Affinage

HORMAD1

HORMA domain-containing protein 1 · UniProt Q86X24

Length
394 aa
Mass
45.2 kDa
Annotated
2026-06-10
34 papers in source corpus 23 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HORMAD1 is a HORMA-domain meiotic chromosome axis protein that coordinates homologue recognition, recombination, and checkpoint surveillance during prophase I, and which becomes a driver of genomic instability when aberrantly expressed in somatic tumors (PMID:19851446, PMID:21079677, PMID:25770156). In meiosis, HORMAD1 is loaded onto chromatin via meiotic cohesins REC8 and RAD21L and assembles onto axial elements together with SYCP2/SYCP3, preferentially marking unsynapsed axes from which it is displaced as the synaptonemal complex forms (PMID:32931493, PMID:19851446). Axis-associated HORMAD1 is required for SPO11-dependent DSB formation and early recombination (γH2AX, DMC1, RAD51, RPA foci), promotes homologue alignment by ensuring sufficient processed DSBs, recruits the ATR checkpoint to unsynapsed chromatin, and is essential for sex-body formation and meiotic sex chromosome inactivation (PMID:21079677, PMID:21478856); it also enforces a prophase checkpoint that eliminates asynaptic oocytes and suppresses DMC1-independent DSB repair (PMID:22530760, PMID:23759310). Its enrichment on unsynapsed axes reflects substage-specific phosphorylation, and its removal upon synapsis is executed by TRIP13 AAA-ATPase and by neddylation-activated SCF(FBXO47)-mediated ubiquitination and degradation (PMID:38897409, PMID:19851446, PMID:42216099). Structurally, HORMAD1 adopts a self-closed conformation in which its HORMA domain engages its own closure motif, and the same surface binds partner Ser-Glu-Pro closure motifs from HORMAD2 and MCM9, an interaction required for its DNA-repair functions (PMID:37794593). In cancer cells HORMAD1 redistributes to DNA-damage and replication-fork sites, where it promotes DSB resection and RAD51/BRCA2-dependent HR repair and protects stalled forks from MRE11-DNA2-BLM degradation, while suppressing mismatch repair by sequestering the MCM8-MCM9 complex from the nucleus (PMID:30333500, PMID:37838177, PMID:36778501, PMID:32647118). These activities generate replication stress and genomic aberrations, conferring dependence on translesion-synthesis and replication-stress genes and sensitivity to HR-targeting and replication-stress agents (PMID:25770156, PMID:35768547). Ectopic HORMAD1 additionally weakens the spindle assembly checkpoint through a MAD2L1-independent HORMAD1–Aurora B/INCENP interaction, generating aneuploidy and sensitizing cells to MPS1, Aurora B, and BUB1 inhibitors (PMID:41813673).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2009 High

    Established HORMAD1 as an axis-resident protein whose distribution is reciprocal to the synaptonemal complex, raising the question of how synapsis status is read out along chromosomes.

    Evidence Immunofluorescence and biochemical fractionation in wild-type and SC-defective mutant mice, plus TRIP13-deficient genetics

    PMID:19686734 PMID:19851446

    Open questions at the time
    • Did not define what triggers HORMAD1 depletion at the molecular level
    • Mechanism of TRIP13-dependent removal not biochemically reconstituted
  2. 2010 High

    Defined HORMAD1 as functionally required for meiotic DSB formation, early recombination, and meiotic sex chromosome inactivation, moving it from a marker to a functional axis factor.

    Evidence Hormad1 knockout mouse with immunofluorescence for DSB markers, SC electron microscopy, and X-chromosome RT-PCR

    PMID:21079677

    Open questions at the time
    • Did not resolve direct vs indirect role in DSB catalysis
    • No structural basis for axis localization
  3. 2011 High

    Showed HORMAD1 couples homologue alignment to ATR checkpoint recruitment in a negative-feedback loop with synapsis, explaining how meiotic progression is monitored.

    Evidence Conditional knockout mouse with genetic epistasis against checkpoint mutants

    PMID:21478856

    Open questions at the time
    • Direct biochemical link between HORMAD1 and ATR not established
    • Did not identify the kinases acting on HORMAD1
  4. 2012 High

    Demonstrated HORMAD1 is required for the asynapsis checkpoint that eliminates defective oocytes and undergoes DSB-independent phosphorylation, separating its checkpoint role from recombination.

