drugs. The Journal of biological chemistry 29 22544748
2016 MFN2-related genetic and clinical features in a cohort of Chinese CMT2 patients. Journal of the peripheral nervous system : JPNS 22 26801520
2014 Phosphorylation regulates the p31Comet-mitotic arrest-deficient 2 (Mad2) interaction to promote spindle assembly checkpoint (SAC) activity. The Journal of biological chemistry 22 24596092
2009 p31comet Induces cellular senescence through p21 accumulation and Mad2 disruption. Molecular cancer research : MCR 22 19276188
1997 Confirmation of a second locus for CMT2 and evidence for additional genetic heterogeneity. Neurogenetics 21 10732809
2018 A novel homozygous MFN2 mutation associated with severe and atypical CMT2 phenotype. European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society 20 29361379
2020 Contiguous and stochastic CHH methylation patterns of plant DRM2 and CMT2 revealed by single-read methylome analysis. Genome biology 17 32762764
2019 Role of Polo-like kinase 1 in the regulation of the action of p31comet in the disassembly of mitotic checkpoint complexes. Proceedings of the National Academy of Sciences of the United States of America 16 31118282
2012 A novel p.Gln175X [corrected] premature stop mutation in the C-terminal end of HSP27 is a cause of CMT2. Journal of the peripheral nervous system : JPNS 14 22734906
2013 p31(comet) inactivates the chemically induced Mad2-dependent spindle assembly checkpoint and leads to resistance to anti-mitotic drugs. SpringerPlus 13 24255856
2013 Coordinated regulation of p31(Comet) and Mad2 expression is required for cellular proliferation. Cell cycle (Georgetown, Tex.) 12 24131926
2010 Seipin S90L mutation in an Italian family with CMT2/dHMN and pyramidal signs. Muscle & nerve 12 20806400
2023 Biallelic variants in MAD2L1BP (p31) cause female infertility characterized by oocyte maturation arrest. eLife 11 37334967
2012 A novel autosomal dominant GDAP1 mutation in an Italian CMT2 family. Journal of the peripheral nervous system : JPNS 11 22971097
2011 Clinical, electrophysiological and pathological findings of a patient with CMT2 due to the p.Ala738Val mitofusin 2 mutation. Journal of the neurological sciences 9 21601224
2023 Biallelic MAD2L1BP (p31comet) mutation is associated with mosaic aneuploidy and juvenile granulosa cell tumors. JCI insight 8 37796616
2020 A novel HSPB1 mutation associated with a late onset CMT2 phenotype: Case presentation and systematic review of the literature. Journal of the peripheral nervous system : JPNS 7 32639100
2020 Deep geno- and phenotyping in two consanguineous families with CMT2 reveals HADHA as an unusual disease-causing gene and an intronic variant in GDAP1 as an unusual mutation. Journal of neurology 7 32897397
2015 Phosphorylation of Xenopus p31(comet) potentiates mitotic checkpoint exit. Cell cycle (Georgetown, Tex.) 7 25892037
2007 Mutation analysis of p31comet gene, a negative regulator of Mad2, in human hepatocellular carcinoma. Experimental & molecular medicine 6 17934339
2018 A novel MFN2 mutation causes variable clinical severity in a multi-generational CMT2 family. Neuromuscular disorders : NMD 5 30642740
2023 O-GlcNAc Modification Alters the Chaperone Activity of HSP27 Charcot-Marie-Tooth Type 2 (CMT2) Variants in a Mutation-Selective Fashion. ACS chemical biology 4 37540114
2017 Pseudodominant inheritance pattern in a family with CMT2 caused by GDAP1 mutations. Journal of the peripheral nervous system : JPNS 4 28837237
2015 p31comet-Induced Cell Death Is Mediated by Binding and Inactivation of Mad2. PloS one 4 26544187
2012 The MFN2 V705I Variant Is Not a Disease-Causing Mutation: A Segregation Analysis in a CMT2 Family. Journal of neurodegenerative diseases 4 26316991
2010 Late-onset CMT2 associated with a novel missense mutation in the cytoplasmic domain of the MPZ gene. Clinical neurology and neurosurgery 4 20800346
2021 The Mad2-Binding Protein p31comet as a Potential Target for Human Cancer Therapy. Current cancer drug targets 2 33511944
2024 CMT2 and distal hereditary motor neuropathy associated with VRK1 variants: Case series. Neuromuscular disorders : NMD 1 39693713
2025 p31Comet Splice Variants Induce Distinct Spindle Assembly Checkpoint Dynamics due to Their Unique N-Termini. International journal of molecular sciences 0 40243841
2025 Linear ubiquitination of p31comet by HOIP couples cytokine response with mitotic regulation. Cell & bioscience 0 40462232