Affinage

HEY1

Hairy/enhancer-of-split related with YRPW motif protein 1 · UniProt Q9Y5J3

Length
304 aa
Mass
32.6 kDa
Annotated
2026-04-28
100 papers in source corpus 37 papers cited in narrative 37 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HEY1 is a bHLH-Orange transcriptional repressor that functions as a central effector of Notch and BMP/Smad signaling to control cell fate decisions in vascular, cardiac, neural, skeletal, and muscle progenitor compartments. HEY1 represses target genes through multiple mechanisms: direct N-box binding (e.g., COL2A1), interaction with SP1-like factors at GC-box elements (e.g., VEGFR2), sequestration of tissue-specific activators such as MyoD into inactive heterodimers, and recruitment of the mSin3A co-repressor complex; its repressive activity on angiogenic genes is maintained by TRIM28-mediated SUMOylation, which stabilizes DNA-binding homodimers, while proangiogenic signals trigger deSUMOylation and heterodimerization with HES1, relieving repression (PMID:38166414, PMID:10964718, PMID:16782059, PMID:11279181, PMID:19369342). In vascular development, Hey1 and Hey2 are redundantly required downstream of Notch for arterial identity specification and great vessel morphogenesis, while Hey1 and HeyL together govern cardiac atrioventricular EMT and muscle satellite cell quiescence (PMID:15107403, PMID:17303760, PMID:21989910). The HEY1-NCOA2 fusion, the defining translocation of mesenchymal chondrosarcoma, retains HEY1 target-gene binding but converts repression into transactivation, upregulating PDGFB/PDGFRA and PI3K/AKT signaling to drive tumorigenesis (PMID:35342947, PMID:37212282).

Mechanistic history

Synthesis pass · year-by-year structured walk · 24 steps
  1. 2000 High

    Identifying HEY1 as a direct Notch transcriptional target resolved how Notch receptor activation is decoded by a specific bHLH repressor, placing HEY1 immediately downstream of RBP-Jκ.

    Evidence Promoter reporter assays with all four activated Notch receptors and RBP-Jκ site mutagenesis

    PMID:10964718

    Open questions at the time
    • Whether Notch-independent inputs also regulate HEY1 promoter in vivo was not addressed
    • Chromatin context of RBP-Jκ binding not examined
  2. 2000 High

    Demonstrating that HEY1 overexpression suppresses VEGFR2 and blocks endothelial tube formation established its first functional role as an anti-angiogenic transcriptional repressor.

    Evidence Bidirectional manipulation (overexpression and antisense knockdown) in primary endothelial cells with proliferation, migration, and tube formation assays

    PMID:11069914

    Open questions at the time
    • Mechanism of VEGFR2 repression (direct vs. indirect) not resolved
    • In vivo angiogenic relevance not tested
  3. 2001 High

    Showing that HEY1 sequesters MyoD into transcriptionally inactive heterodimers via a C-terminal domain (not bHLH or YRPW) revealed a dominant-negative mechanism for blocking myogenesis distinct from canonical bHLH repression.

    Evidence Co-IP, EMSA, and domain mutagenesis in 10T1/2 and C2C12 myogenic conversion assays

    PMID:11279181

    Open questions at the time
    • Structural basis of HEY1-MyoD heterodimer inactivity unknown
    • In vivo relevance to satellite cell biology not yet tested
  4. 2003 High

    In utero electroporation experiments showed that HEY1 maintains neural precursor identity by repressing proneural bHLH genes Mash1 and Math3, expanding the repertoire of HEY1-regulated cell fate decisions beyond the vasculature.

    Evidence In utero electroporation in mouse brain with reporter assay validation for Mash1/Math3 promoters

    PMID:12947105

    Open questions at the time
    • Whether HEY1 binds Mash1/Math3 promoters directly was not shown
    • Redundancy with Hey2/HeyL in neural progenitors not addressed
  5. 2004 High

    Hey1/Hey2 double-knockout lethality with loss of arterial markers phenocopying Notch1 and Jagged1 mutants established these factors as the essential downstream mediators of Notch-driven arterial cell fate specification.

    Evidence Double-knockout mouse genetics with genetic epistasis to Notch1/Jagged1 knockouts and arterial marker immunostaining

    PMID:15107403 PMID:15680351

    Open questions at the time
    • Individual contributions of Hey1 vs. Hey2 to specific arterial genes not dissected
    • Downstream direct target genes mediating arterial fate unknown
  6. 2004 High

    Identification of Runx2 as a direct interaction partner whose transcriptional activity is completely blocked by HEY1 revealed a mechanism for HEY1-mediated inhibition of osteoblast differentiation.

    Evidence siRNA knockdown, Runx2 reporter assays, and mineralization assays in MC3T3 and C2C12 cells

    PMID:15178686

    Open questions at the time
    • Whether HEY1 binds Runx2 on chromatin or sequesters it off-DNA not determined
    • In vivo skeletal phenotype of Hey1 single KO not examined
  7. 2005 High

    Demonstration that HEY1 acts as a corepressor for the androgen receptor AF1 domain, with Notch signaling suppressing AR transactivation through HEY1, linked Notch-HEY1 signaling to androgen-dependent gene regulation in prostate.

    Evidence Reporter assays, corepressor assays, activated Notch constructs, and AR-HEY1 colocalization in prostate epithelium

    PMID:15684393

    Open questions at the time
    • Genome-wide AR target gene regulation by HEY1 not mapped
    • Mechanism of HEY1 nuclear exclusion in prostate cancer not defined
  8. 2006 High

    Mechanistic dissection of VEGFR2 repression showed HEY1 acts through SP1-like factors at GC-box elements rather than direct E-box binding, and that bHLH plus Orange domains suffice while the YRPW motif is dispensable, defining a non-canonical repression mode for TATA-less promoters.

    Evidence Promoter reporter assays with domain mutants; protein-DNA binding studies; TATA vs. non-TATA promoter comparisons

    PMID:16782059

    Open questions at the time
    • Identity of the SP1-like factor mediating HEY1 tethering not determined
    • Whether this mechanism applies genome-wide to other TATA-less targets unknown
  9. 2007 High

    Hey1/HeyL double knockouts revealed that these factors are redundantly required for endocardial EMT and AV valve morphogenesis, while forced Hey1 expression suppresses Tbx2 to regulate AV boundary formation, expanding HEY1's role to cardiac cushion development.

