Affinage

ASCL1

Achaete-scute homolog 1 · UniProt P50553

Length
236 aa
Mass
25.5 kDa
Annotated
2026-06-09
100 papers in source corpus 42 papers cited in narrative 41 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

ASCL1 is a basic helix-loop-helix (bHLH) proneural transcription factor that acts as a context-dependent master regulator of neuronal, glial, and neuroendocrine lineage commitment in development and cancer (PMID:15133515, PMID:28712938). It binds E-box sequences as homodimers or as heterodimers with Neurog2, and functions as a pioneer factor capable of opening closed chromatin to activate neurogenic gene programs; at permissive sites it acts as a non-pioneer remodeler, interacting with BAF SWI/SNF complexes for co-dependent DNA binding and remodeling (PMID:19389376, PMID:28712938, PMID:36931659). During neurogenesis ASCL1 specifies diverse fates—serotonergic neurons via Gata3/Lmx1b/Pet1, GABAergic interneurons, and oligodendrocytes in collaboration with Olig2 and Nkx2-2—and the choice between excitatory and inhibitory output is shaped by partners and downstream targets including Tlx3, Ptf1a, and Notch (PMID:16715081, PMID:15133515, PMID:18287202, PMID:21795554). ASCL1 alone is sufficient to reprogram fibroblasts, ESCs, and astrocytes into functional neurons, dismantling the pluripotency network and driving cell-cycle exit through Tcf7l1/Cdkn1c, while co-expression with MEF2C redirects it toward cardiac fates (PMID:25254342, PMID:26109658, PMID:36206732, PMID:37660160). Its activity is constrained at several levels: multi-site CDK-mediated serine-proline phosphorylation limits genome-wide DNA binding and differentiation-promoting activity, subcellular localization governs Huwe1-mediated ubiquitylation and proteasomal degradation, and protein partners such as Gsx2 and the inhibitor ID2 antagonize its function (PMID:25786414, PMID:29545540, PMID:33577795, PMID:35149717). Upstream, ASCL1 expression is held in check by Hes1, whose sustained versus oscillatory expression gates neural stem cell quiescence versus activation (PMID:30862661). In cancer, ASCL1 drives neuroendocrine identity in small-cell lung cancer—complexing with NKX2-1 and PROX1 and activating NOTCH, RB1, and catecholamine biosynthesis targets—and mediates neuroendocrine lineage plasticity in prostate cancer through large-scale chromatin remodeling (PMID:27452466, PMID:25267614, PMID:34016693, PMID:34466783, PMID:35477723, PMID:39394434). A separable N-terminal domain recruits HDAC1 to repress mesendoderm genes, illustrating that ASCL1 deploys distinct activating and repressive mechanisms for different programs (PMID:26700681).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 2004 High

    Establishing that ASCL1 is not merely a generic proneural factor but a determinant of specific neurotransmitter identity answered how a single bHLH factor links cell-cycle exit to phenotype specification.

    Evidence Mouse Ascl1 knockout with analysis of serotonergic marker activation in vivo

    PMID:15133515

    Open questions at the time
    • Direct binding of ASCL1 to Gata3/Lmx1b/Pet1 loci not shown
    • Mechanism distinguishing proneural from phenotype-specifying functions undefined
  2. 2006 High

    Defining how ASCL1 coordinately controls fate choices clarified that it can both promote inhibitory differentiation and, via Notch, ensure excitatory neuron generation, revealing combinatorial and feedback logic.

    Evidence Mouse knockout and genetic epistasis with Tlx3/Gsh and Ptf1a in spinal cord, plus inducible fate mapping

    PMID:16715081 PMID:17166924

    Open questions at the time
    • Direct vs. indirect regulation of Ptf1a/Tlx3 not fully resolved
    • Temporal switch from neuronal to oligodendrocyte progenitor identity mechanistically unexplained
  3. 2008 High

    Showing ASCL1 cooperates combinatorially with Olig2 and Nkx2-2 extended its role beyond neurons into oligodendrocyte differentiation and gliogenesis.

    Evidence Ascl1 knockout plus gain-of-function combinatorial overexpression in OLP cultures

    PMID:18287202

    Open questions at the time
    • Physical interaction of ASCL1 with Olig2/Nkx2-2 not demonstrated
    • Shared vs. distinct genomic targets unmapped
  4. 2009 High

    Direct ChIP and E-box mutagenesis at the Dll3 promoter established ASCL1 as a sequence-specific DNA binder acting through homodimers and Neurog2 heterodimers, with E-boxes conferring either activation or repression.

    Evidence Transgenic reporter mice, E-box mutagenesis, ChIP, and in vitro DNA binding

    PMID:19389376

    Open questions at the time
    • Identity of additional factors required for efficient binding unknown
    • Structural basis of enhancer vs. repressor E-box discrimination undefined
  5. 2013 High

    Identifying FOXO3 as a co-binding factor that restrains ASCL1-dependent neurogenesis and the Hes1-ASCL1 relationship began mapping the upstream regulatory architecture governing ASCL1 output.

