Affinage

MAD1L1

Mitotic spindle assembly checkpoint protein MAD1 · UniProt Q9Y6D9

Length
718 aa
Mass
83.1 kDa
Annotated
2026-04-28
100 papers in source corpus 53 papers cited in narrative 53 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MAD1L1 encodes a coiled-coil homodimeric protein that functions as the central scaffold of the spindle assembly checkpoint (SAC), constitutively binding closed-conformation Mad2 (C-Mad2) at kinetochores to catalyze conversion of cytosolic open-Mad2 (O-Mad2) into C-Mad2–Cdc20 complexes that inhibit the APC/C and prevent premature anaphase onset (PMID:15694304, PMID:12006501, PMID:11804586). Mad1 is recruited to unattached kinetochores through Mps1-phosphorylated Bub1 via its C-terminal domain and is additionally scaffolded at the kinetochore corona by direct binding of Cyclin B1 to an acidic N-terminal surface, creating a positive-feedback loop that sustains Mps1 recruitment and checkpoint robustness (PMID:24402315, PMID:34013668, PMID:30948704, PMID:32202322). During interphase, Mad1 localizes to nuclear pore complexes through Tpr binding, which stabilizes Mad2 protein levels and primes the Mad1–C-Mad2 complex for rapid kinetochore deployment upon mitotic entry; Cyclin B1–Cdk1 at the NPC promotes timely Mad1 release from Tpr before nuclear envelope breakdown (PMID:11181178, PMID:18981471, PMID:32236513). Beyond its SAC role, a Golgi-localized pool of Mad1 regulates α5-integrin secretion and cell migration independently of Mad2, and overexpression of Mad1 at PML nuclear bodies displaces MDM2 to destabilize p53 (PMID:25447996, PMID:30948704).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 1998 High

    Identification of human MAD1 as a checkpoint homodimer established that the yeast SAC architecture is conserved in mammals and that Mad1 functions through direct Mad2 binding and cell-cycle-dependent hyperphosphorylation.

    Evidence Co-IP, gel filtration, immunofluorescence, and HTLV-I Tax overexpression phenotyping in human cells

    PMID:9546394

    Open questions at the time
    • Kinase(s) responsible for hyperphosphorylation unidentified
    • Mechanism of Tax-mediated checkpoint disruption not resolved
  2. 1999 High

    Demonstrating that Mad1–Mad2 association is constitutive and independent of cell cycle stage resolved that the complex is pre-formed rather than assembled de novo during mitosis, shifting focus to how the stable complex is activated.

    Evidence Gel filtration and co-IP with deletion/mutagenesis in budding yeast

    PMID:10436016

    Open questions at the time
    • How Mad1–Mad2 complex converts cytosolic Mad2 remained unknown
    • Structural basis of constitutive binding unresolved
  3. 2001 High

    Discovery that Mad1 and Mad2 reside at nuclear pore complexes during interphase revealed an unexpected non-mitotic reservoir, raising the question of whether NPC localization functionally contributes to checkpoint competence.

    Evidence Immunofluorescence co-localization with NPC markers and nuclear envelope fractionation

    PMID:11181178

    Open questions at the time
    • NPC-binding partner of Mad1 not identified
    • Functional significance of interphase NPC pool unclear
  4. 2001 High

    Bub1 was established as an upstream scaffold required for Mad1 kinetochore targeting, and kinase-dead Bub1 rescued both localization and checkpoint, indicating a kinase-independent scaffolding mechanism.

    Evidence Immunodepletion and kinase-dead add-back reconstitution in Xenopus egg extracts

    PMID:11402067

    Open questions at the time
    • Direct binding interface between Bub1 and Mad1 not mapped
    • Whether Bub1 kinase activity has additional roles at kinetochore not excluded
  5. 2002 High

    The crystal structure of the Mad1–Mad2 tetramer revealed the 'safety belt' mechanism by which Mad2 C-terminal tails wrap around Mad1, explaining how Mad1 acts as a competitive inhibitor of the Mad2–Cdc20 interaction and establishing the structural foundation of the template model.

    Evidence X-ray crystallography with in vitro competition assays and mutagenesis

    PMID:12006501

    Open questions at the time
    • How O-Mad2 is recruited to the Mad1:C-Mad2 complex remained unknown
    • Full-length Mad1 structure unavailable
  6. 2002 High

    RNAi depletion of Mad1 abolished Mad2 kinetochore localization and checkpoint function, confirming Mad1 is essential for Mad2 activation in mammalian cells; identification of a shared Mad2-binding motif in Mad1 and Cdc20 explained substrate mimicry.

    Evidence RNAi knockdown, in vitro peptide binding, structural analysis of Mad2 conformational change

    PMID:11804586

    Open questions at the time
    • Conformer-specific mechanism of Mad2 conversion not yet demonstrated in vivo
  7. 2005 High

    The 'Mad2 template model' was established: C-Mad2 constitutively bound to Mad1 at kinetochores serves as a catalytic template that recruits and converts O-Mad2 to C-Mad2–Cdc20, answering how a single unattached kinetochore amplifies the checkpoint signal.

    Evidence Conformer-specific binding assays, FRAP, mutagenesis, and in vitro reconstitution

    PMID:15694304

    Open questions at the time
    • Rate-limiting step in the catalytic cycle undefined
    • Role of p31comet in capping the template not fully characterized
  8. 2008 High

    Tpr was identified as the direct NPC anchor for Mad1–Mad2, resolving the interphase binding partner; Tpr depletion reduced Mad1 at both NPCs and kinetochores and diminished Mad2 protein levels, establishing a proteostatic function for the NPC-localized pool.

    Evidence Affinity purification–mass spectrometry, direct binding assay, RNAi with localization and protein level readouts

    PMID:18981471

    Open questions at the time
    • Whether Tpr directly hands off Mad1 to kinetochores or indirectly supports it via protein stabilization not resolved
  9. 2010 High

    Mps1 kinase was shown to be required not just for Mad1 kinetochore recruitment but specifically for O-Mad2 recruitment to the already-bound Mad1:C-Mad2 core, separating two temporally distinct steps in checkpoint activation.

    Evidence Timed chemical inhibition of Mps1 (AZ3146) with immunofluorescence in human cells

    PMID:20624899

    Open questions at the time
    • Direct Mps1 substrate on Mad1 for O-Mad2 recruitment step not identified at this point
  10. 2011 High

    Constitutive Mad1 kinetochore tethering was sufficient for metaphase arrest dependent on Mad1–Mad2 binding, establishing that Mad1 presence at kinetochores is the rate-limiting determinant of checkpoint activation and that downstream kinases (Aurora B, Mps1, BubR1) are needed to maintain but not initiate this arrest.