    Evidence Double-knockout mouse with AV explant EMT assays and MMP-2 analysis; cardiac-specific transgenic misexpression with in situ hybridization

    PMID:17259303 PMID:17303760

    Open questions at the time
    • Whether Hey1 directly binds the Tbx2 promoter not shown
    • Relative contributions of Hey1 vs. HeyL to EMT not separated
  10. 2008 High

    ChIP identification of HEY1 binding to N-box elements in COL2A1 intron 1, where it antagonizes SOX9-mediated activation, established direct N-box binding as a distinct mode of HEY1-mediated transcriptional repression controlling chondrogenesis.

    Evidence ChIP for endogenous HEY1 at COL2A1 intron 1; reporter assays; qPCR for COL2A1 and AGGRECAN

    PMID:18759300

    Open questions at the time
    • Whether HEY1 physically interacts with SOX9 or merely competes for adjacent cis-elements unknown
    • Genome-wide N-box occupancy not mapped
  11. 2008 High

    ChIP evidence that Smad signaling directly activates the Hey1 locus downstream of BMP9 established a Notch-independent route for Hey1 induction, with Runx2 rescue of Hey1 knockdown confirming Hey1 acts upstream of Runx2 in osteogenesis.

    Evidence Smad ChIP at Hey1 locus; siRNA knockdown with in vitro/in vivo osteogenesis assays; Runx2 rescue

    PMID:18986983

    Open questions at the time
    • How Hey1 simultaneously represses and cooperates with Runx2 in different osteogenic contexts not reconciled
  12. 2009 High

    ChIP showing Hey1 occupies myogenin and Mef2C promoters with concomitant displacement of MyoD refined the myogenic repression mechanism from simple MyoD sequestration to active promoter-level competition.

    Evidence ChIP in C2C12 myoblasts for Hey1 and MyoD at myogenin/Mef2C promoters

    PMID:19917614

    Open questions at the time
    • Whether Hey1 recruits specific co-repressors at these promoters not addressed
  13. 2009 High

    Identification of KSHV RTA as an E3 ubiquitin ligase that targets HEY1 for proteasomal degradation and disrupts the HEY1-mSin3A co-repressor complex revealed a viral strategy to overcome HEY1-mediated repression of lytic reactivation.

    Evidence In vitro ubiquitination assay, proteasome inhibitor rescue, Co-IP with mSin3A, RTA domain mutagenesis

    PMID:19369342

    Open questions at the time
    • Whether endogenous cellular E3 ligases regulate HEY1 turnover similarly not explored
    • In vivo relevance to KSHV latency-lytic switch not confirmed
  14. 2009 High

    The Leu94Met polymorphism converting HEY1 from AR corepressor to co-activator while abolishing p53 activation demonstrated that a single residue switch can invert HEY1's functional output, linking HEY1 to p53-dependent cell cycle control.

    Evidence Point mutagenesis with AR corepressor, p53 reporter, and cell-cycle arrest assays

    PMID:19802006

    Open questions at the time
    • Structural basis of how L94M inverts corepressor to co-activator function unknown
    • Population frequency and clinical significance of L94M not established
  15. 2011 High

    Hey1/HeyL double knockout causing premature satellite cell differentiation and age-dependent satellite cell depletion established HEY1 as essential for maintaining muscle stem cell quiescence, linking Notch-HEY1 signaling to adult tissue regeneration.

    Evidence Double-knockout mouse; in vitro myoblast culture showing loss of Pax7+/MyoD− undifferentiated cells; satellite cell counts and regeneration assays

    PMID:21989910

    Open questions at the time
    • Direct chromatin targets of Hey1 in satellite cells not identified genome-wide
  16. 2014 High

    Molecular characterization of the HEY1-NCOA2 fusion in mesenchymal chondrosarcoma identified the diagnostic translocation for this tumor type, implicating conversion of HEY1 repressor function into aberrant transcriptional activation as an oncogenic mechanism.

    Evidence 5' RACE, RT-PCR, FISH in multiple clinical tumor specimens; genome-wide exon array

    PMID:22034177

    Open questions at the time
    • Oncogenic mechanism of the fusion not yet defined
    • Target genes of HEY1-NCOA2 unknown
  17. 2016 High

    Identification of Ser-68 phosphorylation by STK38/STK38L as a modification that stabilizes HEY1 protein but blocks p53 activation revealed a phospho-switch controlling HEY1's pro-apoptotic function, with MDM2 identified as a degradation-promoting interactor opposed by this phosphorylation.

    Evidence MALDI-TOF MS; S68D phosphomimetic mutagenesis; kinase assays; Co-IP with RPL11 and MDM2; p53 reporter and cell-cycle assays

    PMID:27129302

    Open questions at the time
    • In vivo significance of Ser-68 phosphorylation not tested
    • Whether STK38 regulation is context-specific (e.g., tissue type) unknown
  18. 2018 High

    Demonstration that the TrkC killer-fragment is imported to the nucleus via importin-β3/KPNA4 and cooperates with HEY1 to silence MDM2, stabilizing p53 and inducing apoptosis, established a dependence-receptor signaling pathway converging on HEY1-mediated transcriptional repression.

    Evidence Co-IP of TrkC-Hey1 and TrkC-KPNA4; MDM2 promoter reporter; Hey1/p53 knockdown/overexpression; avian neuroblastoma in vivo model

    PMID:29750782

    Open questions at the time
    • Whether HEY1 directly binds the MDM2 promoter not shown by ChIP
    • Generality beyond neuroblastoma not tested
  19. 2019 High

    ChIP-seq revealing that HeyL requires Hes1 to form heterodimers that bind Hey1 target sites showed how combinatorial bHLH pairing determines genome-wide occupancy, explaining the functional redundancy between Hey1 and HeyL in satellite cells.

    Evidence Conditional knockout mice; ChIP-seq for HeyL and HeyL-Hes1; myogenin promoter reporter assay

    PMID:30745427

    Open questions at the time
    • Whether Hey1 also requires a heterodimeric partner for full chromatin occupancy not determined
  20. 2020 High

    Endothelial-specific conditional deletion proved that Hey1 function in pharyngeal arch artery morphogenesis is cell-autonomous to endothelial cells, and identified a distal Notch-responsive enhancer specific to large arteries, defining the cis-regulatory logic of vascular Hey1 expression.