    Evidence ChIP-seq for FOXO3 and ASCL1 with loss-of-function neurogenesis assays in NPCs and fibroblasts

    PMID:23891001

    Open questions at the time
    • Whether FOXO3 acts by direct competition or recruitment unresolved
    • Brain oligodendrogenesis role (PMID 23739972) mechanistically separate from binding studies
  6. 2014 High

    Demonstrating that ASCL1 alone suffices to generate functional neurons from fibroblasts and ESCs established it as a deterministic reprogramming factor and a tool for lineage conversion.

    Evidence Single-factor forced expression with electrophysiology and synaptic characterization

    PMID:25254342

    Open questions at the time
    • Why single-factor neurons default to excitatory identity not explained
    • Chromatin requirements for reprogramming competence not addressed here
  7. 2014 High

    Connecting ASCL1 to cancer, work showed it directly activates RB1 in a phosphorylation-dependent manner and drives oncogenic and NOTCH target programs in SCLC, plus upstream activation by EWS-WT1.

    Evidence ChIP-seq, expression profiling, shRNA, CDK5 inhibition in SCLC; ChIP and reporter assays for EWS-WT1

    PMID:24934812 PMID:25267614 PMID:27452466

    Open questions at the time
    • EWS-WT1 link is Medium-confidence single lab
    • Causal hierarchy among ASCL1 oncogenic targets not dissected
  8. 2015 High

    Defining multi-site CDK phosphorylation as an inhibitory switch answered how ASCL1's differentiation-promoting activity is held in check despite its presence in cycling progenitors.

    Evidence Xenopus phospho-mutant constructs with CDK/MYCN epistasis and AVNA differentiation assays

    PMID:25786414

    Open questions at the time
    • Identity of the specific CDKs acting in each context not fully resolved
    • Phosphatases reversing the modification unknown
  9. 2015 Medium

    Pathway-level studies placed ASCL1 within a NOTCH-ASCL1-RB-p53 axis and a TGF-β-Smad-ASCL1 survival pathway, situating it in cancer signaling networks.

    Evidence In vitro CDK5 inhibition, clinical NGS/IHC, and TβRII/EZH2/TGF-β manipulation in SCLC

    PMID:26340530 PMID:27462425

    Open questions at the time
    • Both are single-lab Medium-confidence
    • Direct vs. indirect Smad regulation of the ASCL1 locus not established
  10. 2017 High

    Direct demonstration of pioneer activity in glioblastoma stem cells showed ASCL1 opens closed chromatin to license a latent neuronal differentiation program suppressed by Notch.

    Evidence ATAC-seq, ChIP-seq, Notch inhibition, and ASCL1 overexpression in patient-derived GSCs with in vivo tumorigenicity

    PMID:28712938

    Open questions at the time
    • Molecular determinants of pioneer-competent sites not defined here
    • Co-factors enabling chromatin opening unidentified
  11. 2018 High

    Linking subcellular localization to ubiquitylation state identified Huwe1-mediated cytoplasmic degradation versus a stable chromatin-bound pool, adding post-translational control of ASCL1 abundance.

    Evidence Subcellular fractionation, ubiquitylation assays, Huwe1 knockdown, and lysine mutagenesis

    PMID:29545540

    Open questions at the time
    • Signals directing cytoplasmic vs. nuclear partitioning unknown
    • Function of short chromatin-associated ubiquitin chains undefined
  12. 2019 High

    Comparative genomics resolved why ASCL1 and Neurog2 induce distinct fates—divergent binding driven by intrinsic E-box preference rather than prior chromatin state—clarifying the basis of bHLH binding specificity.

    Evidence Direct ESC programming with ChIP-seq, ATAC-seq, and E-box motif analysis

    PMID:31086315

    Open questions at the time
    • DNA-binding domain residues conferring preference not mapped
    • Role of downstream factors in reinforcing divergence partially defined
  13. 2019 High

    Demonstrating that oscillatory versus sustained Hes1 gates ASCL1 dynamics established the upstream timer controlling neural stem cell quiescence versus activation, and identified LMO1/MYCN as direct activators of ASCL1 in neuroblastoma.

    Evidence Hes1 conditional KO with live imaging in adult brain; ChIP-seq/RNA-seq with ASCL1 knockdown in neuroblastoma

    PMID:30862661 PMID:31819055

    Open questions at the time
    • How ASCL1 protein level decodes oscillatory input mechanistically unresolved
    • WNT11/CHRNA target regulation (Medium-confidence) less directly validated
  14. 2020 High

    Identifying a direct Gsx2-bHLH interaction that blocks ASCL1 DNA binding revealed a partner-switch mechanism (Gsx2 in VZ vs. E-protein in SVZ) that spatially tunes neurogenic output.