    Evidence Engineered kinetochore-targeted Mad1, chemical kinase inhibitors, live-cell imaging

    PMID:21394085

    Open questions at the time
    • What additional checkpoint function the Mad1 CTD provides beyond Mad2 recruitment remained unclear
  11. 2012 High

    Crystal structure of the Mad1 CTD revealed a homodimeric fold resembling Spc25/Csm1 kinetochore-binding domains, and mutagenesis implicated Bub1 as the direct CTD receptor, providing the first structural basis for Mad1 kinetochore docking.

    Evidence X-ray crystallography with mutagenesis and kinetochore localization assay

    PMID:22493223

    Open questions at the time
    • Atomic-resolution structure of Mad1 CTD–Bub1 complex not yet solved
  12. 2014 High

    Mps1-dependent phosphorylation of Bub1 was reconstituted in vitro as the direct mechanism for Mad1 kinetochore recruitment, closing the kinase–scaffold–effector pathway; artificial Bub1 tethering bypassed Mps1 upstream requirements, confirming Bub1 phosphorylation as the key regulated step.

    Evidence In vitro reconstitution, bypass tethering, mutagenesis in budding yeast

    PMID:24402315

    Open questions at the time
    • Phosphorylation sites on Bub1 not fully mapped in human system at this point
  13. 2014 Medium

    A checkpoint function for Mad1 beyond Mad2 kinetochore recruitment was established: even when C-Mad2 is artificially tethered to kinetochores, Mad1 and specifically its CTD are still required for mitotic arrest, indicating Mad1 scaffolds additional checkpoint signaling.

    Evidence Artificial C-Mad2 tethering, mutagenesis, mitotic index assay

    PMID:24477933

    Open questions at the time
    • Identity of the additional Mad1 CTD interactor(s) required for this function unknown
    • Mechanism not reconstituted in vitro
  14. 2014 Medium

    A Mad2-independent Golgi-localized pool of Mad1 was discovered that regulates α5-integrin secretion, cell adhesion, and directed cell migration, revealing a non-mitotic function entirely separate from the SAC.

    Evidence Golgi co-localization, subcellular fractionation, RNAi with integrin secretion and cell motility assays

    PMID:25447996

    Open questions at the time
    • Molecular mechanism of Mad1 action at the Golgi unknown
    • Whether this pool is regulated during cell cycle not addressed
    • Not independently replicated
  15. 2019 High

    MAD1 was shown to directly recruit Cyclin B1–CDK1 to unattached kinetochores through its N-terminal acidic face, establishing a positive-feedback loop: kinetochore-localized CDK1 sustains Mps1 recruitment, which in turn maintains Mad1 at kinetochores.

    Evidence Proteomics/co-IP, in vitro binding with truncation mutants, live-cell imaging, RNAi

    PMID:30948704

    Open questions at the time
    • CDK1 substrates in this feedback loop not comprehensively identified
  16. 2019 Medium

    Mad1 localization to PML nuclear bodies and direct binding to PML was shown to displace MDM2, leading to p53 destabilization and tumor promotion, establishing a SAC-independent oncogenic mechanism for Mad1 overexpression.

    Evidence Co-IP, direct binding assay, immunofluorescence, sumoylation assay, orthotopic tumor assay

    PMID:30948704

    Open questions at the time
    • Whether PML-body function operates in non-tumor contexts unknown
    • Stoichiometry and regulation of the Mad1–PML interaction not defined
    • Single-lab finding
  17. 2020 High

    Cyclin B1 was identified as the scaffold that anchors Mad1 at the kinetochore corona through a direct interaction with Mad1's N-terminal acidic surface; this corona pool becomes Mps1-independent after establishment, explaining how robust SAC signaling persists even as Mps1 activity fluctuates.

    Evidence In vitro reconstitution, point mutagenesis abolishing interaction, live-cell imaging

    PMID:32202322

    Open questions at the time
    • Structure of the Mad1–Cyclin B1 interface not resolved
    • Whether corona and Bub1-dependent pools function additively or redundantly not fully established
  18. 2020 High

    Cyclin B1–Cdk1 was shown to localize to NPCs via Mad1 binding, where it phosphorylates Tpr to release Mad1 before nuclear envelope breakdown, connecting the interphase NPC pool to rapid kinetochore loading at mitotic entry.

    Evidence Co-IP, live-cell imaging, phosphorylation assays, RNAi

    PMID:32236513

    Open questions at the time
    • Specific Tpr phosphorylation sites mediating Mad1 release not mapped
    • Whether other kinases contribute to NPC release not excluded
  19. 2021 High

    A 1.75 Å crystal structure of Mad1 CTD bound to phospho-Bub1 CD1 peptides defined the atomic contacts: pThr461 of Bub1 contacts Arg617 of the Mad1 RLK motif; asymmetric binding of only one Bub1 peptide per Mad1 homodimer in solution revealed functional consequences of coiled-coil asymmetry.

    Evidence X-ray crystallography, solution binding assay

    PMID:34013668

    Open questions at the time
    • Functional consequence of asymmetric Bub1 binding for checkpoint signaling not determined
    • Full-length Mad1–Bub1 complex structure unavailable

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key open questions include the structural basis of the Mad1–Cyclin B1 corona interface, how the Golgi-localized Mad1 pool regulates integrin trafficking at the molecular level, how the dual NPC and kinetochore pools are coordinately regulated across the cell cycle, and the full-length structure of the Mad1 homodimer.
  • Full-length Mad1 structure unavailable
  • Molecular mechanism of Mad1's Golgi function unknown
  • Quantitative contribution of NPC versus corona versus Bub1 kinetochore pools to checkpoint strength not measured

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 4 GO:0060090 molecular adaptor activity 4
Localization
GO:0005694 chromosome 5 GO:0005635 nuclear envelope 3 GO:0005634 nucleus 1 GO:0005794 Golgi apparatus 1
Pathway
R-HSA-1640170 Cell Cycle 6 R-HSA-9609507 Protein localization 4
Partners
BUB1CCNB1CEP57MAD2L1MPS1NUP153PMLTPR
Complex memberships
MCC (mitotic checkpoint complex)Mad1:C-Mad2 tetramer

