Affinage

HORMAD1

HORMA domain-containing protein 1 · UniProt Q86X24

Length
394 aa
Mass
45.2 kDa
Annotated
2026-04-28
33 papers in source corpus 18 papers cited in narrative 18 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HORMAD1 is a HORMA domain protein that functions as a central coordinator of meiotic chromosome dynamics and, when aberrantly expressed in somatic cancers, reprograms DNA repair and checkpoint signaling. In meiosis, HORMAD1 is loaded onto unsynapsed chromosome axes via meiotic cohesins REC8 and RAD21L, where it promotes SPO11-dependent double-strand break formation, inter-homologue recombination through DMC1/RAD51, ATR-dependent checkpoint surveillance of unsynapsed chromatin, and meiotic sex chromosome inactivation; synaptonemal complex formation triggers its removal by TRIP13 AAA-ATPase, creating a negative feedback loop that couples synapsis completion to checkpoint silencing (PMID:19851446, PMID:21478856, PMID:32931493). A truncating HORMAD1 mutation (p.Gln341*) that ablates nuclear localization causes human male infertility with spermatogenic arrest (PMID:36524333). In cancer cells, HORMAD1 promotes homologous recombination and replication fork protection by facilitating RAD51 loading, sequesters the MCM8–MCM9 complex to impair mismatch repair, weakens the spindle assembly checkpoint through direct interaction with Aurora B/INCENP to generate aneuploidy, and drives p27 degradation to suppress senescence (PMID:30333500, PMID:37838177, PMID:32647118, PMID:41813673, PMID:41868954).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2009 High

    The discovery that HORMAD1 preferentially marks unsynapsed meiotic axes and is actively removed from synapsed regions by TRIP13 established the principle that HORMA domain proteins serve as sensors of synapsis status on meiotic chromosomes.

    Evidence Immunofluorescence on wild-type and Trip13 mutant mouse spermatocytes; biochemical fractionation and SC-mutant analysis

    PMID:19686734 PMID:19851446

    Open questions at the time
    • Mechanism by which TRIP13 catalyzes HORMAD1 removal not defined
    • Whether HORMAD1 displacement requires a direct TRIP13-HORMAD1 interaction or adaptor proteins
  2. 2010 High

    Knockout studies revealed that HORMAD1 is required upstream of meiotic DSB formation, early recombination (γH2AX, DMC1, RAD51 foci), homologue pairing, and sex chromosome inactivation—placing it as a master enabler of meiotic recombination and checkpoint activation.

    Evidence Hormad1 knockout mouse with immunofluorescence and electron microscopy for SC, DSB, and MSCI markers

    PMID:21079677

    Open questions at the time
    • How HORMAD1 mechanistically stimulates SPO11-dependent DSB formation remains unknown
    • Whether HORMAD1 acts catalytically or as a structural scaffold for DSB machinery
  3. 2011 High

    A negative feedback model was established: HORMAD1 promotes DSBs and ATR checkpoint activity on unsynapsed axes, but SC formation depletes HORMAD1, thereby coupling synapsis completion to checkpoint silencing and meiotic progression.

    Evidence Hormad1 knockout mouse, genetic epistasis for ATR recruitment and SC formation

    PMID:21478856

    Open questions at the time
    • Signal that links SC installation to HORMAD1 removal not molecularly defined
    • Relative contributions of HORMAD1-dependent DSBs versus checkpoint signaling to meiotic arrest
  4. 2012 High

    HORMAD1 was shown to operate the meiotic prophase checkpoint in oocytes: Hormad1 deficiency rescued massive oocyte loss in Spo11-null ovaries, demonstrating that HORMAD1 enforces elimination of asynaptic oocytes and undergoes DNA-damage-independent phosphorylation.

    Evidence Hormad1/Spo11 double-KO mice, epistasis for oocyte survival, phosphorylation analysis

    PMID:22530760

    Open questions at the time
    • Kinase(s) responsible for DNA-damage-independent HORMAD1 phosphorylation not identified
    • Whether phosphorylation is required for checkpoint enforcement
  5. 2013 High

    Epistasis with Dmc1 revealed that HORMAD1 enforces DMC1-dependent inter-homologue repair pathway choice; its loss permits DMC1-independent repair that allows asynaptic oocytes to survive.

    Evidence Hormad1/Dmc1 double-KO mice, irradiation rescue of embryonic ovaries, repair foci immunofluorescence

    PMID:23759310

    Open questions at the time
    • Molecular mechanism by which HORMAD1 blocks alternative repair pathways not defined
    • Whether HORMAD1 directly interacts with DMC1 or acts through an intermediary
  6. 2015 High

    The first cancer-context function was identified: aberrant HORMAD1 expression in triple-negative breast cancer suppresses RAD51-dependent HR and promotes alternative repair, generating genomic instability and creating therapeutic vulnerability to PARP inhibitors and platinum agents.