    Evidence Proximity ligation in tissue, Co-IP, DNA-binding interference assays, and in vivo misexpression

    PMID:32122989

    Open questions at the time
    • Structural basis of Gsx2-bHLH contact not determined
    • Whether other homeodomain factors act similarly unknown
  15. 2021 High

    GEMM and complex studies defined ASCL1's repressive role restraining a SOX9 mesenchymal program and its complexing with NKX2-1/PROX1 to maintain neuroendocrine SCLC identity.

    Evidence Genetic ASCL1 depletion in GEMMs with RNA-seq; ChIP-seq, ATAC-seq, and Co-IP of ASCL1/NKX2-1/PROX1

    PMID:34016693 PMID:34466783

    Open questions at the time
    • Mechanism of ASCL1-mediated repression of Hippo/Wnt/Notch genes unresolved
    • Stoichiometry and architecture of the ASCL1/NKX2-1/PROX1 complex undefined
  16. 2022 High

    Mechanistic dissection separated ASCL1's pioneer and non-pioneer modes and identified BAF SWI/SNF as a partner at non-pioneer targets, and showed phosphorylation and ID2 act as differentiation barriers in neuroblastoma and GBM.

    Evidence scRNA-seq, ATAC-seq, ChIP-seq, ASCL1 KO and Co-IP with BAF subunits; phospho-mutant and ID2-deletion functional assays in NB/GBM

    PMID:35149717 PMID:35366798 PMID:36061596 PMID:36931659

    Open questions at the time
    • Determinants selecting pioneer vs. non-pioneer engagement incompletely defined
    • How phosphorylation restricts low-affinity site occupancy mechanistically unresolved
  17. 2022 High

    Cross-lineage and cancer-plasticity studies showed MEF2C redirects ASCL1 to cardiac genes and that ASCL1 drives neuroendocrine prostate plasticity via UHRF1/AMPK-mediated PRC2 disruption.

    Evidence ChIP-seq/RNA-seq cardiac reprogramming; ATAC-seq/ChIP-seq with UHRF1/AMPK manipulation and in vivo prostate tumor models

    PMID:35477723 PMID:36206732

    Open questions at the time
    • How MEF2C physically retargets ASCL1 binding undefined
    • Direct vs. indirect connection between ASCL1 and PRC2 disruption not fully resolved
  18. 2023 High

    Defining the divergent reprogramming logic of ASCL1 (rapid pluripotency dismantling, Tcf7l1/Cdkn1c-dependent cell-cycle exit) clarified the molecular steps by which it overrides existing cell identity, and identified ROR2/ERK/CREB as an upstream activator in prostate cancer.

    Evidence CRISPR KO screen with RNA-seq/ChIP-seq and Cdkn1c rescue; RTK screen with pathway inhibitors in prostate cancer

    PMID:37552603 PMID:37660160

    Open questions at the time
    • Whether Tcf7l1 dependency is direct or via downstream effectors not fully resolved
    • ROR2/CREB-to-ASCL1 link is Medium-confidence single lab
  19. 2024 High

    Stage-specific genetic studies established ASCL1 as required for initiating but not always maintaining neuroendocrine prostate plasticity, defined SMAD4-Myc competition over ASCL1 transcription, and linked ASCL1 to drug tolerance via an EMT program.

    Evidence Conditional Ascl1 deletion at different stages in prostate organoid allografts with scRNA-seq/spatial transcriptomics; CRISPR SMAD4/RB1 KO; PDX scRNA-seq under osimertinib

    PMID:38233864 PMID:38359163 PMID:39264686 PMID:39394434

    Open questions at the time
    • Why established NEPC becomes ASCL1-independent unexplained
    • EMT/drug-tolerance role (Medium-confidence) inferred rather than directly manipulated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ASCL1 integrates phosphorylation state, partner availability, and chromatin context to switch between pioneering, non-pioneering, activating, and repressive modes at the level of structure and recruitment remains unresolved.
  • No structural model of ASCL1 on pioneer-competent nucleosomal DNA
  • Rules dictating activator vs. repressor output at individual E-boxes undefined
  • Phosphatases and full kinase repertoire controlling the phospho-switch unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 5 GO:0003677 DNA binding 3 GO:0042393 histone binding 2
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 2 GO:0005829 cytosol 1
Pathway
R-HSA-1266738 Developmental Biology 5 R-HSA-1643685 Disease 5 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-4839726 Chromatin organization 3
Partners
GSX2HDAC1ID2MEF2CNEUROG2NKX2-1OLIG2PROX1
Complex memberships
ASCL1/NKX2-1/PROX1 complexBAF (SWI/SNF) complex