Evidence

Reading pass · 53 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 Human MAD1 (TXBP181/HsMAD1) is the human homolog of yeast mitotic checkpoint MAD1; it functions as a homodimer, is hyperphosphorylated during S/G2/M phases and upon nocodazole treatment, binds HsMAD2, localizes to the centrosome during metaphase and to the spindle midzone/midbody during anaphase/telophase, and is targeted by HTLV-I oncoprotein Tax, whose expression causes multinucleated cells consistent with loss of MAD1 function. Co-immunoprecipitation, immunofluorescence, gel filtration, transfection/overexpression with phenotypic readout Cell High 9546394
2001 HsMAD1 and HsMAD2 localize to nuclear pore complexes (NPCs) during interphase, as demonstrated by co-labeling with NPC antibodies and co-purification with enriched nuclear envelope fractions; MAD1 associates with MAD2 but not p55CDC in this context. Immunofluorescence co-localization, nuclear envelope fractionation, co-immunoprecipitation Journal of cell science High 11181178
2002 Crystal structure of the tetrameric Mad1-Mad2 core complex reveals an asymmetric tetramer with elongated Mad1 monomers forming a coiled-coil and two connected sub-complexes with Mad2; Mad2 C-terminal tails wrap around Mad1 as 'safety belts'. Mad1 acts as a competitive inhibitor of the Mad2-Cdc20 complex, and unlocking the Mad2 C-terminal tail is required for ligand release. X-ray crystallography, in vitro competition assay, mutagenesis The EMBO journal High 12006501
2002 RNAi-mediated suppression of MAD1 in mammalian cells causes loss of Mad2 kinetochore localization and spindle checkpoint impairment; Mad1 and Cdc20 share a conserved Mad2-binding motif consensus; binding of a Mad1 or Cdc20 motif peptide triggers extensive rearrangement of Mad2 tertiary structure. RNAi knockdown, in vitro binding assay, structural analysis Molecular cell High 11804586
2001 Mad2 forms incompatible complexes with Mad1 and Cdc20 (neither requiring Mad2 oligomerization); interaction of Mad2 with Mad1 is crucial for kinetochore localization of Mad2, where Mad2 then interacts with Cdc20. Co-immunoprecipitation, mutagenesis, cell microinjection, kinetochore localization assay The EMBO journal High 11707408
2005 A closed conformer of Mad2 constitutively bound to Mad1 (C-Mad2) serves as the kinetochore receptor for cytosolic open Mad2 (O-Mad2); interaction of open and closed Mad2 conformers is essential for the spindle assembly checkpoint. This 'Mad2 template' model proposes that C-Mad2 bound to Mad1 acts as a template for conversion of O-Mad2 into C-Mad2 bound to Cdc20. Conformer-specific binding assays, fluorescence imaging (FRAP), mutagenesis, in vitro reconstitution Current biology : CB High 15694304
2002 Hec1 is required for recruitment of Mps1 kinase and Mad1/Mad2 complexes to kinetochores; depletion of Hec1 by RNAi impairs chromosome congression and causes persistent spindle checkpoint activation. RNAi depletion, immunofluorescence kinetochore localization Science High 12351790
2001 Bub1 is required for kinetochore localization of Mad1, Mad2, Bub3, and CENP-E in Xenopus egg extracts; immunodepletion of Bub1 abolishes checkpoint and kinetochore binding of these proteins; reintroduction of kinase-deficient Bub1 restores checkpoint and localization, demonstrating kinase-independent scaffolding. Immunodepletion, add-back reconstitution, kinase-dead mutant, immunofluorescence The Journal of cell biology High 11402067
2002 BubR1 immunodepletion in Xenopus egg extracts greatly reduces kinetochore binding of Mad1, Mad2, Bub1, Bub3, and CENP-E; localization and hyperphosphorylation of BubR1 at kinetochores depends on Bub1 and Mad1 (but not Mad2), placing Mad1 upstream of BubR1 phosphorylation. Immunodepletion, kinetochore localization assay, phosphorylation analysis The Journal of cell biology High 12163471
1999 Mad2 forms a tight complex with Mad1 in budding yeast, independent of cell cycle stage and other checkpoint proteins; this association is critical for checkpoint function and for hyperphosphorylation of Mad1. Deletion/mutation analysis confirms that Mad1-Mad2 association is required for spindle checkpoint. Gel filtration, co-immunoprecipitation, deletion/mutagenesis analysis Molecular biology of the cell High 10436016
2008 Tpr (a nuclear pore complex component) directly binds Mad1 and Mad2; Tpr depletion disrupts NPC localization of Mad1 and Mad2 during interphase, decreases levels of Mad1-bound Mad2, and decreases Mad1 at kinetochores during prometaphase, correlating with inability of Mad1 to activate Mad2 and inhibit APC/Cdc20. Mass spectrometry of affinity-purified Mad2 complexes, direct binding assay, RNAi depletion, immunofluorescence Genes & development High 18981471
2010 Mps1 kinase activity is required for recruitment of O-Mad2 to the kinetochore-bound Mad1-C-Mad2 core complex; inhibiting Mps1 before mitosis abolishes Mad1 and Mad2 kinetochore recruitment, whereas inhibiting it after mitotic entry leaves the Mad1-C-Mad2 core bound but prevents O-Mad2 recruitment. Mps1 can dimerize and transphosphorylate. Small-molecule Mps1 inhibitor (AZ3146), immunofluorescence, biochemical fractionation The Journal of cell biology High 20624899
2014 Mad1 kinetochore localization in budding yeast is mediated by Mps1-dependent phosphorylation of a region within Bub1; tethering this Bub1 region to kinetochores bypasses Mps1-mediated upstream checkpoint requirements; Mad1-Bub1 interaction and kinetochore association can be reconstituted in vitro with Mps1 and Mad2. In vitro reconstitution, mutagenesis, epistasis (bypass tethering), kinetochore localization assay Genes & development High 24402315