    Evidence HORMAD1 knockdown/overexpression in TNBC lines, HR reporter assays, genomic copy-number profiling

    PMID:25770156

    Open questions at the time
    • Apparent contradiction with later studies showing HORMAD1 promotes HR in other cancer contexts
    • Whether HR suppression is dose- or context-dependent not resolved
  7. 2018 High

    Domain dissection in lung cancer cells showed that the HORMA domain and C-terminal oligomerization motif are both required for HORMAD1 localization to DNA damage foci, where it promotes DSB end resection and RAD51 loading for HR repair independently of meiotic partners HORMAD2 and CCDC36.

    Evidence Domain mutant analysis, HR/NHEJ reporter assays, RPA and RAD51 immunofluorescence in lung adenocarcinoma cells

    PMID:30333500

    Open questions at the time
    • Reconciliation of HR-promoting versus HR-suppressing roles of HORMAD1 across cancer types
    • How the C-terminal oligomerization motif contributes mechanistically to resection
  8. 2020 High

    The initial chromatin-loading mechanism for HORMAD1 was defined: meiotic cohesins REC8 and RAD21L physically recruit HORMAD1 to chromatin prior to axial element assembly, with HORMAD1 also binding AE components SYCP2/SYCP3, establishing the hierarchical order of axis assembly.

    Evidence Co-immunoprecipitation, Sycp2-KO, Hormad1/Rec8 and Hormad1/Rad21L double-KO mice

    PMID:32931493

    Open questions at the time
    • Whether REC8 and RAD21L bind HORMAD1 through its HORMA domain closure-motif interface not tested
    • Stoichiometry and dynamics of the cohesin–HORMAD1 interaction unknown
  9. 2020 Medium

    A second oncogenic mechanism was uncovered: HORMAD1 sequesters the MCM8–MCM9 complex away from chromatin, reducing MLH1 loading and causing DNA mismatch repair deficiency in cancer cells.

    Evidence Co-immunoprecipitation, nuclear fractionation, MMR assays in HORMAD1-expressing cancer lines

    PMID:32647118

    Open questions at the time
    • Single-lab finding without reciprocal validation of MCM8–MCM9 cytoplasmic sequestration in vivo
    • Whether HORMAD1-MCM9 interaction uses the same closure-motif interface as meiotic partners not yet determined at that time
  10. 2022 Medium

    Super-resolution imaging demonstrated that HORMAD1 loss alters the lifetime, size, and configuration of RAD51/DMC1 recombination intermediates and inhibits SC coiling, revealing a nanoscale structural role in organizing the recombination machinery.

    Evidence Three-color dSTORM on Hormad1−/− spermatocytes

    PMID:35857787

    Open questions at the time
    • Whether altered intermediate configurations reflect a direct structural role or indirect consequence of reduced DSBs
    • Single imaging study awaits independent replication
  11. 2023 High

    Structural determination of the HORMAD1 HORMA domain revealed a self-closed conformation with an intramolecular closure motif; peptides from HORMAD2 and MCM9 bind this same interface via a conserved Ser-Glu-Pro motif, unifying the meiotic and cancer-context partner interactions through a shared structural mechanism.

    Evidence Crystal structure, biochemical binding assays, structure-guided mutants in MMR and HR reporter assays

    PMID:37794593

    Open questions at the time
    • Full-length HORMAD1 structure with partners not determined
    • Whether TRIP13-catalyzed conformational change uses the same open/closed transition seen in other HORMA proteins
  12. 2023 High

    HORMAD1 was found to associate with the replisome and protect stalled replication forks by promoting RAD51 loading; its loss exposes nascent DNA to MRE11–DNA2–BLM-mediated degradation, establishing a replication fork protection function distinct from its DSB repair role.

    Evidence iPOND for replisome association, DNA fiber assays, MRE11/DNA2/BLM inhibitor epistasis in HORMAD1-KO cells

    PMID:37838177

    Open questions at the time
    • Whether fork protection is relevant in meiotic S-phase not tested
    • Mechanism of HORMAD1 recruitment to the replisome unknown
  13. 2023 Medium

    A human truncating HORMAD1 mutation (p.Gln341*) that removes the nuclear localization signal causes cytoplasmic mislocalization and spermatogenic arrest, providing the first direct genetic link between HORMAD1 loss-of-function and human male infertility.