    Evidence Tek-Cre conditional knockout; enhancer identification and functional testing in vivo; Notch vs. ALK1 signaling manipulations

    PMID:33454003

    Open questions at the time
    • Transcription factors binding the distal enhancer besides Notch not identified
    • Whether the enhancer is relevant to non-pharyngeal arteries unknown
  21. 2021 High

    Live imaging revealed that Hey1 is expressed in a non-oscillatory, stationary pattern in slowly dividing neural progenitors, contrasting with oscillatory Hes1/Hes5, establishing expression dynamics as a mechanism by which Notch effector choice biases stem cell maintenance vs. proliferation.

    Evidence Live imaging of Hey1 dynamics; comparison with Hes1/Hes5 oscillations; Notch manipulation in embryonic NPCs; adult NSC lineage tracing

    PMID:34772946

    Open questions at the time
    • Molecular basis for why Hey1 does not oscillate unknown
    • Whether stationary expression is intrinsic to the Hey1 mRNA/protein or imposed by cell cycle state not resolved
  22. 2022 High

    Genome-wide ChIP-seq and RNA-seq of the HEY1-NCOA2 fusion showed it binds canonical HEY1 target promoters but converts them from repressed to activated, directly upregulating PDGFB/PDGFRA and hyperactivating PI3K/AKT, providing the mechanistic basis for how the fusion drives mesenchymal chondrosarcoma.

    Evidence ChIP-seq and RNA-seq in iPSC-derived MSCs with inducible HEY1-NCOA2 vs. wildtype HEY1/NCOA2 isogenic controls

    PMID:35342947

    Open questions at the time
    • Whether PDGFB/PDGFRA are necessary and sufficient for transformation not tested
    • Structural basis of repressor-to-activator conversion not resolved
  23. 2023 High

    An in vivo mesenchymal chondrosarcoma mouse model showed that the HEY1-NCOA2 fusion physically interacts with Runx2 and that Runx2 contributes to but is not solely required for tumorigenesis, while HDAC inhibition suppresses fusion-driven gene expression and tumor growth.

    Evidence Mouse tumor model; ChIP-seq; Co-IP of HEY1-NCOA2 with Runx2; Runx2 conditional KO; panobinostat treatment in vitro and in vivo

    PMID:37212282

    Open questions at the time
    • Which Runx2-independent pathways sustain tumor growth unknown
    • Mechanism by which HDAC inhibition specifically disrupts fusion activity not defined
  24. 2024 High

    Discovery that TRIM28-mediated SUMOylation stabilizes HEY1 homodimers and E-box binding while proangiogenic deSUMOylation switches HEY1 to inactive HES1 heterodimers provided a unified post-translational mechanism governing the angiogenic switch through HEY1 dimerization control.

    Evidence IP-MS identifying SUMOylation sites; ChIP, EMSA, dual luciferase for DNA binding; Co-IP for dimerization; SUMOylation-deficient mutant mice; multiple in vivo angiogenesis models

    PMID:38166414

    Open questions at the time
    • The deSUMOylase responsible for proangiogenic HEY1 modification not identified
    • Whether SUMOylation regulates HEY1 in non-endothelial contexts unknown
    • Structural basis of how SUMOylation favors homodimer over heterodimer not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for HEY1 dimerization switching, genome-wide direct target identification across multiple tissue contexts, the identity of endogenous E3 ligases and deSUMOylases regulating HEY1 turnover outside viral contexts, and the precise mechanism by which the HEY1-NCOA2 fusion converts repression to activation.
  • No crystal or cryo-EM structure of HEY1 or its complexes
  • Comprehensive genome-wide binding data for wildtype HEY1 across tissues lacking
  • Endogenous ubiquitin ligases for HEY1 turnover not identified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 10 GO:0003677 DNA binding 4
Localization
GO:0005634 nucleus 3
Pathway
R-HSA-1266738 Developmental Biology 7 R-HSA-74160 Gene expression (Transcription) 6 R-HSA-1643685 Disease 3
Partners
ARBABAM2HES1MYOD1NTRK3RBPJRUNX2TRIM28
Complex memberships
HEY1-HES1 heterodimerHEY1-MyoD heterodimerHEY1-mSin3A co-repressor complex