2012 Crystal structure of the C-terminal domain (CTD) of human Mad1 reveals a homodimer with fold similar to kinetochore-binding domains of Spc25 and Csm1; mutagenesis of the CTD interface diminishes kinetochore targeting and implicates Bub1 as the Mad1 CTD receptor. X-ray crystallography, mutagenesis, kinetochore localization assay Proceedings of the National Academy of Sciences of the United States of America High 22493223
2021 Crystal structure of the Mad1 CTD bound to two phosphorylated Bub1 CD1 peptides at 1.75 Å resolution shows that phosphorylated Bub1 Thr461 directly contacts Arg617 of the Mad1 RLK motif and caps the CD1 α-helix dipole; in solution, only one Bub1 CD1 peptide binds the Mad1 homodimer, reflecting inherent coiled-coil asymmetry. X-ray crystallography, solution binding assay EMBO reports High 34013668
2011 Mad2 requires association with Mad1 to adopt the closed conformation (C-Mad2) in vivo; p31comet-dependent 'capping' regulates the activity of the Mad1:C-Mad2 complex; microinjection of C-Mad2-specific antibody or Mad1-neutralizing antibody abruptly terminates the spindle assembly checkpoint and accelerates mitotic progression. Conformation-specific monoclonal antibody, antibody microinjection, live-cell imaging The EMBO journal High 21772247
2011 Constitutive targeting of Mad1 to bioriented kinetochores (via engineered construct) is sufficient to cause metaphase arrest dependent on Mad1-Mad2 binding; Aurora B, Mps1, and BubR1 kinases (but not Polo-like kinase) are needed to maintain checkpoint arrest when Mad1 is present at kinetochores, placing them downstream of Mad1-Mad2 recruitment. Kinetochore-targeted Mad1 construct, chemical kinase inhibitors, live-cell imaging, mutagenesis Nature cell biology High 21394085
2014 Recruiting Mad1 to metaphase kinetochores via chemically induced dimerization (CID) is sufficient to reactivate the spindle assembly checkpoint without increasing Mps1 or BubR1 at kinetochores; Mad2 binding and a conserved C-terminal motif of Mad1 are both required for checkpoint reactivation, suggesting Mad1 scaffolds formation of a higher-order mitotic checkpoint complex. Chemically induced dimerization, live-cell imaging, mutagenesis The Journal of cell biology High 24637323
2019 MAD1 directly interacts with the N-terminal 100 amino acids of CDK1-CCNB1 (Cyclin B1); CCNB1 is recruited to unattached kinetochores through this interaction in an MPS1-dependent manner; this MAD1-dependent pool of CDK1-CCNB1 creates a positive feedback loop for timely MPS1 kinetochore recruitment and sustained checkpoint arrest. Proteomics/co-immunoprecipitation, in vitro binding with truncation mutants, live-cell imaging, RNAi The Journal of cell biology High 30674583
2020 Cyclin B1 directly binds to an acidic face in the N-terminal region of MAD1 (mapped by in vitro reconstitution) and scaffolds MAD1 to the kinetochore corona; point mutations abolishing this interaction eliminate MAD1 corona localization and weaken the spindle assembly checkpoint; corona-localized MAD1 loses dependence on MPS1 kinase after corona establishment, ensuring robust SAC. In vitro reconstitution, mutagenesis, live-cell imaging, RNAi The EMBO journal High 32202322
2020 Cyclin B1-Cdk1 is targeted to the nuclear pore complex by binding an acidic face of MAD1; localized Cyclin B1-Cdk1 is required for proper release of MAD1 from Tpr at the NPC, allowing MAD1 recruitment to kinetochores before nuclear envelope breakdown. Co-immunoprecipitation, live-cell imaging, phosphorylation assays, RNAi The Journal of cell biology High 32236513
2014 MAD-1 (C. elegans) interacts with BUB-1 through a specific segment of the MAD-1 coiled coil; mutations selectively disrupting BUB-1 interaction eliminate MAD-1 localization to unattached kinetochores and meiotic chromosomes and abrogate checkpoint signaling; this BUB-1 C-terminal/kinase domain region mediates MAD-1 kinetochore targeting independently of kinase activity. Mutagenesis, co-immunoprecipitation, kinetochore localization assay, C. elegans genetics The Journal of cell biology High 24567362
2003 Tpr is required for Mad1-c-Mad2 recruitment to nuclear pores during interphase and stabilizes Mad1 and Mad2 protein levels; Tpr depletion reduces Mad2 (but not Mad1) at kinetochores, and the SAC robustness depends on Mad2 kinetochore levels maintained by Tpr. Co-immunoprecipitation, RNAi, immunofluorescence, protein half-life measurements The Journal of cell biology High 24344181
2010 Nup153 directly binds Mad1 via Nup153's N-terminal domain; Nup153 overexpression causes hypophosphorylation of Mad1 and spindle checkpoint inactivation; Nup153 depletion reduces Mad1 at nuclear pores and delays Mad1 dissociation from kinetochores at metaphase. Nup153 binding to Mad1 affects Mad1 phosphorylation status but not its interaction with Mad2. In vitro direct binding assay, overexpression, RNAi, immunofluorescence, phosphorylation analysis Nucleus Medium 21327106
2003 Human CENP-I is required for kinetochore localization of MAD1, MAD2, and CENP-F; CENP-I depletion prevents mitotic arrest despite unattached kinetochores, and the delay that does occur is MAD2-dependent, indicating that collective signal from many unattached kinetochores is needed to sustain arrest. RNAi depletion, immunofluorescence, cell cycle analysis Nature cell biology High 12640463