Evidence

Reading pass · 41 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 Ascl1 controls excitatory vs. inhibitory cell fate in spinal sensory interneurons by coordinately regulating Tlx3 expression (with Gsh1/2) during early neurogenesis and, at later stages, controlling Ptf1a expression in dIL(A) progenitors to promote inhibitory neuron differentiation while upregulating Notch signaling to ensure generation of dIL(B) excitatory neurons. Mouse genetic loss-of-function (Ascl1 knockout), genetic epistasis, in vivo analysis of transcription factor expression Nature neuroscience High 16715081
2004 Ascl1 is required for the birth of central serotonergic neurons, functioning both as a proneural gene for the production of postmitotic neuronal precursors and as a determinant of the serotonergic phenotype by activating Gata3, Lmx1b, and Pet1 in parallel. Mouse Ascl1 knockout, analysis of 5-HT neuron production and serotonergic marker expression in vivo Nature neuroscience High 15133515
2006 Ascl1 marks sequentially generated lineage-restricted progenitors in the developing spinal cord: at E11 it identifies neuronal-restricted precursors that become dorsal horn neurons, and by E16 it identifies oligodendrocyte-restricted precursors. Ascl1-null spinal cord cells have diminished capacity for neuronal differentiation, with a subset retaining immature glial characteristics. Genetic fate mapping (Ascl1-CreER / conditional Cre-flox), Ascl1 knockout mouse, temporal inducible lineage tracing Development (Cambridge, England) High 17166924
2008 Ascl1 is required for oligodendrocyte development in the spinal cord: Ascl1-/- mice show deficiency in myelin-expressing oligodendrocyte differentiation; Ascl1 collaborates with Olig2 and Nkx2-2 to promote oligodendrocyte precursor differentiation, with the combinatorial action of Ascl1+Olig2 or Ascl1+Nkx2-2 required for full differentiation beyond OLP specification. Ascl1 knockout mouse, in vitro OLP culture studies, gain-of-function overexpression of Ascl1/Olig2/Nkx2-2 combinations Development (Cambridge, England) High 18287202
2009 Ascl1 regulates Delta-like 3 (Dll3) expression in the neural tube by binding E-boxes in the conserved Dll3 proximal promoter. Distinct E-boxes confer enhancer or repressor properties; Ascl1 forms homodimers and Ascl1/Neurog2 heterodimers that bind specific E-box sites, sometimes requiring additional undefined factors for efficient DNA binding. Transgenic reporter mice (Dll3-GFP), E-box mutagenesis, chromatin immunoprecipitation (ChIP), in vitro DNA binding assays, genetic loss-of-function Developmental biology High 19389376
2011 Ascl1 is present in progenitors of all glial and neuronal cell types arising from the cerebellar ventricular zone. Conditional deletion of Ascl1 in the cerebellum causes major decreases in three types of GABAergic interneurons and an imbalance of oligodendrocytes and astrocytes; Ptf1a functions with Ascl1 in generating interneurons and Purkinje cells (double-mutant epistasis). Genetic inducible fate mapping (Ascl1-CreER), conditional Ascl1 knockout, double-mutant (Ascl1/Ptf1a) analysis The Journal of neuroscience High 21795554
2013 FOXO3 shares common genomic targets with ASCL1 in adult neural progenitor cells (NPCs); FOXO3-bound sites are enriched for bHLH motifs; FOXO3 inhibits ASCL1-dependent neurogenesis in NPCs and direct neuronal conversion in fibroblasts, and restrains neurogenesis in vivo. ChIP-seq (FOXO3 and ASCL1), chromatin landscape analysis, loss-of-function neurogenesis assays in NPCs and fibroblasts, in vivo neurogenesis assay Cell reports High 23891001
2013 Ascl1 is required for brain oligodendrogenesis during myelination and remyelination: Ascl1 positively regulates OPC specification from SVZ progenitors and the balance between OPC differentiation and proliferation in the neonatal cortex; remyelinating oligodendrocytes derive from Ascl1+ progenitors and Ascl1 is required for proper remyelination. Multiple genetic Ascl1 deletion strategies in cortical progenitors and OPCs, demyelination mouse models, analysis of human MS lesions The Journal of neuroscience High 23739972
2014 ASCL1 alone is sufficient to generate functional induced neuronal (iN) cells from mouse and human fibroblasts and embryonic stem cells; ASCL1-induced single-factor neurons are predominantly excitatory, demonstrating ASCL1 is permissive but not deterministic for the inhibitory neuronal lineage. Forced expression of single transcription factor ASCL1 in MEFs and human fibroblasts/ESCs; electrophysiology, synaptic marker analysis, neuronal morphology assessment Stem cell reports High 25254342
2014 ASCL1 directly transcriptionally activates the RB1 gene via phosphorylation-dependent inactivation; this is reversible by CDK5 inhibition. ASCL1 targets include MYCL1, RET, SOX2, NFIB (oncogenic genes), and multiple NOTCH pathway genes including DLL3, as determined by ChIP-seq in SCLC. ChIP-seq, whole-genome microarray expression analysis, shRNA knockdown, CDK5 inhibition in vitro Cell reports / PNAS High 25267614 27452466