Evidence

Reading pass · 37 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 HEY1 (Hey1) promoter is directly activated by all four mammalian Notch receptors via two functional RBP-Jκ binding sites, establishing Hey1 as a direct Notch target gene. Cotransfection/promoter reporter assays with activated Notch constructs and site-directed mutagenesis of RBP-Jκ binding sites Biochemical and biophysical research communications High 10964718
2000 HESR1/HEY1 overexpression in endothelial cells downregulates VEGFR2 mRNA levels and blocks endothelial cell proliferation, migration, and capillary-like network formation in vitro. Overexpression and antisense oligonucleotide knockdown in primary endothelial cells with tube formation, proliferation, and migration assays The Journal of biological chemistry High 11069914
2001 CHF2/HEY1 inhibits MyoD-dependent myogenin promoter activation, blocks myogenic conversion, and forms an inactive heterodimeric complex with MyoD; the repressive activity maps to a hydrophobic C-terminal region, not the bHLH or YRPW motifs. Transient transfection reporter assays, EMSA, co-immunoprecipitation, and mutational analysis in 10T1/2 fibroblasts and C2C12 cells The Journal of biological chemistry High 11279181
2002 Notch signaling activation during endothelial capillary network formation induces HESR1/HEY1 expression, which in turn downregulates VEGFR2, reducing VEGF-mediated EC proliferation but not bFGF-mediated proliferation. Dominant-negative and constitutively active Notch constructs in endothelial cells; reporter assays and RT-PCR for VEGFR2 and HESR1 Microvascular research Medium 12453432
2003 Hey1 (Hesr1) misexpression in mouse brain transiently maintains neural precursor cells by negatively regulating neuronal bHLH genes Mash1 and Math3, increasing late-born superficial-layer neurons; at later stages it inhibits neurogenesis and promotes astroglial fate. In utero electroporation of mouse brain; transient transfection reporter assays for Mash1/Math3 transcription The Journal of biological chemistry High 12947105
2003 BOIP, a conserved protein, interacts with the Orange domain of HEY1/HRT1, and this interaction recruits BOIP to the nucleus, identifying Orange-domain binding as a mechanism for regulating HEY1 activity. Yeast two-hybrid screen, co-localization studies showing nuclear recruitment upon binding Developmental dynamics Medium 14648848
2004 Combined knockout of Hey1 and Hey2 in mice results in embryonic lethality with failure of vascular remodeling, loss of arterial endothelial markers (CD44, neuropilin1, ephrin-B2), establishing Hey1/Hey2 as essential downstream transducers of Notch signals in arterial cell fate specification. Mouse double-knockout genetics; comparison with Notch1 and Jagged1 knockout phenotypes (genetic epistasis); immunostaining for arterial markers Genes & development High 15107403
2004 Hey1 completely abrogates Runx2 transcriptional activity via direct interaction, and siRNA-mediated inhibition of Hey1 increases osteoblast matrix mineralization, identifying Hey1 as a negative regulator of osteoblast differentiation acting through Runx2. siRNA knockdown, reporter assays for Runx2 transcriptional activity, mineralization assays in MC3T3 and C2C12 cells The Journal of biological chemistry High 15178686
2005 Hey1 functions as a corepressor for AF1 in the androgen receptor (AR), inhibiting transcription from androgen-dependent target genes; activated Notch represses endogenous AR transactivation through Hey1. Hey1 co-localizes with AR in prostate epithelium and is excluded from the nucleus in most prostate cancers. Transient transfection reporter assays, coactivator/corepressor assays; immunofluorescence colocalization; constitutively active Notch constructs Molecular and cellular biology High 15684393
2005 Hesr1/Hey1 and Hesr2/Hey2 are redundantly required for cardiovascular Notch signaling: double knockout mice exhibit embryonic lethality recapitulating most cardiovascular phenotypes of Notch pathway mutants including arterial-venous specification defects, septation, and cushion formation defects. Hesr1/Hesr2 double-knockout mouse genetics; phenotypic and molecular analysis of cardiovascular defects Developmental biology High 15680351
2006 HESR1/HEY1 represses VEGFR2 transcription not through direct E-box binding but through interactions with GC-box/SP1-like binding proteins; the bHLH and Orange domains are sufficient for repression; the YRPW motif is dispensable; a TATA box renders the promoter resistant to HESR1 repression. Promoter reporter assays with HESR1 domain mutants, protein-DNA binding studies, promoter comparison across TATA vs. non-TATA promoters Biochemical and biophysical research communications High 16782059
2006 KSHV RTA induces HEY1 expression; HEY1 represses the RTA promoter as part of a repressor complex (without direct DNA binding), interacts with co-repressor mSin3A, and this interaction is abolished by RTA, suggesting a feedback repression mechanism in KSHV latency. Luciferase reporter assays, ChIP, co-immunoprecipitation of HEY1 with mSin3A, siRNA knockdown Biochemical and biophysical research communications Medium 16678790
2006 HESR1/HEY1 directly binds the 3′ non-coding region of the dopamine transporter (DAT1) gene and represses its expression; Hesr1 knockout mice show upregulation of multiple dopamine-related genes and altered dopaminergic behavior. Direct DNA-binding assay; RT-PCR gene expression in knockout mice; behavioral testing Journal of neuroscience research Medium 16998899
2007 Combined loss of Hey1 and HeyL causes impaired epithelial-to-mesenchymal transition (EMT) in atrioventricular endocardial explants, accompanied by reduced MMP-2 expression and reduced mesenchymal cell density, resulting in ventricular septal defects and valve dysplasia. Hey1/HeyL double-knockout mouse genetics; AV explant EMT assay; MMP-2 expression analysis; comparison with Hey2 and Notch1 knockouts (genetic epistasis) Circulation research High 17303760
2007 Forced expression of Hesr1/Hey1 in the cardiac lineage suppresses AV canal boundary formation and reduces Bmp2 and Tbx2 expression, indicating that Hey1 directly suppresses Tbx2 to regulate AV boundary formation, independently of Notch2 signaling. Cardiac lineage-specific transgenic misexpression; in situ hybridization and immunostaining for AV markers; pharmacological Notch2 inhibition Development High 17259303
2008 HEY1 binds to N-box domains adjacent to the SOX9 enhancer site in intron 1 of COL2A1, repressing SOX9-mediated transcriptional activation of COL2A1 and AGGRECAN to block chondrogenic differentiation; overexpression of HEY1 represses COL2A1 ~80-fold. ChIP for endogenous HEY1 binding to COL2A1 intron 1; transfection reporter assays; qPCR for COL2A1 and AGGRECAN Arthritis and rheumatism High 18759300
2008 Hey1 is a direct target of BMP9-induced Smad signaling (ChIP evidence); Hey1 loss diminishes BMP9-induced osteogenesis and promotes chondrogenic fate; Hey1 and Runx2 act synergistically, with Runx2 downstream of Hey1, and exogenous Runx2 rescues Hey1-knockdown osteogenic defects. ChIP for Smad binding to Hey1 locus; siRNA knockdown with in vitro/in vivo osteogenesis assays; Runx2 rescue experiments The Journal of biological chemistry High 18986983
2009 Hey1 is recruited to the promoter regions of myogenin and Mef2C in myoblasts, correlating with reduced MyoD recruitment to these promoters, establishing that Hey1 represses myogenesis by blocking key myogenic target gene expression rather than directly inhibiting MyoD intrinsic activity. ChIP in C2C12 myoblasts for Hey1 and MyoD at myogenin and Mef2C promoters; Hey1 overexpression with differentiation assays The Journal of biological chemistry High 19917614
2009 KSHV RTA acts as an E3 ubiquitin ligase targeting HEY1 for ubiquitination and proteasomal degradation; a Cys-plus-His-rich region of RTA is required; HEY1 interacts with co-repressor mSin3A; RTA disrupts the HEY1-mSin3A interaction. Ubiquitination assay, proteasome inhibitor rescue, co-immunoprecipitation of HEY1 with mSin3A, domain mutant analysis of RTA Journal of virology High 19369342
2009 A naturally occurring Leu94Met polymorphism in HEY1 converts it from an AR corepressor to an AR co-activator and abolishes HEY1-mediated p53 activation and p53-dependent cell-cycle arrest, without affecting its intrinsic transcriptional repressive domains. Transient transfection reporter assays, cell-cycle analysis, sensitivity assays to p53-activating drugs; mutagenesis of HEY1 localization motifs Oncogene High 19802006