    Evidence Hormad1/Spo11 double-mutant epistasis with oocyte counting and phosphorylation analysis

    PMID:22530760

    Open questions at the time
    • Phosphorylation sites and responsible kinases not mapped here
    • Mechanism of pseudo sex body formation unresolved
  5. 2013 Medium

    Revealed that HORMAD1 normally restrains DMC1-independent DSB repair, defining its role in enforcing inter-homologue recombination fidelity.

    Evidence Hormad1/Dmc1 double-mutant rescue epistasis with gamma-irradiation and repair-marker immunofluorescence

    PMID:23759310

    Open questions at the time
    • Single lab; pathway choice mechanism not reconstituted
    • Identity of the alternative repair pathway unclear
  6. 2015 High

    Opened the cancer dimension by showing aberrant HORMAD1 suppresses RAD51-dependent HR and generates copy-number aberrations, linking it to therapy sensitivity.

    Evidence Knockdown/overexpression in TNBC with HR reporter assays and genomic copy-number profiling

    PMID:25770156

    Open questions at the time
    • Apparent HR-suppressive role conflicts with later HR-promoting findings
    • Molecular mechanism of pathway redirection undefined here
  7. 2018 High

    Showed in lung adenocarcinoma that HORMAD1 relocalizes to IR-induced foci and promotes DSB resection and HR independently of its meiotic partners, defining a context-specific somatic repair function.

    Evidence Depletion plus HR/NHEJ reporter assays, DSB-marker imaging, and domain-deletion analysis

    PMID:30333500

    Open questions at the time
    • Reconciliation with HR-suppressive TNBC data not addressed
    • Recruitment mechanism to damage sites not defined
  8. 2020 Medium

    Identified HORMAD1 sequestration of the MCM8-MCM9 complex from the nucleus as a mechanism for mismatch-repair suppression in cancer, explaining a mutator phenotype.

    Evidence Reciprocal Co-IP, nuclear/cytoplasmic fractionation, and MLH1 chromatin-binding and MMR functional assays

    PMID:32647118

    Open questions at the time
    • Single lab; quantitative stoichiometry of sequestration unknown
    • Whether MMR suppression is direct or via downstream effects unclear
  9. 2020 High

    Defined the order of meiotic axis assembly by showing cohesins REC8/RAD21L load HORMAD1 before axial-element formation and that HORMAD1 binds SYCP2/SYCP3.

    Evidence Sycp2-KO and double-knockout mice with Co-IP and immunofluorescence

    PMID:32931493

    Open questions at the time
    • Direct binding interface between HORMAD1 and cohesins not mapped
    • Hierarchy of loading vs retention not fully separated
  10. 2022 Medium

    Used super-resolution imaging to show HORMAD1 tunes recombinase intermediate dynamics and inhibits SC coiling, adding a structural-dynamic role at DSB sites.

    Evidence Three-color dSTORM microscopy in Hormad1-/- vs wild-type spermatocytes

    PMID:35857787

    Open questions at the time
    • Single lab; molecular basis of coiling control unknown
    • Effect on recombinase kinetics correlative
  11. 2022 Medium

    Mapped the synthetic vulnerabilities created by HORMAD1, showing dependence on translesion-synthesis and replication-stress tolerance genes.

    Evidence siRNA screens in inducible HORMAD1 SUM159 cells with clonogenic validation

    PMID:35768547

    Open questions at the time
    • Mechanistic link between HORMAD1 and TLS dependence not resolved
    • Single cell-line model
  12. 2023 High

    Provided the structural basis for HORMAD1 function: a self-closed HORMA conformation that also binds HORMAD2 and MCM9 closure motifs, an interaction required for MMR and HR activities.

    Evidence Crystal structure with peptide-binding biochemistry and cell-based MMR/HR assays using interaction-deficient mutants

    PMID:37794593

    Open questions at the time
    • Conformational conversion enzymology (e.g. TRIP13 action) not structurally captured
    • Stoichiometry of oligomeric assemblies undefined
  13. 2023 High

    Established a replication-fork protection function whereby HORMAD1 prevents nascent DNA degradation and supports RAD51/BRCA2 loading at stalled forks.