2003 Depletion of either Nuf2 or Hec1 by RNAi leads to 5-fold or greater reduction of Mad1 and Mad2 at kinetochores during a prometaphase block; Mad1/Mad2 reduction is reversible upon spindle depolymerization, indicating Nuf2/Hec1 prevent microtubule-dependent stripping of Mad1/Mad2. RNAi, quantitative immunofluorescence Current biology : CB Medium 14654001
2004 NEK2A interacts with MAD1 in vitro and in vivo via a leucine zipper-containing C-terminal domain of MAD1; NEK2A localizes to kinetochores; NEK2A depletion by siRNA abolishes MAD2 (but not MAD1, BUB1, or HEC1) kinetochore association and impairs spindle checkpoint signaling. Co-immunoprecipitation, in vitro binding, siRNA, immunofluorescence The Journal of biological chemistry Medium 14978040
2007 PRP4 kinase is required for recruitment or maintenance of MPS1, MAD1, and MAD2 at kinetochores; PRP4 depletion by RNAi induces mitotic acceleration, lagging chromatids, aneuploidy, and failure to arrest after nocodazole treatment. RNAi, immunofluorescence, mitotic index assay The Journal of cell biology Medium 17998396
2002 Two leucine zipper domains (amino acids 501-522 and 557-571) in human MAD1 are required for binding MAD2; a polymorphism at codon 558 (Arg→His) reduces MAD2 binding and mitotic checkpoint enforcement, representing loss-of-heterozygosity at the MAD1 locus in a human breast cancer. Mutagenesis, co-immunoprecipitation, mitotic index assay The Journal of biological chemistry High 12042300
2003 Human Mad2 is phosphorylated on multiple serine residues in a cell-cycle-dependent manner; only unphosphorylated Mad2 interacts with Mad1 or the APC/C in vivo; a phosphomimetic Mad2 mutant fails to interact with Mad1 or APC/C and acts as dominant-negative. In vivo phosphorylation analysis, co-immunoprecipitation, dominant-negative mutagenesis The EMBO journal Medium 12574116
1999 BUB1 phosphorylates MAD1 in vitro; BUB1 and BUB3 form a complex and interact with MAD1; BUB1 autophosphorylation and MAD1 phosphorylation require Lys821 in the BUB1 kinase motif. In vitro kinase assay, co-immunoprecipitation Biochemical and biophysical research communications Medium 10198256
2014 ATM kinase phosphorylates Mad1 at Serine 214; this phosphorylation promotes Mad1 homodimerization and heterodimerization with Mad2, contributes to spindle assembly checkpoint activation, and is required for chromosomal stability. In vitro kinase assay, phospho-specific antibody, co-immunoprecipitation, flow cytometry Carcinogenesis Medium 24728176
2019 ULK1 phosphorylates Mad1 at Ser546, promoting Mad1 kinetochore recruitment; phosphorylated Ser546-Mad1 shows enhanced interaction with the RZZ (Rod/ZW10/Zwilch) complex, which may serve as its kinetochore receptor; ULK1 deletion increases chromosomal instability. In vitro kinase assay, co-immunoprecipitation, RNAi, immunofluorescence Nucleic acids research Medium 31291454
2017 MAD1 N-terminal domain (NTD) and C-terminal domain (CTD) both bind O-Mad2 and C-Mad2 conformers (unlike the MIM which binds only C-Mad2); NTD and CTD interact with each other and with MPS1 kinase; MPS1 phosphorylates both NTD and CTD, decreasing their mutual interaction and CTD's interaction with MPS1; phosphorylation of CTD residue Thr-716 compromises Mad2 binding and checkpoint responses. Co-immunoprecipitation, in vitro kinase assay, mutagenesis, conformer-specific binding assay The Journal of biological chemistry Medium 29162720
2014 A Golgi-localized pool of Mad1 (independent of Mad2) controls secretion of α5 integrin; Mad1 depletion impairs integrin secretion, cell attachment, adhesion, FAK activation, and cell motility; Mad1 overexpression accelerates directed cell migration. Immunofluorescence co-localization with Golgi markers, subcellular fractionation, RNAi, integrin secretion assay, cell motility assay Current biology : CB Medium 25447996
2019 Upregulated Mad1 localizes to PML nuclear bodies; the C-terminus of Mad1 directly interacts with PML (interaction enhanced by sumoylation); upregulated Mad1 displaces MDM2 from PML, freeing MDM2 to ubiquitinate and destabilize p53, thereby promoting tumor growth. Co-immunoprecipitation, direct binding assay, immunofluorescence, sumoylation assay, orthotopic tumor assay Nature communications Medium 30948704
2015 Fission yeast Mad1 binds the kinesin-5 motor Cut7 (Eg5 homolog); Mad1 recruits Cut7 to kinetochores of misaligned chromosomes to promote chromosome congression; human Mad1 similarly recruits CENP-E motor to kinetochores, revealing a conserved dual function of Mad1 in checkpoint signaling and chromosome gliding. Protein-protein interaction screen, co-immunoprecipitation, live-cell imaging, genetic analysis Nature cell biology Medium 26258632
2014 Mad1 has a direct role in the spindle assembly checkpoint beyond Mad2 kinetochore recruitment: even when C-Mad2 is artificially recruited to kinetochores, Mad1 is still required for mitotic arrest; the C-terminal globular domain of Mad1 and conserved residues within it are required for this additional checkpoint function. Artificial C-Mad2 kinetochore tethering, mutagenesis, mitotic index assay EMBO reports Medium 24477933
2016 Cep57 localizes to kinetochores, binds Mis12 (KMN network), and interacts with Mad1; Cep57 depletion decreases Mad1-Mad2 kinetochore localization and reduces spindle checkpoint signaling; Cep57 microtubule-binding activity is involved in timely Mad1 removal from kinetochores. Co-immunoprecipitation, RNAi, immunofluorescence, spindle checkpoint assay Nature communications Medium 26743940