2011 Hesr1/Hey1 and Hesr3/HeyL are required together for the generation of undifferentiated quiescent satellite cells during postnatal muscle development; double knockout leads to premature myogenic differentiation (MyoD, myogenin, Ki67 expression in satellite cells) and age-dependent loss of satellite cells. Hesr1/Hesr3 double-knockout mouse analysis; in vitro myoblast culture showing loss of Pax7+/MyoD− undifferentiated cells; in vivo satellite cell counts and regeneration assays Development High 21989910
2014 HEY1-NCOA2 fusion protein (derived from t(8;8) in mesenchymal chondrosarcoma) results from fusion of HEY1 exon 4 to NCOA2 exon 13 and is present in virtually all mesenchymal chondrosarcomas, defining this as the diagnostic gene fusion for this sarcoma. 5' RACE, RT-PCR, FISH in clinical tumor specimens; genome-wide exon array expression screening Genes, chromosomes & cancer High 22034177
2014 KSHV LANA stabilizes HEY1 protein by inhibiting its degradation, and HEY1 stabilized by LANA promotes neoplastic vasculature; HEY1 knockdown reduces new blood vessel formation in vivo (Matrigel plug assay). Whole-transcriptome sequencing, IHC on patient specimens, Matrigel plug angiogenesis assay in mice, siRNA knockdown of HEY1 Cancer research Medium 24523441
2015 Hey1 expression in endothelial cells is induced by BMP9 (an Alk1 ligand) in serum, independent of canonical Notch/γ-secretase signaling; soluble Alk1 (but not Alk3) receptor abolishes this induction. Gamma-secretase inhibition, dominant-negative MAML1 expression, soluble BMP receptor pretreatment, RT-PCR for Hey1 in primary human endothelial cells PloS one Medium 25799559
2016 HEY1 is a direct downstream effector of FRA1 in the c-Met/HGF signaling pathway; CAF-derived HGF activates FRA1 in an ERK1/2-dependent manner, which in turn drives HEY1 expression to regulate liver tumor-initiating cells. Functional shRNA knockdown and overexpression assays; ChIP/reporter assays placing HEY1 downstream of FRA1; STAM NASH-HCC mouse model validation Cell reports High 27134167
2016 HEY1 phosphorylation at Ser-68 by STK38 and STK38L increases HEY1 protein stability but inhibits its ability to enhance p53 transcriptional activity; the phosphomimetic S68D mutant fails to induce p53-dependent cell-cycle arrest. HEY1 also interacts with MDM2 and is subject to MDM2-mediated degradation, and this interaction is prevented by Ser-68 phosphorylation. MALDI-TOF/TOF MS identification of phosphorylation site; mutagenesis (S68D phosphomimetic); kinase interaction and phosphorylation assays; co-immunoprecipitation with RPL11 and MDM2; p53 reporter assays; cell-cycle analysis Bioscience reports High 27129302
2019 Hey1 and HeyL function cell-autonomously and redundantly in muscle stem cells (satellite cells); HeyL requires Hes1 to form heterodimers that bind Hey1 target sites in chromatin with high affinity; HeyL-Hes1 heterodimer and Hey1 act synergistically to suppress myogenin promoter activity. Conditional and genetic null mice; cultured satellite cell assays; ChIP-seq for HeyL and HeyL-Hes1; myogenin promoter reporter assay Development High 30745427
2019 BMP9 specifically induces Hey1 expression; Hey1 forms complexes with Id4 in osteoblasts; BMP9-induced overexpression of Hey1 overcomes Id4 inhibition and suppresses osteopontin (Opn) promoter activity, preventing OPN-type osteoblast differentiation. ChIP, immunoprecipitation (Hey1-Id4 complex), site-directed mutagenesis of Opn promoter, Opn promoter reporter assays International journal of biochemistry & cell biology High 31550547
2019 HIF-1α directly binds a hypoxia response element (HRE) in the HEY1 promoter under hypoxia; HEY1 then directly represses PINK1 transcription; HCC cells with HEY1 knockdown re-express PINK1, and HEY1 overexpression reduces mitochondrial mass and oxidative stress. ChIP and luciferase reporter assays for HRE in HEY1 promoter; ChIP-seq and transcriptome sequencing to identify PINK1 as HEY1 target; siRNA knockdown of HEY1 with mitochondrial phenotype readouts Cell death & disease High 31819034
2021 Hey1 displays non-oscillatory stationary expression in slowly dividing neural progenitors (in contrast to oscillatory Hes1/Hes5 in fast-cycling progenitors), contributing to long-term maintenance of adult neural stem cells downstream of Notch; cell cycle arrest biases Notch effector selection toward Hey1. Live imaging of Hey1 expression dynamics; comparison with Hes1/Hes5 oscillations; Notch manipulation in embryonic NPCs; adult NSC lineage tracing Nature communications High 34772946
2022 HEY1-NCOA2 fusion protein preferentially binds promoter regions of canonical HEY1 targets (ChIP-seq) but converts them from repressed to transactivated; the fusion directly targets and upregulates PDGFB and PDGFRA, and dramatically increases phospho-AKT (Ser473). ChIP-seq and RNA-seq in iPSC-derived MSCs with inducible HEY1-NCOA2 expression; comparison with wildtype HEY1 and NCOA2 The Journal of pathology High 35342947
2023 HEY1-NCOA2 expression in embryonic superficial zone chondrocyte precursors induces mesenchymal chondrosarcoma in mice; the fusion protein physically interacts with Runx2 via NCOA2 C-terminal domains; Runx2 knockout delays but does not abolish tumor onset; HDAC inhibitor panobinostat suppresses tumor growth by abrogating HEY1-NCOA2/Runx2-downstream gene expression. Mouse mesenchymal chondrosarcoma model via gene transduction and transplantation; ChIP-seq; co-immunoprecipitation of HEY1-NCOA2 with Runx2; Runx2 conditional knockout; in vitro and in vivo panobinostat treatment JCI insight High 37212282
2024 HEY1 is SUMOylated at conserved lysines by the E3 ligase TRIM28 in endothelial cells; SUMOylation facilitates HEY1 homodimer formation and preserves E-box promoter binding capability, maintaining HEY1's repressive activity on angiogenic RTK and Notch pathway genes. Proangiogenic stimuli induce HEY1 deSUMOylation, causing heterodimerization with HES1, loss of DNA binding, and relief of repression. Immunoprecipitation + mass spectrometry identifying SUMOylation sites; ChIP, dual luciferase, EMSA for DNA binding; co-immunoprecipitation for dimerization; SUMOylation-deficient mutant mice; multiple in vivo angiogenesis models (embryonic vascular growth, matrigel plug, wound healing, OIR, tumor angiogenesis) Circulation research High 38166414
2018 Hey1 interacts directly with the TrkC intracellular domain and importin-α3/KPNA4; the cleaved TrkC killer-fragment is translocated to the nucleus by importins and interacts with Hey1 there; Hey1 and TrkC-KF together transcriptionally silence MDM2, contributing to p53 stabilization and induction of apoptosis in neuroblastoma. Co-immunoprecipitation identifying TrkC-Hey1 and TrkC-KPNA4 interactions; MDM2 promoter reporter assays; Hey1 and p53 knockdown/overexpression; avian neuroblastoma in vivo model PLoS biology High 29750782
2015 Hey1 null mice on C57BL/6N background exhibit perinatal lethality due to abnormal fourth pharyngeal arch artery (PAA4) development, resulting in aortic arch malformations; endothelial cells in PAA4 differentiate normally but are structurally disorganized and vascular smooth muscle cells are absent, associated with downregulation of endothelial Jag1. Hrt1/Hey1 knockout mouse analysis; histology, immunostaining for endothelial and VSMC markers; Jag1 expression analysis Mechanisms of development High 26577899
2020 Hey1 expression in vascular endothelial cells (not smooth muscle cells) is essential for pharyngeal arch artery development and great vessel morphogenesis; endothelial-specific Tek-Cre-mediated Hey1 deletion impairs endothelial tube formation and smooth muscle differentiation. A distal endothelial enhancer controlling Hey1 expression is conserved, specific to large-caliber arteries, and regulated by Notch (not ALK1) signaling. Cell type-specific conditional knockout (Tek-Cre); enhancer identification and functional testing in vivo; Notch vs ALK1 signaling manipulations The Journal of biological chemistry High 33454003
2022 Babam2 interacts with Hey1 to inhibit Nfatc1 transcription, negatively regulating osteoclastogenesis; silencing Hey1 largely abolishes the anti-osteoclastogenic effects of Babam2 overexpression. Co-immunoprecipitation (Babam2-Hey1 interaction); Nfatc1 promoter reporter assays; Babam2 transgenic mice; siRNA knockdown epistasis experiments International journal of biological sciences Medium 35864959