    Evidence DNA fiber assays, replisome co-localization, and RAD51/BRCA2 loading and chromosomal aberration analysis in HORMAD1-deleted cells (published plus preprint)

    PMID:36778501 PMID:37838177

    Open questions at the time
    • Direct binding to fork components not defined
    • Relationship to its HR-promoting role at DSBs not fully integrated
  14. 2023 Medium

    Localized a C-terminal nuclear localization signal by showing a truncation mutant mislocalizes to the cytoplasm, defining a determinant of HORMAD1 nuclear function.

    Evidence Transfection of GFP-tagged wild-type and p.Gln341* mutant with immunofluorescence and immunoblotting

    PMID:36524333

    Open questions at the time
    • NLS sequence not precisely delimited
    • Import receptor not identified
  15. 2023 Low

    Linked HORMAD1 to pro-tumorigenic signalling and to its upstream regulation, implicating Wnt/β-catenin, NF-κB, and STRA8.

    Evidence Western-blot pathway analysis, fractionation, knockdown/overexpression and xenografts across lung, squamous, and gastric cancer models

    PMID:35347116 PMID:37371097 PMID:37854207

    Open questions at the time
    • Pathway links rest on phospho-blots without direct reconstitution
    • Whether signalling effects are direct or secondary to genomic instability unknown
  16. 2026 High

    Identified a mitotic checkpoint defect caused by ectopic HORMAD1 acting through Aurora B/INCENP, independently of MAD2L1, explaining aneuploidy and revealing targetable vulnerabilities.

    Evidence Inducible HORMAD1 expression, mitotic arrest assays, HORMAD1-Aurora B Co-IP, signalling readouts, MAD2L1 epistasis, and inhibitor sensitivity

    PMID:41813673

    Open questions at the time
    • Direct HORMAD1-Aurora B binding interface not structurally defined
    • How HORMA conformation relates to Aurora B engagement unknown
  17. 2026 Medium

    Defined the degradation machinery removing HORMAD1 at synapsis, showing neddylation-activated SCF(FBXO47) ubiquitinates HORMAD1 and that loss causes meiotic arrest.

    Evidence Germ-cell Nedd8-KO mice, MLN4924 inhibition, and in vitro/in vivo ubiquitination assays with SC-marker imaging

    PMID:42216099

    Open questions at the time
    • Direct FBXO47-HORMAD1 substrate recognition not structurally resolved
    • Coordination with TRIP13-mediated removal not integrated
  18. 2026 Low

    Connected HORMAD1 to senescence escape by linking its loss to p27 accumulation and senescence in TNBC.

    Evidence Co-IP, western blot for p27/ubiquitin components, and senescence assays with overexpression/knockdown

    PMID:41868954

    Open questions at the time
    • Direct ubiquitination of p27 by a HORMAD1-dependent ligase not reconstituted
    • Single lab; causality between p27 and senescence not isolated

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how a single self-closed HORMA conformation is mechanistically redeployed to drive opposite outcomes across meiotic recombination, somatic HR/fork protection, MMR suppression, and mitotic checkpoint weakening.
  • No unified structural model connecting conformational state to each functional context
  • Switch between HR-suppressive and HR-promoting roles unexplained
  • How partner closure-motif selection (HORMAD2 vs MCM9 vs Aurora B) is regulated is unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140097 catalytic activity, acting on DNA 3 GO:0005198 structural molecule activity 2 GO:0060089 molecular transducer activity 2 GO:0140313 molecular sequestering activity 1
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 3 GO:0005694 chromosome 1
Pathway
R-HSA-1474165 Reproduction 3 R-HSA-1643685 Disease 3 R-HSA-73894 DNA Repair 3 R-HSA-1640170 Cell Cycle 1
Partners
AURKBHORMAD2MCM8MCM9RAD21LREC8SYCP2SYCP3
Complex memberships
meiotic chromosome axis / axial element