2014 CENP-I is required for stable association of RZZ complex and Mad1 with kinetochores and inhibits their dynein-mediated removal; Aurora B regulates RZZ/Mad1 association; CENP-I and Aurora B act as a molecular switch controlling Mad1 kinetochore dynamics. RNAi, Aurora B inhibitor, immunofluorescence, kinetochore localization quantification The Journal of cell biology Medium 24862574
2015 The RZZ complex localizes to the N-terminus of KNL1 downstream of Bub1, and mediates robust Mad1/Mad2 kinetochore localization in human cells; both Bub1/KNL1-dependent and KNL1/Bub1-independent mechanisms exist for RZZ and Mad1/Mad2 kinetochore recruitment. RNAi, kinetochore localization quantification, rescue experiments Open biology Medium 26581576
1996 Mad1 heterodimerizes with Max and represses transcription from E-box-containing promoters (competing with Myc:Max); the SIN3 corepressor interaction domain at the N-terminus of Mad1 and the PAH2 domain of Sin3 are required for transcriptional repression; Mad1 inhibits cell cycle progression from G1 to S phase, and this inhibitory activity requires its transcriptional repression function. Transcription reporter assay, cell cycle analysis (FACS), mutagenesis, co-immunoprecipitation Molecular and cellular biology High 8649388
1999 Amino acids 8-20 of Mad1 are sufficient for SID:PAH2 interaction; these residues form an amphipathic alpha-helix, and hydrophobic residues on the helix face are required for mSin3A PAH2 binding; this minimal SID can function as an autonomous portable repression domain. Mutagenesis, NMR/structural analysis, in vitro binding assay, transcription reporter assay The Journal of biological chemistry High 10551834
2000 NMR solution structure of the Sin3B PAH2 domain in complex with the N-terminal Mad1 peptide reveals a 'wedged helical bundle'; four α-helices of PAH2 form a hydrophobic cleft accommodating an amphipathic Mad1 α-helix; Mad1 binding stabilizes PAH2 secondary structure elements. NMR structure determination Nature structural biology High 11101889
2008 c-IAP1 (a RING finger E3 ubiquitin ligase) catalyzes ubiquitination of Mad1 (the Myc/Max/Mad transcriptional repressor), accelerating its degradation via the 26S proteasome, thereby reducing Mad1 levels and cooperating with Myc to promote cell proliferation. In vitro ubiquitination assay, co-immunoprecipitation, proteasome inhibitor experiments, cell proliferation assay Molecular cell High 18082613
2008 RSK (p90 ribosomal kinase) and S6K (p70 S6 kinase) phosphorylate Serine 145 of Mad1 (Myc/Max/Mad family member) upon serum or insulin stimulation; Ser-145 phosphorylation accelerates Mad1 ubiquitination and degradation via the 26S proteasome, promoting Myc transcriptional activity. In vitro kinase assay, mutagenesis, ubiquitination assay, pulse-chase degradation analysis Proceedings of the National Academy of Sciences of the United States of America High 18451027
2009 Mad1 (Myc/Max/Mad family) recruits the histone demethylase RBP2 to the hTERT gene promoter; Mad1-RBP2 interaction and co-occupancy at the hTERT promoter correlates with H3-K4 demethylation and transcriptional repression during differentiation; RBP2 depletion derepresses hTERT expression. Co-immunoprecipitation, chromatin immunoprecipitation (ChIP), RNAi, histone methylation assay FASEB journal Medium 19762557
2004 Mad1 (Myc/Max/Mad) interacts directly with the UBF promoter and represses rDNA transcription; granulocytic cells lacking Mad1 display increased rDNA transcription, protein synthesis, and cell volume; siRNA knockdown shows UBF is required for c-MYC-induced rDNA transcription. Nuclear run-on assay, chromatin immunoprecipitation, siRNA, cell size measurement The EMBO journal Medium 15282543
2001 During differentiation of HL60 cells, c-Myc occupancy at hTERT E-boxes is replaced by Mad1 occupancy in vivo, correlating with reduced histone acetylation at the promoter; histone deacetylase inhibitor trichostatin A attenuates hTERT repression during differentiation. Chromatin immunoprecipitation (ChIP), reporter assay, HDAC inhibitor treatment Proceedings of the National Academy of Sciences of the United States of America Medium 11274400
2003 p53 represses MAD1 transcription through a novel 38-bp element in the MAD1 promoter distinct from canonical p53 binding sites; p53, HDAC1, and mSin3A associate with the MAD1 promoter in vivo (by ChIP); HDAC inhibitor trichostatin A relieves p53-mediated MAD1 repression. Promoter reporter assay, ChIP, HDAC inhibitor treatment The Journal of biological chemistry Medium 12876282
2012 miR-125b represses Mad1 (spindle checkpoint) expression post-transcriptionally; exogenous miR-125b overexpression downregulates Mad1, delays cells at metaphase, and promotes apoptotic death with elevated chromosomal abnormalities. miRNA overexpression, immunoblot, cell cycle analysis, chromosome aberration assay Cell death and differentiation Medium 23099851
2012 Overexpression of Mad1 (spindle checkpoint) causes aneuploidy and chromosomal instability through mislocalization of Mad2 away from kinetochores, weakening the mitotic checkpoint; cells overexpressing Mad1 are resistant to microtubule poisons. Mad1 overexpression, immunofluorescence quantification of Mad2 kinetochore levels, chromosome counting, drug sensitivity assay Proceedings of the National Academy of Sciences of the United States of America Medium 22778409
2017 RARS-MAD1L1 fusion protein interacts with AIMP2 (by co-immunoprecipitation), resulting in activation of the FUBP1/c-Myc pathway; silencing of FUBP1 or c-Myc inhibitor abrogates cancer stem cell-like characteristics induced by the fusion. Co-immunoprecipitation, ChIP, siRNA, colony/sphere formation assay Clinical cancer research Medium 29133573