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 The Notch target genes Hey1 and Hey2 are required for embryonic vascular development. Genes & development 538 15107403
2016 Cancer-Associated Fibroblasts Regulate Tumor-Initiating Cell Plasticity in Hepatocellular Carcinoma through c-Met/FRA1/HEY1 Signaling. Cell reports 273 27134167
2011 Identification of a novel, recurrent HEY1-NCOA2 fusion in mesenchymal chondrosarcoma based on a genome-wide screen of exon-level expression data. Genes, chromosomes & cancer 244 22034177
2000 Comparative analysis of the human and mouse Hey1 promoter: Hey genes are new Notch target genes. Biochemical and biophysical research communications 208 10964718
2004 Coordinated activation of notch, Wnt, and transforming growth factor-beta signaling pathways in bone morphogenic protein 2-induced osteogenesis. Notch target gene Hey1 inhibits mineralization and Runx2 transcriptional activity. The Journal of biological chemistry 190 15178686
2002 Notch activation during endothelial cell network formation in vitro targets the basic HLH transcription factor HESR-1 and downregulates VEGFR-2/KDR expression. Microvascular research 173 12453432
2008 Hey1 basic helix-loop-helix protein plays an important role in mediating BMP9-induced osteogenic differentiation of mesenchymal progenitor cells. The Journal of biological chemistry 156 18986983
2019 Hypoxia regulates the mitochondrial activity of hepatocellular carcinoma cells through HIF/HEY1/PINK1 pathway. Cell death & disease 154 31819034
2005 Mouse hesr1 and hesr2 genes are redundantly required to mediate Notch signaling in the developing cardiovascular system. Developmental biology 150 15680351
2007 Combined loss of Hey1 and HeyL causes congenital heart defects because of impaired epithelial to mesenchymal transition. Circulation research 144 17303760
2003 The basic helix-loop-helix genes Hesr1/Hey1 and Hesr2/Hey2 regulate maintenance of neural precursor cells in the brain. The Journal of biological chemistry 137 12947105
2007 Integrative genomic analyses on HES/HEY family: Notch-independent HES1, HES3 transcription in undifferentiated ES cells, and Notch-dependent HES1, HES5, HEY1, HEY2, HEYL transcription in fetal tissues, adult tissues, or cancer. International journal of oncology 132 17611704
2000 The basic helix-loop-helix transcription factor HESR1 regulates endothelial cell tube formation. The Journal of biological chemistry 128 11069914
2011 Hesr1 and Hesr3 are essential to generate undifferentiated quiescent satellite cells and to maintain satellite cell numbers. Development (Cambridge, England) 122 21989910
2005 Hey1, a mediator of notch signaling, is an androgen receptor corepressor. Molecular and cellular biology 114 15684393
2007 Hesr1 and Hesr2 regulate atrioventricular boundary formation in the developing heart through the repression of Tbx2. Development (Cambridge, England) 103 17259303
2008 Hesr1 and Hesr2 may act as early effectors of Notch signaling in the developing cochlea. Developmental biology 84 18291358
2009 The Notch effector Hey1 associates with myogenic target genes to repress myogenesis. The Journal of biological chemistry 78 19917614
2008 Repression of chondrogenesis through binding of notch signaling proteins HES-1 and HEY-1 to N-box domains in the COL2A1 enhancer site. Arthritis and rheumatism 77 18759300
2017 The NOTCH4-HEY1 Pathway Induces Epithelial-Mesenchymal Transition in Head and Neck Squamous Cell Carcinoma. Clinical cancer research : an official journal of the American Association for Cancer Research 75 29146722
2000 Characterization of the human and mouse HEY1, HEY2, and HEYL genes: cloning, mapping, and mutation screening of a new bHLH gene family. Genomics 69 10860664
2009 Kaposi's sarcoma-associated herpesvirus RTA promotes degradation of the Hey1 repressor protein through the ubiquitin proteasome pathway. Journal of virology 67 19369342
2008 A role for the transcription factor HEY1 in glioblastoma. Journal of cellular and molecular medicine 65 18363832
2001 Regulation of myogenic terminal differentiation by the hairy-related transcription factor CHF2. The Journal of biological chemistry 63 11279181
2009 Ubiquitous overexpression of Hey1 transcription factor leads to osteopenia and chondrocyte hypertrophy in bone. Bone 54 19857617
2014 Hey1 and Hey2 control the spatial and temporal pattern of mammalian auditory hair cell differentiation downstream of Hedgehog signaling. The Journal of neuroscience : the official journal of the Society for Neuroscience 49 25232121
2020 CAFs-derived MFAP5 promotes bladder cancer malignant behavior through NOTCH2/HEY1 signaling. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 45 32293074
2011 Inhibition of the Notch-Hey1 axis blocks embryonal rhabdomyosarcoma tumorigenesis. Clinical cancer research : an official journal of the American Association for Cancer Research 44 21948088
2019 Cell-autonomous and redundant roles of Hey1 and HeyL in muscle stem cells: HeyL requires Hes1 to bind diverse DNA sites. Development (Cambridge, England) 40 30745427
2014 Latency-associated nuclear antigen of Kaposi sarcoma-associated herpesvirus promotes angiogenesis through targeting notch signaling effector Hey1. Cancer research 39 24523441
2020 The NOTCH1-HEY1 pathway regulates self-renewal and epithelial-mesenchymal transition of salivary adenoid cystic carcinoma cells. International journal of biological sciences 38 32025208