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 HORMAD1 preferentially associates with unsynapsed meiotic chromosome axes and is depleted from synapsed axes; SC formation directly or indirectly promotes HORMAD1 depletion from chromosome axes. TRIP13 AAA-ATPase is required for the reciprocal distribution of HORMADs and SYCP1/SC-components along chromosome axes. Immunofluorescence/cytology of wild-type and mutant mice (SC-defective and DSB-processing mutants); genetic analysis of TRIP13-deficient mice PLoS genetics High 19851446
2009 Mouse HORMAD1 associates with the meiotic chromosome axis and localizes to unsynapsed or desynapsed chromosomal regions during prophase I; establishment of the SC is required for displacement of HORMAD1 from the chromosome axis. Biochemical fractionation, immunofluorescence in wild-type and SC-component mutant mice Experimental cell research High 19686734
2010 HORMAD1 is required for double-strand break (DSB) formation and early recombination events in meiosis; HORMAD1 deficiency causes drastic decreases in γH2AX, DMC1, RAD51, and RPA foci. HORMAD1 co-localizes with γH2AX to the sex body and is required for ATR, BRCA1, and γH2AX localization to sex chromosomes and meiotic sex chromosome inactivation. Hormad1 knockout mouse model; immunofluorescence for DSB markers, electron microscopy for SC, RT-PCR for X-chromosome transcription PLoS genetics High 21079677
2011 HORMAD1 promotes homologue alignment by ensuring sufficient processed DSBs are available for homology search, and is required for efficient ATR checkpoint kinase recruitment to unsynapsed chromatin. SC formation depletes HORMAD1 from chromosome axes, forming a negative feedback loop coordinating meiotic progression with homologue alignment. Hormad1 conditional knockout mouse; immunofluorescence, genetic epistasis with checkpoint mutants Nature cell biology High 21478856
2012 HORMAD1 is required for a meiotic prophase checkpoint that eliminates asynaptic oocytes; Hormad1 deficiency abrogates massive oocyte loss in Spo11-deficient ovaries (epistasis). HORMAD1 is also required for pseudo sex body formation in Spo11-deficient gonads, and HORMAD1 undergoes extensive DSB-independent phosphorylation in Spo11-deficient testes and ovaries. Hormad1/Spo11 double-mutant genetic epistasis; immunofluorescence, oocyte counting, phosphorylation analysis Genes to cells High 22530760
2013 HORMAD1 deficiency promotes DMC1-independent DSB repair in oocytes; Hormad1 deficiency rescues Dmc1-/- oocytes from loss, indicating HORMAD1 normally suppresses alternative (DMC1-independent) DSB repair pathways. Hormad1/Dmc1 double-mutant epistasis; gamma-irradiation of embryonic ovaries; immunofluorescence for γH2AX, RAD51, DMC1 Biology of reproduction Medium 23759310
2015 Elevated HORMAD1 expression in cancer cells suppresses RAD51-dependent homologous recombination and drives use of alternative DNA repair pathways, generating allelic imbalance copy-number aberrations and sensitizing cells to HR-targeting therapies (platinum, PARP inhibitors). HORMAD1 knockdown/overexpression in TNBC cells; HR reporter assays; genomic copy-number profiling Cancer discovery High 25770156
2018 In lung adenocarcinoma cells, HORMAD1 redistributes to nuclear foci co-localizing with γH2AX after IR/chemotherapy; HORMAD1 promotes DSB resection (RPA-ssDNA foci and RAD51 redistribution to DSBs) and HR repair but not NHEJ. The HORMA domain and C-terminal disordered oligomerization motif are required for localization to IR-induced foci. HORMAD1-mediated HR is independent of its meiotic partners HORMAD2 and CCDC36. HORMAD1 depletion in lung adenocarcinoma cells; HR and NHEJ reporter assays; immunofluorescence for DSB repair markers; domain-deletion analysis Scientific reports High 30333500