    Evidence Whole-exome sequencing of infertile patient, GFP-tagged WT vs. mutant transfection, immunofluorescence

    PMID:36524333

    Open questions at the time
    • Single family; additional independent cases needed
    • Whether partial nuclear localization persists in patient tissue not examined
  14. 2024 Medium

    Substage-specific differential phosphorylation of HORMAD1 at Ser307 (DSB-independent, from leptotene) and Ser378 (partially SPO11-dependent, from mid-zygotene onward) was mapped, suggesting that distinct phospho-forms encode different functional states during meiotic prophase.

    Evidence Phospho-specific antibodies, immunofluorescence on wild-type and Spo11−/− spermatocytes

    PMID:38897409

    Open questions at the time
    • Functional consequences of each phosphorylation site not tested by mutagenesis
    • Kinase identity for each site unknown
  15. 2026 High

    HORMAD1 was shown to weaken the spindle assembly checkpoint in mitotic cancer cells through direct interaction with Aurora B, impairing Aurora B/INCENP signaling independently of MAD2L1, thereby generating aneuploidy and creating vulnerability to MPS1, Aurora B, and BUB1 inhibitors.

    Evidence Co-IP of HORMAD1 with Aurora B, live-cell mitotic arrest assays, inducible HORMAD1 TNBC lines, aneuploidy quantification, inhibitor sensitivity

    PMID:41813673

    Open questions at the time
    • Whether the HORMAD1–Aurora B interaction uses the HORMA closure-motif interface not tested
    • In vivo validation of inhibitor sensitivity in HORMAD1-expressing tumors lacking
  16. 2026 Medium

    HORMAD1 was found to promote ubiquitin-mediated p27 degradation, preventing cellular senescence in TNBC; its depletion leads to p27 accumulation and senescence, revealing a proliferation-sustaining mechanism in cancer.

    Evidence Co-IP, p27 ubiquitination western blot, senescence flow cytometry, HORMAD1 knockdown/overexpression in TNBC cells

    PMID:41868954

    Open questions at the time
    • E3 ubiquitin ligase mediating HORMAD1-dependent p27 degradation not identified
    • Single lab, single study; independent confirmation needed

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include how HORMAD1 mechanistically stimulates SPO11-dependent DSB formation, the identity of kinases phosphorylating HORMAD1 at functionally distinct sites, the structural basis of TRIP13-mediated HORMAD1 removal from synapsed axes, and how HORMAD1's apparently opposing effects on HR (promoting in some cancer contexts, suppressing in others) are reconciled by cellular context or dosage.
  • No reconstituted system for HORMAD1-dependent DSB stimulation
  • No full-length HORMAD1 structure with TRIP13 or cohesin partners
  • Context-dependent HR regulation mechanism undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005694 chromosome 4 GO:0005634 nucleus 3
Pathway
R-HSA-1474165 Reproduction 4 R-HSA-73894 DNA Repair 4 R-HSA-1643685 Disease 3 R-HSA-1640170 Cell Cycle 1
Partners
AURKBCDKN1BHORMAD2MCM9RAD21LREC8SYCP2TRIP13