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1998 Human T cell leukemia virus type 1 oncoprotein Tax targets the human mitotic checkpoint protein MAD1. Cell 433 9546394
2002 Role of Hec1 in spindle checkpoint signaling and kinetochore recruitment of Mad1/Mad2. Science (New York, N.Y.) 366 12351790
2005 The Mad1/Mad2 complex as a template for Mad2 activation in the spindle assembly checkpoint. Current biology : CB 354 15694304
2010 Sustained Mps1 activity is required in mitosis to recruit O-Mad2 to the Mad1-C-Mad2 core complex. The Journal of cell biology 278 20624899
2002 The Mad2 spindle checkpoint protein undergoes similar major conformational changes upon binding to either Mad1 or Cdc20. Molecular cell 268 11804586
2002 Crystal structure of the tetrameric Mad1-Mad2 core complex: implications of a 'safety belt' binding mechanism for the spindle checkpoint. The EMBO journal 264 12006501
2001 Switch from Myc/Max to Mad1/Max binding and decrease in histone acetylation at the telomerase reverse transcriptase promoter during differentiation of HL60 cells. Proceedings of the National Academy of Sciences of the United States of America 264 11274400
2007 The MAD1 adhesin of Metarhizium anisopliae links adhesion with blastospore production and virulence to insects, and the MAD2 adhesin enables attachment to plants. Eukaryotic cell 210 17337634
2008 Activation of PI3K/Akt and MAPK pathways regulates Myc-mediated transcription by phosphorylating and promoting the degradation of Mad1. Proceedings of the National Academy of Sciences of the United States of America 203 18451027
2001 Spindle checkpoint protein Bub1 is required for kinetochore localization of Mad1, Mad2, Bub3, and CENP-E, independently of its kinase activity. The Journal of cell biology 196 11402067
2000 Expression of the hTERT gene is regulated at the level of transcriptional initiation and repressed by Mad1. Cancer research 175 10786671
2002 BubR1 is essential for kinetochore localization of other spindle checkpoint proteins and its phosphorylation requires Mad1. The Journal of cell biology 164 12163471
2001 Mitotic checkpoint proteins HsMAD1 and HsMAD2 are associated with nuclear pore complexes in interphase. Journal of cell science 162 11181178
2014 Mad1 kinetochore recruitment by Mps1-mediated phosphorylation of Bub1 signals the spindle checkpoint. Genes & development 159 24402315
1999 The spindle checkpoint of budding yeast depends on a tight complex between the Mad1 and Mad2 proteins. Molecular biology of the cell 155 10436016
2007 Heterozygous deletion of mitotic arrest-deficient protein 1 (MAD1) increases the incidence of tumors in mice. Cancer research 154 17210695
2004 MAD1 and c-MYC regulate UBF and rDNA transcription during granulocyte differentiation. The EMBO journal 152 15282543
2003 Nuf2 and Hec1 are required for retention of the checkpoint proteins Mad1 and Mad2 to kinetochores. Current biology : CB 139 14654001
2011 Constitutive Mad1 targeting to kinetochores uncouples checkpoint signalling from chromosome biorientation. Nature cell biology 138 21394085
2001 Mad2 binding to Mad1 and Cdc20, rather than oligomerization, is required for the spindle checkpoint. The EMBO journal 136 11707408
2003 Human CENP-I specifies localization of CENP-F, MAD1 and MAD2 to kinetochores and is essential for mitosis. Nature cell biology 129 12640463
2008 Tpr directly binds to Mad1 and Mad2 and is important for the Mad1-Mad2-mediated mitotic spindle checkpoint. Genes & development 128 18981471
1996 Inhibition of cell proliferation by the Mad1 transcriptional repressor. Molecular and cellular biology 118 8649388
2002 Spindle checkpoint requires Mad1-bound and Mad1-free Mad2. Molecular biology of the cell 115 12006648
1998 Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation. The EMBO journal 113 9451002
2004 NEK2A interacts with MAD1 and possibly functions as a novel integrator of the spindle checkpoint signaling. The Journal of biological chemistry 106 14978040
2014 A Bub1-Mad1 interaction targets the Mad1-Mad2 complex to unattached kinetochores to initiate the spindle checkpoint. The Journal of cell biology 97 24567362
2001 Mutations in the mitotic check point gene, MAD1L1, in human cancers. Oncogene 89 11423979
2012 Structure of human Mad1 C-terminal domain reveals its involvement in kinetochore targeting. Proceedings of the National Academy of Sciences of the United States of America 87 22493223
2003 Mad2 phosphorylation regulates its association with Mad1 and the APC/C. The EMBO journal 85 12574116
2012 Up-regulation of the mitotic checkpoint component Mad1 causes chromosomal instability and resistance to microtubule poisons. Proceedings of the National Academy of Sciences of the United States of America 84 22778409
2001 Mad-1 is the exclusive JC virus strain present in the human colon, and its transcriptional control region has a deleted 98-base-pair sequence in colon cancer tissues. Journal of virology 84 11160700
2002 Modulation of T-lymphocyte development, growth and cell size by the Myc antagonist and transcriptional repressor Mad1. The EMBO journal 82 12234922
2005 Partial downregulation of MAD1 causes spindle checkpoint inactivation and aneuploidy, but does not confer resistance towards taxol. Oncogene 78 15782113
2019 MAD1-dependent recruitment of CDK1-CCNB1 to kinetochores promotes spindle checkpoint signaling. The Journal of cell biology 70 30674583
2011 Probing the in vivo function of Mad1:C-Mad2 in the spindle assembly checkpoint. The EMBO journal 65 21772247
2007 c-IAP1 cooperates with Myc by acting as a ubiquitin ligase for Mad1. Molecular cell 65 18082613
1997 Function of the c-Myc antagonist Mad1 during a molecular switch from proliferation to differentiation. Molecular and cellular biology 65 9111304
1994 Beta II-spectrin (fodrin) and beta I epsilon 2-spectrin (muscle) contain NH2- and COOH-terminal membrane association domains (MAD1 and MAD2). The Journal of biological chemistry 64 7961888
2020 Cyclin B1 scaffolds MAD1 at the kinetochore corona to activate the mitotic checkpoint. The EMBO journal 62 32202322
2004 HBP1 and Mad1 repressors bind the Sin3 corepressor PAH2 domain with opposite helical orientations. Nature structural & molecular biology 61 15235594
2007 PRP4 is a spindle assembly checkpoint protein required for MPS1, MAD1, and MAD2 localization to the kinetochores. The Journal of cell biology 60 17998396
2015 Mad1 promotes chromosome congression by anchoring a kinesin motor to the kinetochore. Nature cell biology 59 26258632
1999 Two MAD tails: what the recent knockouts of Mad1 and Mxi1 tell us about the MYC/MAX/MAD network. Biochimica et biophysica acta 59 10382539
2005 The roles of MAD1, MAD2 and MAD3 in meiotic progression and the segregation of nonexchange chromosomes. Nature genetics 58 15951820
2013 Spindle assembly checkpoint robustness requires Tpr-mediated regulation of Mad1/Mad2 proteostasis. The Journal of cell biology 57 24344181
2002 MAD1 and p27(KIP1) cooperate to promote terminal differentiation of granulocytes and to inhibit Myc expression and cyclin E-CDK2 activity. Molecular and cellular biology 57 11940659
1996 SIN3-dependent transcriptional repression by interaction with the Mad1 DNA-binding protein. Molecular and cellular biology 55 8754821
1999 A 13-amino acid amphipathic alpha-helix is required for the functional interaction between the transcriptional repressor Mad1 and mSin3A. The Journal of biological chemistry 54 10551834
2014 Recruitment of Mad1 to metaphase kinetochores is sufficient to reactivate the mitotic checkpoint. The Journal of cell biology 53 24637323
2000 Analysis of Myc/Max/Mad network members in adipogenesis: inhibition of the proliferative burst and differentiation by ectopically expressed Mad1. Journal of cellular physiology 52 10797315