2018 HORMAD1 repair activity in cancer is independent of its meiotic partners HORMAD2 and CCDC36; depletion causes sensitivity to IR and camptothecin. siRNA depletion, clonogenic survival assays, reporter assays Scientific reports Medium 30333500
2020 HORMAD1 interacts with the MCM8-MCM9 complex and prevents its efficient nuclear localization, leading to reduced MLH1 chromatin binding and DNA mismatch repair (MMR) defects in cancer cells. Co-immunoprecipitation, nuclear/cytoplasmic fractionation, MLH1 chromatin binding assays, MMR functional assays in HORMAD1-expressing cancer cells Cell death & disease Medium 32647118
2020 Meiotic cohesins REC8 and RAD21L mediate initial chromatin loading of HORMAD1 prior to axial element formation; HORMAD1 interacts with meiotic cohesins (REC8, RAD21L) and AE components (SYCP2, SYCP3). In Sycp2-KO, HORMAD1 localizes along cohesin axial cores independently of SYCP2/SYCP3. Sycp2-KO and Hormad1/Rad21L and Hormad1/Rec8 double-knockout mice; Co-immunoprecipitation; immunofluorescence PLoS genetics High 32931493
2022 Using super-resolution dSTORM microscopy in Hormad1-/- spermatocytes, HORMAD1 was shown to influence the lifetime/dynamics of RAD51/DMC1 recombinase intermediates at DSB sites and to inhibit coil formation in the synaptonemal complex; SPO11 plays a similar but weaker coiling role and SYCP1 has the opposite effect. Three-color dSTORM super-resolution microscopy in Hormad1-/- vs wild-type spermatocytes PLoS genetics Medium 35857787
2022 HORMAD1 expression in TNBC induces dependencies on translesion synthesis (TLS) polymerases POLH, POLK, REV1, REV3L, REV7 and replication stress tolerance genes (ATR, BRIP1, TDP1, XRCC1); depletion of these genes selectively inhibits growth of HORMAD1-expressing cells. siRNA screens in doxycycline-inducible HORMAD1 SUM159 cell model; clonogenic survival validation Oncogene Medium 35768547
2023 The crystal structure of human HORMAD1 reveals a self-closed conformation with an intramolecular HORMA domain-closure motif interaction. Partner peptides from HORMAD2 and MCM9 interact with HORMAD1 similarly to its own closure motif via a conserved Ser-Glu-Pro sequence. This HORMA-closure motif interaction is required for HORMAD1-dependent DNA mismatch repair and HR repair in cells. Crystal structure determination; biochemical peptide-binding assays; cell-based MMR and HR repair assays with interaction-deficient mutants Structure High 37794593
2023 HORMAD1 associates with the replisome and protects stalled DNA replication forks; loss of HORMAD1 leads to nascent DNA degradation via the MRE11-DNA2-BLM pathway, reduced RAD51 and BRCA2 loading onto stalled forks, increased DNA breaks and chromosomal defects exacerbated by replication stress. DNA fiber assays, co-localization with replisome components, RAD51/BRCA2 ChIP at stalled forks, chromosomal aberration analysis in HORMAD1-deleted lung adenocarcinoma cells The Journal of biological chemistry High 36778501 37838177
2023 HORMAD1 activates the Wnt/β-catenin pathway in lung cancer cells by increasing AKT phosphorylation (Ser473) and GSK-3β phosphorylation (Ser9), which decreases β-catenin phosphorylation (Ser33/37/Thr41) and enhances cytoplasmic/nuclear accumulation of β-catenin, promoting EMT. Western blot for phosphorylation states, β-catenin nuclear fractionation, in vitro and in vivo lung cancer models with HORMAD1 overexpression/knockdown Cell death discovery Medium 35347116