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 HORMAD1 and HORMAD2 preferentially associate with unsynapsed meiotic chromosome axes and are depleted from synapsed axes; TRIP13 AAA-ATPase is required for this depletion, establishing a mutually exclusive relationship between HORMAD-rich domains and synapsed chromatin. Immunofluorescence on wild-type and mutant mouse spermatocytes; genetic analysis of TRIP13 mutants PLoS genetics High 19851446
2009 HORMAD1 associates biochemically and cytologically with the meiotic chromosome axis, accumulating during leptotene-to-zygotene and disappearing from synapsed regions at pachytene, then reappearing upon desynapsis at diplotene; establishment of the synaptonemal complex is required for displacement of HORMAD1 from the axis. Biochemical fractionation, immunofluorescence, analysis of synaptonemal complex mutant strains Experimental cell research High 19686734
2010 HORMAD1 is a component of the synaptonemal complex required for double-strand break formation, early recombination events (γH2AX, DMC1, RAD51, RPA foci), homologous chromosome pairing, and meiotic sex chromosome inactivation (MSCI); HORMAD1 co-localizes with γH2AX, ATR, and BRCA1 at the sex body, and its loss abolishes their localization to sex chromosomes. Hormad1 knockout mouse, immunofluorescence, electron microscopy PLoS genetics High 21079677
2011 HORMAD1 ensures sufficient processed DSBs for homology search, promotes synaptonemal complex formation, and is required for efficient recruitment of ATR checkpoint kinase activity to unsynapsed chromatin; SC formation leads to HORMAD1 depletion from chromosome axes, forming a negative feedback loop that coordinates meiotic progression with homologue alignment. Hormad1 knockout mouse, immunofluorescence, genetic epistasis Nature cell biology High 21478856
2012 HORMAD1 is required for the meiotic prophase checkpoint that eliminates asynaptic oocytes; Hormad1 deficiency abrogates massive oocyte loss in Spo11-deficient ovaries (epistasis); HORMAD1 undergoes extensive phosphorylation in Spo11-deficient testes and ovaries through DNA damage-independent signaling. Hormad1/Spo11 double mutant mice, genetic epistasis, immunofluorescence, phosphorylation analysis Genes to cells High 22530760
2013 HORMAD1 deficiency in oocytes promotes DMC1-independent DSB repair, which enables asynaptic oocytes to resist perinatal loss; Hormad1 deficiency rescues Dmc1−/− oocytes, placing HORMAD1 upstream of DMC1-dependent repair pathway choice. Hormad1/Dmc1 double mutant mice, irradiation of embryonic ovaries, immunofluorescence for γH2AX, RAD51, DMC1 Biology of reproduction High 23759310
2015 Elevated HORMAD1 expression in triple-negative breast cancer suppresses RAD51-dependent homologous recombination and drives use of alternative DNA repair pathways, generating allelic-imbalanced copy-number aberrations and sensitizing cancer cells to platinum-based chemotherapy and PARP inhibitors. HORMAD1 knockdown/overexpression in cancer cell lines, 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; the HORMA domain and C-terminal disordered oligomerization motif are required for IRIF localization; HORMAD1 promotes DSB resection (RPA-ssDNA foci and RAD51 redistribution to DSBs) and HR-mediated repair but not NHEJ; HORMAD1-mediated HR is independent of meiotic partners HORMAD2 and CCDC36. HORMAD1 depletion, domain mutant analysis, HR and NHEJ reporter assays, immunofluorescence for RPA and RAD51 Scientific reports High 30333500
2018 HORMAD1 promotes repair of radiation-induced DSBs at the synaptonemal complex axis and influences DNA repair pathway choice in mouse meiocytes; Spo11/Hormad1 double-KO spermatocytes showed fewer remaining DSB repair foci after irradiation compared to Spo11-KO, indicating HORMAD1 slows repair (repair inhibition role). Spo11/Hormad1 double knockout mouse, irradiation, immunofluorescence for DSB repair foci DNA repair Medium 29414051
2020 Meiotic cohesins REC8 and RAD21L mediate initial chromatin loading of HORMAD1 prior to axial element formation; HORMAD1 physically interacts with meiotic cohesins (REC8, RAD21L) and with AE components SYCP2 and SYCP3; in Sycp2-KO, HORMAD1 still localizes along cohesin axial cores via cohesins; Hormad1/Rec8-dKO but not Hormad1/Rad21L-dKO shows precocious sister chromatid axis separation. Co-immunoprecipitation, Sycp2 null mice, Hormad1/Rad21L and Hormad1/Rec8 double KO mice, immunofluorescence PLoS genetics High 32931493
2020 Aberrantly expressed HORMAD1 in cancer cells interacts with the MCM8-MCM9 complex and prevents its efficient nuclear localization, causing reduced MLH1 chromatin binding and DNA mismatch repair defects. Co-immunoprecipitation, nuclear fractionation, MMR assays in HORMAD1-expressing cancer cell lines Cell death & disease Medium 32647118
2022 HORMAD1 loss-of-function in Hormad1−/− spermatocytes alters the lifetime and size of RAD51/DMC1 recombination intermediate configurations and inhibits coil formation in the synaptonemal complex; SPO11 plays a similar but weaker role in coiling and SYCP1 has an opposite effect. Three-color dSTORM super-resolution microscopy on Hormad1−/− spermatocytes PLoS genetics Medium 35857787
2023 The human HORMAD1 HORMA domain adopts a self-closed conformation with an intra-molecular closure motif interaction; peptide motifs from HORMAD2 and MCM9 bind HORMAD1 in a mode highly similar to the self-closure, sharing a conserved Ser-Glu-Pro sequence; this HORMA-closure motif interaction contributes to DNA mismatch repair and HR repair. Crystal structure determination, biochemical binding assays, cell-based MMR and HR reporter assays with structure-guided mutants Structure High 37794593
2023 HORMAD1 associates with the replisome and protects stalled DNA replication forks; loss of HORMAD1 leads to nascent DNA strand degradation mediated by the MRE11-DNA2-BLM pathway and reduced RAD51 loading onto stalled forks, resulting in increased DNA breaks and chromosomal defects exacerbated by replication stress. DNA fiber assay, iPOND (replisome association), RAD51/BRCA2 ChIP/foci analysis, MRE11/DNA2/BLM inhibitor epistasis in HORMAD1-KO cells The Journal of biological chemistry High 37838177
2023 A truncating HORMAD1 mutation (p.Gln341*) that removes the nuclear localization signal causes cytoplasmic rather than nuclear localization of the protein, corresponding to spermatogenic arrest at the primary spermatocyte stage in humans. Whole exome sequencing, cell transfection with GFP-tagged wild-type vs. mutant HORMAD1, immunoblotting, immunofluorescence microscopy Human reproduction Medium 36524333
2024 Mouse HORMAD1 is differentially phosphorylated at two serine clusters (Ser307 and Ser378) in a substage-specific manner during meiotic prophase I: Ser307 phosphorylation occurs from early leptotene independently of SPO11 (primary, DSB-independent), while Ser378 phosphorylation is abundant on unsynapsed axes after mid-zygotene and is partially SPO11-dependent; Ser307 is phosphorylated on sex chromosome axes but unphosphorylated on desynapsed axes in diplotene. Phospho-specific antibody generation, immunofluorescence on wild-type and Spo11−/− spermatocytes Experimental cell research Medium 38897409
2026 Out-of-context HORMAD1 expression in mitotic cancer cells perturbs mitotic arrest and generates aneuploidy by weakening the spindle assembly checkpoint through a direct HORMAD1/Aurora B interaction that impairs Aurora B/INCENP signalling; these effects are MAD2L1-independent and confer sensitivity to MPS1, Aurora B, and BUB1 inhibitors. Co-immunoprecipitation of HORMAD1 with Aurora B, live-cell mitotic arrest assays, doxycycline-inducible HORMAD1 TNBC cell lines, aneuploidy quantification, inhibitor sensitivity assays Nature communications High 41813673
2026 HORMAD1 depletion in TNBC cells induces cellular senescence through accumulation of p27; HORMAD1 promotes ubiquitin-mediated degradation of p27, and ectopic HORMAD1 expression blocks p27-mediated senescence and enhances TNBC cell growth. Co-immunoprecipitation, flow cytometry for senescence, western blot for p27 ubiquitination, HORMAD1 knockdown/overexpression American journal of translational research Medium 41868954