2015 Ascl1 alone is sufficient to convert dorsal midbrain astrocytes into functional induced neurons in vivo; GFAP-AAV-mediated Ascl1 expression converts astrocytes in dorsal midbrain, striatum, and somatosensory cortex of postnatal and adult mice into neurons that form synaptic inputs and outputs with existing neurons. GFAP-AAV viral delivery in postnatal and adult mice, morphological analysis, electrophysiology, synaptic connectivity tracing The Journal of neuroscience High 26109658
2015 Multi-site phosphorylation of Ascl1 at serine-proline motifs by CDKs inhibits its ability to induce differentiation of AVNA (anteroventral noradrenergic) cells; a phospho-mutant Ascl1 drives differentiation even when CDKs or MYCN are overexpressed, whereas wild-type Ascl1 is inhibited. This was shown in a Xenopus developmental model. Xenopus in vivo gain- and loss-of-function, phospho-mutant ASCL1 constructs, CDK overexpression, Xenopus AVNA cell differentiation assays Disease models & mechanisms High 25786414
2015 The NOTCH-ASCL1-RB-p53 signaling axis drives secondary SCLC: NOTCH inactivating mutations lead to ASCL1 activation; ASCL1 inactivates RB via phosphorylation (reversible by CDK5 inhibition); this pathway was experimentally verified in vitro and validated by genetic alterations in vivo. In vitro cell line experiments with CDK5 inhibition, NGS of clinical samples, IHC, FISH; pathway epistasis analysis International journal of cancer Medium 26340530
2015 EZH2 promotes SCLC progression by epigenetically silencing TGF-β type II receptor (TβRII), thereby suppressing the TGF-β-Smad-ASCL1 pathway; ASCL1 is a Smad-dependent transcriptional target of TGF-β signaling that induces cell survival in SCLC. TβRII overexpression in SCLC cells, TGF-β treatment, EZH2 functional analysis, in vitro growth/apoptosis assays, in vivo tumor formation Cell discovery Medium 27462425
2017 ASCL1 functions as a pioneer factor in glioblastoma stem cells (GSCs), opening closed chromatin to activate a neurogenic gene expression program; ASCL1hi GSCs have latent capacity for terminal neuronal differentiation upon Notch inhibition, and increasing ASCL1 in ASCL1lo GSCs restores neuronal lineage potential, promotes differentiation, and attenuates tumorigenicity. ATAC-seq, ChIP-seq, Notch inhibition, ASCL1 overexpression in patient-derived GSCs, in vivo tumorigenicity assays, chromatin accessibility analysis Cell stem cell High 28712938
2018 Subcellular localization modulates ASCL1 ubiquitylation and degradation: cytoplasmic ASCL1 harbors long ubiquitin chains and is targeted for proteasomal destruction via the E3 ligase Huwe1, with ubiquitin conjugated to lysines in the bHLH domain; chromatin-bound ASCL1 associates with short ubiquitin chains (on N-terminal or bHLH lysines, not mediated by Huwe1) and is not targeted for destruction. Subcellular fractionation, ubiquitylation assays, E3 ligase (Huwe1) knockdown/inhibition, site-directed mutagenesis of lysine residues Scientific reports High 29545540
2019 Proneural factors Ascl1 and Neurog2 induce different neuronal fates by binding largely different genomic sites; their divergent binding patterns are not determined by prior chromatin state but are distinguished by enrichment of specific E-box sequences reflecting DNA-binding domain preferences. Divergent binding results in distinct chromatin accessibility and enhancer activity profiles that differentially shape binding of downstream transcription factors. Direct neuronal programming of ESCs, ChIP-seq, ATAC-seq, comparative genomic binding analysis, E-box motif analysis Nature neuroscience High 31086315
2019 High Hes1 expression in quiescent adult neural stem cells continuously suppresses Ascl1, keeping cells quiescent; oscillatory Hes1 drives cyclic Ascl1 expression in active neural stem cells, promoting proliferation. Inactivation of Hes1-related genes upregulates Ascl1 and increases neurogenesis, causing NSC depletion; sustained Hes1 represses Ascl1 and maintains quiescence. Induction of Ascl1 oscillations (rather than sustained expression) activates NSCs. Hes1 conditional knockout in adult mouse brain, live imaging of oscillatory expression, Hes1 sustained overexpression, neurogenesis quantification in vivo Genes & development High 30862661
2019 ASCL1 is a direct transcriptional target of LMO1 and MYCN in neuroblastoma; regulatory elements of ASCL1 are bound by LMO1, MYCN, and CRC transcription factors GATA3, HAND2, PHOX2B, TBX2, ISL1. ASCL1 is required for neuroblastoma cell growth and arrest of differentiation, and directly regulates expression of CRC genes. ChIP-seq, RNA-seq, ASCL1 knockdown functional assays in neuroblastoma cell lines Nature communications High 31819055
2020 Physical interaction between Gsx2 homeodomain protein and the bHLH domain of Ascl1 interferes with Ascl1 DNA binding, inhibiting neurogenesis in LGE ventricular zone progenitors; Ascl1-Gsx2 interactions are enriched in LGE VZ progenitors while Ascl1-E-protein (Tcf3) interactions predominate in the SVZ. Luciferase transcriptional assays, protein-protein interaction (Co-IP/proximity ligation assay in tissue sections), DNA-binding assays, Ascl1 misexpression in dorsal progenitors, Gsx2/Ascl1 co-expression experiments Development (Cambridge, England) High 32122989