2023 shRNA-mediated depletion of HORMAD1 in squamous cell carcinoma cells increases genomic instability, DNA damage, and etoposide sensitivity; conversely, HORMAD1 overexpression is protective. The upstream meiosis transcription factor STRA8 was identified as a regulator of HORMAD1 expression. shRNA knockdown, overexpression, DNA damage markers (γH2AX), clonogenic survival, etoposide sensitivity assays Cells Medium 37371097
2023 HORMAD1 promotes gastric cancer growth and invasion via activation of the NF-κB pathway; HORMAD1 overexpression increases phosphorylation of NF-κB p65 and IκK-β and downstream targets c-Myc and CyclinD1, promoting EMT. Western blot for NF-κB pathway components and phosphorylation, in vitro invasion/proliferation assays, in vivo xenograft with HORMAD1 KD/OE American journal of translational research Low 37854207
2024 Mouse HORMAD1 is phosphorylated at two distinct serine clusters (Ser307 and Ser378) in a substage-specific manner during meiotic prophase I. Ser307 phosphorylation begins at early leptotene and is SPO11-independent, while Ser378 phosphorylation appears after mid-zygotene and preferentially marks unsynapsed axes. Phospho-specific antibody generation; immunofluorescence on wild-type and Spo11-/- spermatocytes at different prophase substages Experimental cell research Medium 38897409
2026 Out-of-context HORMAD1 expression in mitotic cells perturbs mitotic arrest and generates aneuploidy by weakening the spindle assembly checkpoint (SAC) and/or kinetochore-microtubule error correction via a HORMAD1-Aurora B interaction that causes defective Aurora B/INCENP signalling; these effects are MAD2L1-independent. HORMAD1-expressing cells are sensitized to MPS1, Aurora B, and BUB1 inhibitors. Inducible HORMAD1 expression in mitotic cells; mitotic arrest assays; Co-IP of HORMAD1 with Aurora B; Aurora B/INCENP signalling readouts; pharmacological inhibition; MAD2L1 epistasis Nature communications High 41813673
2026 Neddylation of Cullin1 activates the SKP1-Cullin1-FBXO47 (SCF) E3 ubiquitin ligase complex to ubiquitinate and degrade HORMAD1 during synapsis; NEDD8 deficiency in spermatocytes causes persistent HORMAD1 on unsynapsed axes, meiotic arrest at zygotene, defective SC assembly, and infertility. Germ-cell-specific Nedd8-knockout mice; MLN4924 neddylation inhibitor; in vivo and in vitro ubiquitination assays; immunofluorescence for HORMAD1 and SC markers Cell & bioscience Medium 42216099
2026 HORMAD1 depletion in TNBC cells induces cellular senescence through accumulation of p27, caused by impairment of ubiquitin-mediated degradation of p27; ectopic HORMAD1 expression blocks p27-driven senescence, promoting TNBC cell growth. Co-immunoprecipitation, western blot for p27 and ubiquitin pathway components, senescence assays (flow cytometry), HORMAD1 overexpression/KD American journal of translational research Low 41868954
2023 HORMAD1 is critical for protecting stalled DNA replication forks in lung adenocarcinoma; loss leads to nascent DNA degradation mediated by MRE11-DNA2-BLM, accumulation of ssDNA, and failure to load RAD51 and BRCA2 onto stalled forks. (Preprint version of PMID:37838177.) DNA fiber assay, ssDNA accumulation, RAD51/BRCA2 loading assays in HORMAD1-deleted LUAD cells bioRxivpreprint Medium 36778501
2023 Human cell transfection experiments showed that a truncated HORMAD1 protein (p.Gln341*, lacking the nuclear localization signal) is expressed but displays cytoplasmic rather than nuclear localization, establishing that the C-terminal region of HORMAD1 contains a nuclear localization signal required for nuclear import. Cell transfection with GFP-tagged wild-type and mutant HORMAD1; immunoblotting; immunofluorescence microscopy Human reproduction Medium 36524333