2012 Detection of HEY1-NCOA2 fusion by fluorescence in-situ hybridization in formalin-fixed paraffin-embedded tissues as a possible diagnostic tool for mesenchymal chondrosarcoma. Pathology international 37 23252872
2011 Notch signaling proteins HES-1 and Hey-1 bind to insulin degrading enzyme (IDE) proximal promoter and repress its transcription and activity: implications for cellular Aβ metabolism. Biochimica et biophysica acta 37 22036964
2021 Notch signaling via Hey1 and Id2b regulates Müller glia's regenerative response to retinal injury. Glia 36 34415582
2021 Cell cycle arrest determines adult neural stem cell ontogeny by an embryonic Notch-nonoscillatory Hey1 module. Nature communications 36 34772946
2015 Serum induces transcription of Hey1 and Hey2 genes by Alk1 but not Notch signaling in endothelial cells. PloS one 34 25799559
2014 Chromosome aberrations and HEY1-NCOA2 fusion gene in a mesenchymal chondrosarcoma. Oncology reports 34 24839999
2006 HESR1/CHF2 suppresses VEGFR2 transcription independent of binding to E-boxes. Biochemical and biophysical research communications 33 16782059
2014 Prostate tumor OVerexpressed-1 (PTOV1) down-regulates HES1 and HEY1 notch targets genes and promotes prostate cancer progression. Molecular cancer 31 24684754
2018 Nuclear Factor I Represses the Notch Effector HEY1 in Glioblastoma. Neoplasia (New York, N.Y.) 30 30195713
2018 CCN3 and DLL1 co-regulate osteogenic differentiation of mouse embryonic fibroblasts in a Hey1-dependent manner. Cell death & disease 27 30538222
2015 Cyclic stretch enhances bone morphogenetic protein-2-induced osteoblastic differentiation through the inhibition of Hey1. International journal of molecular medicine 27 26647760
2017 Methylation regulates HEY1 expression in glioblastoma. Oncotarget 25 28574840
2004 her7 and hey1, but not lunatic fringe show dynamic expression during somitogenesis in medaka (Oryzias latipes). Gene expression patterns : GEP 24 15261833
2021 LncRNA MAGI2-AS3 inhibits tumor progression and angiogenesis by regulating ACY1 via interacting with transcription factor HEY1 in clear cell renal cell carcinoma. Cancer gene therapy 22 34002044
2009 HEY1 Leu94Met gene polymorphism dramatically modifies its biological functions. Oncogene 22 19802006
2006 Hesr1 knockout mice exhibit behavioral alterations through the dopaminergic nervous system. Journal of neuroscience research 22 16998899
2022 Mesenchymal chondrosarcoma of the head and neck with HEY1::NCOA2 fusion: A clinicopathologic and molecular study of 13 cases with emphasis on diagnostic pitfalls. Genes, chromosomes & cancer 21 35672279
2018 MiR-769 Inhibits Colorectal Cancer Cell Proliferation and Invasion by Targeting HEY1. Medical science monitor : international medical journal of experimental and clinical research 21 30565566
2022 Genomic profiling identifies genes and pathways dysregulated by HEY1-NCOA2 fusion and shines a light on mesenchymal chondrosarcoma tumorigenesis. The Journal of pathology 20 35342947
2010 Expression of the transcription factor HEY1 in glioblastoma: a preliminary clinical study. Tumori 20 20437865
2020 IMPAD1 functions as mitochondrial electron transport inhibitor that prevents ROS production and promotes lung cancer metastasis through the AMPK-Notch1-HEY1 pathway. Cancer letters 19 32417395
2020 Long noncoding RNA LINC00982 upregulates CTSF expression to inhibit gastric cancer progression via the transcription factor HEY1. American journal of physiology. Gastrointestinal and liver physiology 19 33236952
2024 SUMOylation Fine-Tunes Endothelial HEY1 in the Regulation of Angiogenesis. Circulation research 18 38166414
2016 HEY1 functions are regulated by its phosphorylation at Ser-68. Bioscience reports 18 27129302
2006 KSHV RTA induces a transcriptional repressor, HEY1 that represses rta promoter. Biochemical and biophysical research communications 18 16678790
2006 Protective effects of transcription factor HESR1 on retinal vasculature. Microvascular research 18 17028039
2003 Identification of BOIP, a novel cDNA highly expressed during spermatogenesis that encodes a protein interacting with the orange domain of the hairy-related transcription factor HRT1/Hey1 in Xenopus and mouse. Developmental dynamics : an official publication of the American Association of Anatomists 17 14648848
2023 HEY1-NCOA2 expression modulates chondrogenic differentiation and induces mesenchymal chondrosarcoma in mice. JCI insight 15 37212282
2016 Expression of activated Notch1 and Hey1 in papillary thyroid carcinoma. Histopathology 15 27542980
2020 Lidocaine Suppresses Cell Proliferation and Aerobic Glycolysis by Regulating circHOMER1/miR-138-5p/HEY1 Axis in Colorectal Cancer. Cancer management and research 14 32612388
2018 Hey1- and p53-dependent TrkC proapoptotic activity controls neuroblastoma growth. PLoS biology 14 29750782
2002 Isolation and characterization of Xenopus Hey-1: a downstream mediator of Notch signaling. Developmental dynamics : an official publication of the American Association of Anatomists 14 12454931
2017 LDB2 inhibits proliferation and migration in liver cancer cells by abrogating HEY1 expression. Oncotarget 13 29212240
2015 Pharyngeal arch artery defects and lethal malformations of the aortic arch and its branches in mice deficient for the Hrt1/Hey1 transcription factor. Mechanisms of development 13 26577899
2008 Cyclosporine inhibition of angiogenesis involves the transcription factor HESR1. The Journal of surgical research 13 18694572