2021 Ascl1 directly regulates a set of target genes during astrocyte-to-neuron conversion including Klf10 (neuritogenesis), Myt1/Myt1l (electrophysiological maturation), and Neurod4/Chd7 (conversion efficiency); ChIP-seq identified 107 genes whose regulatory regions are directly bound by ASCL1 during early conversion. RNA-seq, ChIP-seq, siRNA knockdown of individual targets during astrocyte-to-neuron conversion, electrophysiology, morphological analysis Stem cell reports High 33577795
2021 ASCL1 represses a SOX9+/RUNX1/RUNX2 neural crest stem-like program in MYC-driven SCLC; ASCL1 loss in MYC-driven SCLC promotes emergence of a SOX9+ mesenchymal state and osteosarcoma/chondroid tumors, while promoting neuroendocrine fate and NKX2-1/FOXA2/INSM1 expression; ASCL1 also represses Hippo/Wnt/Notch developmental pathway genes. Genetically engineered mouse models (GEMMs), genetic ASCL1 depletion, RNA-seq, in vivo tumor analysis, human SCLC cell SOX9 expression analysis Genes & development High 34016693
2021 ASCL1 complexes with NKX2-1 and PROX1 to co-regulate genes functioning in NOTCH signaling, catecholamine biosynthesis, and cell-cycle processes in ASCL1-high SCLC; ASCL1 depletion reduces expression of multiple DepMap-defined essential genes. ChIP-seq, ATAC-seq, super-enhancer analysis, ASCL1 knockdown, Co-immunoprecipitation/interaction analysis of ASCL1/NKX2-1/PROX1 iScience High 34466783
2022 ASCL1 acts as a pioneer factor to open closed chromatin and as a non-pioneer remodeler at permissive chromatin during human neural differentiation; ASCL1 interacts with BAF SWI/SNF chromatin remodeling complexes primarily at non-pioneer targets, with codependent DNA binding and remodeling at a subset of ASCL1/SWI/SNF co-targets. Single-cell transcriptomics, ASCL1 knockout model, ATAC-seq, ChIP-seq, Co-IP of ASCL1 with BAF complex subunits, chromatin conformation analysis Genes & development High 36931659
2022 Ascl1 possesses cross-lineage reprogramming potential; together with Mef2c, it drives efficient cardiac reprogramming. MEF2C shifts ASCL1 binding away from neuronal genes toward cardiac genes, guiding cooperative epigenetic and transcriptional activity. ChIP-seq, RNA-seq, direct cardiac reprogramming assays, comparison of ASCL1 binding in neuronal vs. cardiac reprogramming contexts Cell stem cell High 36206732
2022 Elevated ASCL1 activity in neuroblastoma cells creates numerous additional low-affinity binding sites beyond endogenous sites; multi-site phosphorylation of ASCL1 limits this additional binding; preventing phosphorylation (phospho-mutant) further increases genome-wide binding and gene activation, redirecting the transcriptome from proliferative neuroblast state toward neuronal differentiation. ASCL1 overexpression and phospho-mutant expression in neuroblastoma cells, ChIP-seq, RNA-seq, genome-wide binding site analysis BMC genomics High 35366798
2022 ASCL1 acts as a driver of neuroendocrine lineage plasticity in prostate cancer via large-scale chromatin remodeling; ASCL1 motif is enriched in hyper-accessible chromatin regions after ARPI treatment; targeting ASCL1 switches neuroendocrine lineage back to luminal epithelial state via UHRF1/AMPK-mediated disruption of polycomb repressive complex-2. ATAC-seq, ChIP-seq, ASCL1 knockdown/overexpression, chromatin architecture analysis, UHRF1/AMPK pathway manipulation, in vivo tumor models Nature communications High 35477723
2022 ASCL1 phospho-mutant (Ascl1-SA6, six serine-to-alanine substitutions at SP motifs) is more effective than wild-type Ascl1 at converting adult cortical astrocytes to neurons in vivo; Ascl1-SA6 more efficiently represses astrocytic markers SOX9 and GFAP, promotes dendritic arbor maturation, and transduced astrocytes exhibit neuronal electrophysiological responses (faster decay of evoked potentials). AAV delivery in adult mouse cerebral cortex, Rosa reporter mice, immunofluorescence, patch-clamp electrophysiology, ChR2 optogenetic stimulation Frontiers in neuroscience High 36061596
2022 ASCL1 phosphorylation at SP sites and upregulation of ID2 are barriers to ASCL1-driven differentiation in GBM stem cells; a phospho-mutant ASCL1 (non-phosphorylatable at SP sites) drives GBM cells to neuronal lineage and out of cell cycle more efficiently; the effect is further enhanced by deletion of ID2. Phospho-mutant ASCL1 overexpression in GBM stem cells, CRISPR-mediated ID2 deletion, cell cycle analysis, neuronal differentiation assays Scientific reports High 35149717
2023 Ascl1 rapidly dismantles the pluripotency network during ESC-to-neuron conversion, while Ngn2 generates a neural stem cell-like intermediate via incomplete pluripotency network shutdown; Ascl1 relies more on Tcf7l1 for cell cycle exit (in Tcf7l1 KO, Ascl1 represses pluripotency genes but fails to exit cell cycle; overexpression of Cdkn1c restores cell cycle exit and neuronal generation). CRISPR-Cas9 KO screening, RNA-seq, ChIP-seq, direct ESC-to-neuron conversion, Cdkn1c overexpression rescue experiments Nature communications High 37660160