Source papers

Stage 0 corpus · 34 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Mouse HORMAD1 and HORMAD2, two conserved meiotic chromosomal proteins, are depleted from synapsed chromosome axes with the help of TRIP13 AAA-ATPase. PLoS genetics 333 19851446
2011 Meiotic homologue alignment and its quality surveillance are controlled by mouse HORMAD1. Nature cell biology 198 21478856
2010 Hormad1 mutation disrupts synaptonemal complex formation, recombination, and chromosome segregation in mammalian meiosis. PLoS genetics 184 21079677
2009 A novel mammalian HORMA domain-containing protein, HORMAD1, preferentially associates with unsynapsed meiotic chromosomes. Experimental cell research 109 19686734
2015 Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers. Cancer discovery 97 25770156
2005 Identification of CT46/HORMAD1, an immunogenic cancer/testis antigen encoding a putative meiosis-related protein. Cancer immunity 78 15999985
2012 HORMAD1-dependent checkpoint/surveillance mechanism eliminates asynaptic oocytes. Genes to cells : devoted to molecular & cellular mechanisms 71 22530760
2018 The Cancer/Testes (CT) Antigen HORMAD1 promotes Homologous Recombinational DNA Repair and Radioresistance in Lung adenocarcinoma cells. Scientific reports 47 30333500
2013 Mouse HORMAD1 is a meiosis i checkpoint protein that modulates DNA double- strand break repair during female meiosis. Biology of reproduction 43 23759310
2020 Aberrantly expressed HORMAD1 disrupts nuclear localization of MCM8-MCM9 complex and compromises DNA mismatch repair in cancer cells. Cell death & disease 40 32647118
2020 Meiotic cohesins mediate initial loading of HORMAD1 to the chromosomes and coordinate SC formation during meiotic prophase. PLoS genetics 40 32931493
2018 Repair of exogenous DNA double-strand breaks promotes chromosome synapsis in SPO11-mutant mouse meiocytes, and is altered in the absence of HORMAD1. DNA repair 31 29414051
2012 Biological significance of HORMA domain containing protein 1 (HORMAD1) in epithelial ovarian carcinoma. Cancer letters 29 22776561
2012 HORMAD2/CT46.2, a novel cancer/testis gene, is ectopically expressed in lung cancer tissues. Molecular human reproduction 28 22893617
2018 Epigenetic activation of HORMAD1 in basal-like breast cancer: role in Rucaparib sensitivity. Oncotarget 25 30046392
2021 HORMAD1 promotes docetaxel resistance in triple negative breast cancer by enhancing DNA damage tolerance. Oncology reports 24 34036395
2022 The cancer/testis antigen HORMAD1 mediates epithelial-mesenchymal transition to promote tumor growth and metastasis by activating the Wnt/β-catenin signaling pathway in lung cancer. Cell death discovery 20 35347116
2022 Functional screening reveals HORMAD1-driven gene dependencies associated with translesion synthesis and replication stress tolerance. Oncogene 13 35768547
2012 Single-nucleotide polymorphisms in HORMAD1 may be a risk factor for azoospermia caused by meiotic arrest in Japanese patients. Asian journal of andrology 12 22407170
2023 Structural and biochemical insights into the interaction mechanism underlying HORMAD1 and its partner proteins. Structure (London, England : 1993) 8 37794593
2023 A biallelic loss of function variant in HORMAD1 within a large consanguineous Turkish family is associated with spermatogenic arrest. Human reproduction (Oxford, England) 7 36524333
2023 HORMAD1 overexpression predicts response to anthracycline-cyclophosphamide and survival in triple-negative breast cancers. Molecular oncology 6 36852691
2023 The cancer testes antigen, HORMAD1, limits genomic instability in cancer cells by protecting stalled replication forks. The Journal of biological chemistry 5 37838177
2022 Multi-color dSTORM microscopy in Hormad1-/- spermatocytes reveals alterations in meiotic recombination intermediates and synaptonemal complex structure. PLoS genetics 5 35857787
2023 Ectopically Expressed Meiosis-Specific Cancer Testis Antigen HORMAD1 Promotes Genomic Instability in Squamous Cell Carcinomas. Cells 4 37371097
2023 The cancer/testis antigen HORMAD1 promotes gastric cancer progression by activating the NF-κB signaling pathway and inducing epithelial-mesenchymal transition. American journal of translational research 4 37854207
2021 [Corrigendum] HORMAD1 promotes docetaxel resistance in triple negative breast cancer by enhancing DNA damage tolerance. Oncology reports 2 34296290
2025 HORMAD1 Polymorphisms Influence Susceptibility to Esophageal Squamous Cell Carcinoma Through Gene-Smoking Interaction. Molecular carcinogenesis 1 40875139
2024 Differential phosphorylation of two serine clusters in mouse HORMAD1 during meiotic prophase I progression. Experimental cell research 1 38897409
2026 Tumour specific HORMAD1 expression perturbs mitotic arrest and drives sensitivity to mitotic kinase inhibitors. Nature communications 0 41813673
2026 HORMAD1 inhibits senescence and promotes proliferation of triple negative breast cancer by facilitating ubiquitination-mediated degradation of p27. American journal of translational research 0 41868954
2026 Neddylation is indispensable for early meiotic progression in spermatocytes via destabilizing HORMAD1 by SCF ubiquitin E3 ligase during synapsis. Cell & bioscience 0 42216099
2024 Expression of HORMAD1 in Chronic Rhinosinusitis and Its Correlation with Inflammatory Factors. Journal of the College of Physicians and Surgeons--Pakistan : JCPSP 0 38185961
2023 The Cancer Testes Antigen, HORMAD1, is a Tumor-Specific Replication Fork Protection Factor. bioRxiv : the preprint server for biology 0 36778501

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