2022 Babam2 negatively regulates osteoclastogenesis by interacting with Hey1 to inhibit Nfatc1 transcription. International journal of biological sciences 12 35864959
2014 Primary spinal intradural mesenchymal chondrosarcoma with detection of fusion gene HEY1-NCOA2: A paediatric case report and review of the literature. Oncology letters 12 25202377
2012 Theoretical studies on the kinetics and mechanism of the gas-phase reactions of CHF(2)OCHF (2) with OH radicals. Journal of molecular modeling 12 22562169
2020 Importance of endothelial Hey1 expression for thoracic great vessel development and its distal enhancer for Notch-dependent endothelial transcription. The Journal of biological chemistry 11 33454003
2019 Design, synthesis and SAR study of 3rd-generation taxoids bearing 3-CH3, 3-CF3O and 3-CHF2O groups at the C2-benzoate position. Bioorganic chemistry 11 31911305
2016 Pancreatic involvement by mesenchymal chondrosarcoma harboring the HEY1-NCOA2 gene fusion. Human pathology 11 27544802
2020 Reciprocal activation of HEY1 and NOTCH4 under SOX2 control promotes EMT in head and neck squamous cell carcinoma. International journal of oncology 10 33491747
2019 Primary mesenchymal chondrosarcoma of the kidney without HEY1-NCOA2 and IRF2BP2-CDX1 fusion: A case report and review. Oncology letters 10 31897203
2014 Mesenchymal chondrosarcoma diagnosed on FISH for HEY1-NCOA2 fusion gene. Pediatrics international : official journal of the Japan Pediatric Society 10 25336010
2021 Hey1 promotes migration and invasion of melanoma cells via GRB2/PI3K/AKT signaling cascade. Journal of Cancer 9 34729100
2019 BMP9 prevents induction of osteopontin in JNK-inactivated osteoblasts via Hey1-Id4 interaction. The international journal of biochemistry & cell biology 9 31550547
2015 The Anti-Adipogenic Potential of COUP-TFII Is Mediated by Downregulation of the Notch Target Gene Hey1. PloS one 9 26719988
2022 Transcription Factor HEY1 Improves Brain Vascular Endothelial Cell Function and Alleviates Ischemic Stroke by Upregulating NOTCH3. Neurochemical research 8 35316462
2022 HEY1-mediated cisplatin resistance in lung adenocarcinoma via epithelial-mesenchymal transition. Medical oncology (Northwood, London, England) 8 36396748
2017 Hey1 functions as a positive regulator of odontogenic differentiation in odontoblast‑lineage cells. International journal of molecular medicine 8 29138798
2021 8q21.11 microdeletion syndrome: Delineation of HEY1 as a candidate gene in neurodevelopmental and cardiac defects. Molecular genetics & genomic medicine 7 34549899
2021 Patient-derived xenografts and in vitro model show rationale for imatinib mesylate repurposing in HEY1-NCoA2-driven mesenchymal chondrosarcoma. Laboratory investigation; a journal of technical methods and pathology 7 34837064
2017 Hey1 and Hey2 are differently expressed during mouse tooth development. Gene expression patterns : GEP 7 29155305
2024 Atomoxetine suppresses radioresistance in glioblastoma via circATIC/miR-520d-5p/Notch2-Hey1 axis. Cell communication and signaling : CCS 6 39501373
2020 Consecutive Hypoxia Decreases Expression of NOTCH3, HEY1, CC10, and FOXJ1 via NKX2-1 Downregulation and Intermittent Hypoxia-Reoxygenation Increases Expression of BMP4, NOTCH1, MKI67, OCT4, and MUC5AC via HIF1A Upregulation in Human Bronchial Epithelial Cells. Frontiers in cell and developmental biology 6 33015064
2018 Minute mesenchymal chondrosarcoma within osteochondroma: an unexpected diagnosis confirmed by HEY1-NCOA2 fusion. Human pathology 6 29596896
2013 Enhanced prepulse inhibition and low sensitivity to a dopamine agonist in HESR1 knockout mice. Journal of neuroscience research 6 24431082
2020 Intracranial Mesenchymal Chondrosarcoma Lacking the Typical Histopathological Features Diagnosed by HEY1-NCOA2 Gene Fusion. NMC case report journal 5 32322450
2017 Role of Jagged1-Hey1 Signal in Angiotensin II-induced Impairment of Myocardial Angiogenesis. Chinese medical journal 5 28139517
2015 Qingyihuaji Formula Inhibits Pancreatic Cancer and Prolongs Survival by Downregulating Hes-1 and Hey-1. Evidence-based complementary and alternative medicine : eCAM 5 26783407
2022 HOCI Probe CPP Induces the Differentiation of Human Dermal Fibroblasts into Vascular Endothelial Cells through PHD2/HIF-1α/HEY1 Signaling Pathway. Cells 4 36231088
2016 Reinvestigation of the Unimolecular Reactions of CHF2CHF2: Identification of the 1,1-HF Elimination Component from Addition of :CFCHF2 to trans-2-Butene. The journal of physical chemistry. A 4 27798960
2023 Sox9 Inhibits Cochlear Hair Cell Fate by Upregulating Hey1 and HeyL Antagonists of Atoh1. Cells 3 37681879
2023 Inhibition of Pi4kb activity causes malformation of vestibular apparatus in zebrafish by downregulating hey1. Gene 3 38135256
2025 EOGT knockdown promotes ferroptosis and inhibits hepatocellular carcinoma proliferation by regulating SLC7A11 via HEY1. Cellular signalling 2 40154588
2025 Orbital mesenchymal chondrosarcoma and its specific fusion gene HEY1-NCOA2. BMC ophthalmology 2 40301759
2024 Inhibition of Notch3/Hey1 ameliorates peribiliary hypoxia by preventing hypertrophic hepatic arteriopathy in biliary atresia progression. Histochemistry and cell biology 2 38597939
2024 Case report: A mesenchymal chondrosarcoma with alternative HEY1::NCOA2 fusions in the sella turcica. Pathology oncology research : POR 2 39165647
2022 Novel low-grade renal spindle cell neoplasm with HEY1::NCOA2 fusion that is distinct from mesenchymal chondrosarcoma. Genes, chromosomes & cancer 2 36416671