2014 EWS-WT1 oncoprotein directly activates ASCL1 transcription by binding the proximal ASCL1 promoter through multiple WT1-responsive elements; EWS-WT1 silencing in DSRCT cells reduces ASCL1 expression and cell viability. ChIP assay, luciferase reporter assays with ASCL1 promoter, EWS-WT1 knockdown/transgenic mouse, DSRCT cell functional assays Cancer research Medium 24934812
2011 Gli2 directly binds multiple regulatory regions (promoter and enhancer) of the Ascl1 gene and activates its promoter in vitro; Gli2 upregulates Ascl1 to induce neurogenesis, and dominant-negative Gli2 significantly downregulates Ascl1 expression, causing delayed neurogenesis. ChIP assays, luciferase reporter assays with Ascl1 promoter, Gli2 overexpression and dominant-negative Gli2 in P19 cells PloS one Medium 21559470
2010 ASCL1 regulates expression of the CHRNA5/A3/B4 nicotinic acetylcholine receptor gene cluster in SCLC; knockdown of ASCL1 specifically decreases alpha3 and beta4 subunit expression without affecting other nAChR genes, indicating a specific regulatory relationship. ASCL1 shRNA knockdown in SCLC and non-SCLC cells, qRT-PCR, in silico promoter analysis identifying ASCL1 binding sites Molecular cancer research : MCR Medium 20124469
2019 ASCL1 regulates Wnt11 expression via H3K27 acetylation at the WNT11 gene enhancer region; ASCL1 knockdown downregulates Wnt11 in SCLC; Wnt11 in turn controls neuroendocrine differentiation, cell proliferation, and E-cadherin expression downstream of ASCL1, with AKT and p38 MAPK phosphorylation increased by Wnt11. ASCL1 transfection into A549 cells, ASCL1 knockdown in SCLC lines, ChIP for H3K27ac at WNT11 enhancer, WNT11 knockdown functional assays Laboratory investigation Medium 31231131
2011 Phorbol ester (PMA) suppresses hASH1 (ASCL1) synthesis via distinct sequential mechanisms: short-term inhibition through mRNA destabilization dependent mainly on protein kinase C activity; prolonged suppression (48h) through decreased ASCL1 promoter activity and inhibition of mRNA translation. Reporter gene assays (promoter-luciferase and UTR-luciferase), PKC inhibitor experiments, mRNA stability assays in neuroblastoma-derived Kelly cells Frontiers in molecular neuroscience Medium 21441980
2015 Maternal Ascl1 protein in Xenopus represses VegT-induced mesendoderm (but not Nodal-induced mesendoderm); a previously uncharacterized N-terminal domain of Ascl1 interacts with HDAC1 to inhibit mesendoderm gene expression via histone deacetylation at VegT target promoters; this N-terminal domain is dispensable for neurogenic function, indicating distinct mechanisms for different functions. Gain- and loss-of-function experiments in Xenopus, domain deletion mutants, HDAC interaction assay, HDAC inhibitor treatment, ChIP for histone acetylation at target gene promoters Development (Cambridge, England) High 26700681
2023 ROR2 receptor tyrosine kinase activates the ERK/CREB signaling pathway to modulate ASCL1 expression in prostate cancer; ROR2 upregulation following AR pathway inhibition feeds into lineage plasticity via ASCL1 activation. RTK screen, ROR2 knockdown/overexpression, ERK/CREB pathway inhibitor experiments, ASCL1 expression analysis in prostate cancer cells Cell reports Medium 37552603
2024 ASCL1 is required for neuroendocrine differentiation in prostate cancer in vivo; genetic loss of Ascl1 in RPM (Rb1-/-/Trp53-/-/Myc+) mouse prostate organoid allografts decreases NE identity and increases basal-like identity without affecting tumor incidence, growth, or metastasis. Genetically engineered mouse prostate organoids with Cre-induced Rb1/Trp53 loss and Myc overexpression, Ascl1 conditional genetic deletion, histopathology, immunofluorescence, scRNA-seq Cancer research High 39264686
2024 ASCL1+ cells arise from KRT8+ luminal cells during neuroendocrine prostate cancer (NEPC) transition; Ascl1 loss before transplantation abrogates lineage plasticity, resulting in castration-sensitive adenocarcinomas, while Ascl1 deletion in established NEPC causes only transient regression. Multiplexed immunofluorescence, spatial transcriptomics, Ascl1 conditional deletion at different stages, in vivo mouse prostate organoid transplantation model Nature cancer High 39394434
2024 SMAD4 competes with Myc to regulate ASCL1 transcription in NSCLC cells; SMAD4 deficiency accelerates SCLC transition by inducing neuroendocrine phenotype through increased ASCL1 transcription, independently of RB1 status in TP53-deficient cells. CRISPR-Cas9 SMAD4/RB1 knockout in HCC827 and A549-TP53-/- cells, Myc inhibitor treatment, in vitro and in vivo tumor models, mRNA and protein expression analysis Cell communication and signaling Medium 38233864
2024 ASCL1 confers drug tolerance to osimertinib in EGFR mutant lung cancer by initiating an epithelial-to-mesenchymal gene-expression program in permissive cellular contexts; this effect is context-specific and not observed in all tumor types. Patient-derived xenograft models, single-cell transcriptional profiling, osimertinib treatment to maximal regression, ASCL1 expression analysis in residual disease Cancer research Medium 38359163