Source papers

Stage 0 corpus · 33 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 327 19851446
2011 Meiotic homologue alignment and its quality surveillance are controlled by mouse HORMAD1. Nature cell biology 194 21478856
2010 Hormad1 mutation disrupts synaptonemal complex formation, recombination, and chromosome segregation in mammalian meiosis. PLoS genetics 178 21079677
2009 A novel mammalian HORMA domain-containing protein, HORMAD1, preferentially associates with unsynapsed meiotic chromosomes. Experimental cell research 108 19686734
2015 Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers. Cancer discovery 96 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 70 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 41 23759310
2020 Meiotic cohesins mediate initial loading of HORMAD1 to the chromosomes and coordinate SC formation during meiotic prophase. PLoS genetics 39 32931493
2020 Aberrantly expressed HORMAD1 disrupts nuclear localization of MCM8-MCM9 complex and compromises DNA mismatch repair in cancer cells. Cell death & disease 35 32647118
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 28 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 23 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 19 35347116
2022 Functional screening reveals HORMAD1-driven gene dependencies associated with translesion synthesis and replication stress tolerance. Oncogene 12 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 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 Structural and biochemical insights into the interaction mechanism underlying HORMAD1 and its partner proteins. Structure (London, England : 1993) 7 37794593
2023 HORMAD1 overexpression predicts response to anthracycline-cyclophosphamide and survival in triple-negative breast cancers. Molecular oncology 6 36852691
2022 Multi-color dSTORM microscopy in Hormad1-/- spermatocytes reveals alterations in meiotic recombination intermediates and synaptonemal complex structure. PLoS genetics 5 35857787
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
2023 Ectopically Expressed Meiosis-Specific Cancer Testis Antigen HORMAD1 Promotes Genomic Instability in Squamous Cell Carcinomas. Cells 3 37371097
2023 The cancer testes antigen, HORMAD1, limits genomic instability in cancer cells by protecting stalled replication forks. The Journal of biological chemistry 3 37838177
2021 [Corrigendum] HORMAD1 promotes docetaxel resistance in triple negative breast cancer by enhancing DNA damage tolerance. Oncology reports 2 34296290
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
2025 HORMAD1 Polymorphisms Influence Susceptibility to Esophageal Squamous Cell Carcinoma Through Gene-Smoking Interaction. Molecular carcinogenesis 0 40875139
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