2000 The Mad1-Sin3B interaction involves a novel helical fold. Nature structural biology 52 11101889
2012 The Mad1-Mad2 balancing act--a damaged spindle checkpoint in chromosome instability and cancer. Journal of cell science 51 23093575
2009 Chromatin remodeling: recruitment of histone demethylase RBP2 by Mad1 for transcriptional repression of a Myc target gene, telomerase reverse transcriptase. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 51 19762557
2004 Localization of mitotic arrest deficient 1 (MAD1) in mouse oocytes during the first meiosis and its functions as a spindle checkpoint protein. Biology of reproduction 51 15342357
2003 Transcriptional regulation of mitotic checkpoint gene MAD1 by p53. The Journal of biological chemistry 51 12876282
2017 The RARS-MAD1L1 Fusion Gene Induces Cancer Stem Cell-like Properties and Therapeutic Resistance in Nasopharyngeal Carcinoma. Clinical cancer research : an official journal of the American Association for Cancer Research 50 29133573
2012 Functional interaction between the Arabidopsis orthologs of spindle assembly checkpoint proteins MAD1 and MAD2 and the nucleoporin NUA. Plant molecular biology 50 22457071
2010 The nucleoporin Nup153 affects spindle checkpoint activity due to an association with Mad1. Nucleus (Austin, Tex.) 50 21327106
2003 Spindle checkpoint proteins Mad1 and Mad2 are required for cytostatic factor-mediated metaphase arrest. The Journal of cell biology 50 14691134
2015 The RZZ complex requires the N-terminus of KNL1 to mediate optimal Mad1 kinetochore localization in human cells. Open biology 49 26581576
2006 Gain of a region on 7p22.3, containing MAD1L1, is the most frequent event in small-cell lung cancer cell lines. Genes, chromosomes & cancer 48 16130125
2002 Signaling disrupts mSin3A binding to the Mad1-like Sin3-interacting domain of TIEG2, an Sp1-like repressor. The EMBO journal 46 12006497
2000 Inhibition of proliferation and apoptosis by the transcriptional repressor Mad1. Repression of Fas-induced caspase-8 activation. The Journal of biological chemistry 46 10744730
2012 Dissection of the NUP107 nuclear pore subcomplex reveals a novel interaction with spindle assembly checkpoint protein MAD1 in Caenorhabditis elegans. Molecular biology of the cell 45 22238360
2005 Assembly of b/HLH/z proteins c-Myc, Max, and Mad1 with cognate DNA: importance of protein-protein and protein-DNA interactions. Biochemistry 45 16128587
2004 HAT cofactor Trrap regulates the mitotic checkpoint by modulation of Mad1 and Mad2 expression. The EMBO journal 44 15549134
2020 Cyclin B1-Cdk1 facilitates MAD1 release from the nuclear pore to ensure a robust spindle checkpoint. The Journal of cell biology 43 32236513
2014 CENP-I and Aurora B act as a molecular switch that ties RZZ/Mad1 recruitment to kinetochore attachment status. The Journal of cell biology 42 24862574
2010 Functional evaluation of missense variations in the human MAD1L1 and MAD2L1 genes and their impact on susceptibility to lung cancer. Journal of medical genetics 42 20516147
1999 Phosphorylation of human MAD1 by the BUB1 kinase in vitro. Biochemical and biophysical research communications 42 10198256
2002 Expression of mitotic spindle checkpoint protein hsMAD1 correlates with cellular proliferation and is activated by a gain-of-function p53 mutant. Cancer research 39 11980658
2002 Characterization of regions in hsMAD1 needed for binding hsMAD2. A polymorphic change in an hsMAD1 leucine zipper affects MAD1-MAD2 interaction and spindle checkpoint function. The Journal of biological chemistry 39 12042300
2016 Bub3-Bub1 Binding to Spc7/KNL1 Toggles the Spindle Checkpoint Switch by Licensing the Interaction of Bub1 with Mad1-Mad2. Current biology : CB 38 27618268
2001 The Mad1 transcription factor is a novel target of activin and TGF-beta action in keratinocytes: possible role of Mad1 in wound repair and psoriasis. Oncogene 38 11709721
2011 MAD1 and its life as a MYC antagonist: an update. European journal of cell biology 37 21917351
2014 Endopolyploidization and flowering time are antagonistically regulated by checkpoint component MAD1 and immunity modulator MOS1. Nature communications 36 25429892
2014 Conditional targeting of MAD1 to kinetochores is sufficient to reactivate the spindle assembly checkpoint in metaphase. Chromosoma 33 24695965
2011 A mitotic role for Mad1 beyond the spindle checkpoint. Journal of cell science 32 21511728
2011 Centromere-tethered Mps1 pombe homolog (Mph1) kinase is a sufficient marker for recruitment of the spindle checkpoint protein Bub1, but not Mad1. Proceedings of the National Academy of Sciences of the United States of America 32 22184248
2019 Mad1 destabilizes p53 by preventing PML from sequestering MDM2. Nature communications 31 30948704
2014 A direct role of Mad1 in the spindle assembly checkpoint beyond Mad2 kinetochore recruitment. EMBO reports 31 24477933
1999 Silencing of the Epstein-Barr virus latent membrane protein 1 gene by the Max-Mad1-mSin3A modulator of chromatin structure. Journal of virology 31 10074148
2017 Direct interactions of mitotic arrest deficient 1 (MAD1) domains with each other and MAD2 conformers are required for mitotic checkpoint signaling. The Journal of biological chemistry 30 29162720
2016 Epigenetic Variability across Human Populations: A Focus on DNA Methylation Profiles of the KRTCAP3, MAD1L1 and BRSK2 Genes. Genome biology and evolution 30 27503294
2013 Nitric oxide induces cotyledon senescence involving co-operation of the NES1/MAD1 and EIN2-associated ORE1 signalling pathways in Arabidopsis. Journal of experimental botany 29 24336389
2012 miR-125b promotes cell death by targeting spindle assembly checkpoint gene MAD1 and modulating mitotic progression. Cell death and differentiation 29 23099851
2021 Molecular mechanism of Mad1 kinetochore targeting by phosphorylated Bub1. EMBO reports 28 34013668
2011 Solution structure of the mSin3A PAH2-Pf1 SID1 complex: a Mad1/Mxd1-like interaction disrupted by MRG15 in the Rpd3S/Sin3S complex. Journal of molecular biology 28 21440557
2016 Cep57 is a Mis12-interacting kinetochore protein involved in kinetochore targeting of Mad1-Mad2. Nature communications 27 26743940
2014 ATM-mediated Mad1 Serine 214 phosphorylation regulates Mad1 dimerization and the spindle assembly checkpoint. Carcinogenesis 26 24728176
2005 The telomere repeat binding protein Trf1 interacts with the spindle checkpoint protein Mad1 and Nek2 mitotic kinase. Cell cycle (Georgetown, Tex.) 26 15611654
2004 Functional analysis of the Mad1-mSin3A repressor-corepressor interaction reveals determinants of specificity, affinity, and transcriptional response. Molecular and cellular biology 26 15024060
1999 Dwarfism and dysregulated proliferation in mice overexpressing the MYC antagonist MAD1. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 26 10616903
2018 Replicated associations of FADS1, MAD1L1, and a rare variant at 10q26.13 with bipolar disorder in Chinese population. Translational psychiatry 25 30531795
2019 ULK1 phosphorylates Mad1 to regulate spindle assembly checkpoint. Nucleic acids research 24 31291454
2018 MAD1: Kinetochore Receptors and Catalytic Mechanisms. Frontiers in cell and developmental biology 24 29868582
2014 A Golgi-localized pool of the mitotic checkpoint component Mad1 controls integrin secretion and cell migration. Current biology : CB 24 25447996
2007 Combined IFN-gamma and retinoic acid treatment targets the N-Myc/Max/Mad1 network resulting in repression of N-Myc target genes in MYCN-amplified neuroblastoma cells. Molecular cancer therapeutics 24 17938259
2002 Repression of in vivo growth of Myc/Ras transformed tumor cells by Mad1. Oncogene 24 11821957