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2020 SCLC Subtypes Defined by ASCL1, NEUROD1, POU2F3, and YAP1: A Comprehensive Immunohistochemical and Histopathologic Characterization. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer 431 33011388
2016 ASCL1 and NEUROD1 Reveal Heterogeneity in Pulmonary Neuroendocrine Tumors and Regulate Distinct Genetic Programs. Cell reports 419 27452466
2014 Generation of induced neuronal cells by the single reprogramming factor ASCL1. Stem cell reports 300 25254342
2014 ASCL1 is a lineage oncogene providing therapeutic targets for high-grade neuroendocrine lung cancers. Proceedings of the National Academy of Sciences of the United States of America 230 25267614
2015 Ascl1 Converts Dorsal Midbrain Astrocytes into Functional Neurons In Vivo. The Journal of neuroscience : the official journal of the Society for Neuroscience 203 26109658
2015 NOTCH, ASCL1, p53 and RB alterations define an alternative pathway driving neuroendocrine and small cell lung carcinomas. International journal of cancer 158 26340530
2006 Ascl1 and Gsh1/2 control inhibitory and excitatory cell fate in spinal sensory interneurons. Nature neuroscience 155 16715081
2004 Ascl1/Mash1 is required for the development of central serotonergic neurons. Nature neuroscience 154 15133515
2017 ASCL1 Reorganizes Chromatin to Direct Neuronal Fate and Suppress Tumorigenicity of Glioblastoma Stem Cells. Cell stem cell 144 28712938
2006 Ascl1 defines sequentially generated lineage-restricted neuronal and oligodendrocyte precursor cells in the spinal cord. Development (Cambridge, England) 140 17166924
2019 High Hes1 expression and resultant Ascl1 suppression regulate quiescent vs. active neural stem cells in the adult mouse brain. Genes & development 132 30862661
2013 FOXO3 shares common targets with ASCL1 genome-wide and inhibits ASCL1-dependent neurogenesis. Cell reports 128 23891001
2022 ASCL1 activates neuronal stem cell-like lineage programming through remodeling of the chromatin landscape in prostate cancer. Nature communications 122 35477723
2011 Ascl1 genetics reveals insights into cerebellum local circuit assembly. The Journal of neuroscience : the official journal of the Society for Neuroscience 119 21795554
2008 Ascl1 (Mash1) lineage cells contribute to discrete cell populations in CNS architecture. Molecular and cellular neurosciences 118 18585058
2013 Ascl1/Mash1 promotes brain oligodendrogenesis during myelination and remyelination. The Journal of neuroscience : the official journal of the Society for Neuroscience 117 23739972
2011 Ascl1 expression defines a subpopulation of lineage-restricted progenitors in the mammalian retina. Development (Cambridge, England) 106 21771810
2019 Proneural factors Ascl1 and Neurog2 contribute to neuronal subtype identities by establishing distinct chromatin landscapes. Nature neuroscience 100 31086315
2015 EZH2 promotes progression of small cell lung cancer by suppressing the TGF-β-Smad-ASCL1 pathway. Cell discovery 99 27462425
2005 Upregulation of ASCL1 and inhibition of Notch signaling pathway characterize progressive astrocytoma. Oncogene 99 16103883
2009 Ascl1 and Neurog2 form novel complexes and regulate Delta-like3 (Dll3) expression in the neural tube. Developmental biology 91 19389376
2008 Ascl1 is required for oligodendrocyte development in the spinal cord. Development (Cambridge, England) 82 18287202
2004 hASH1 expression is closely correlated with endocrine phenotype and differentiation extent in pulmonary neuroendocrine tumors. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 81 14657947
2019 ASCL1 is a MYCN- and LMO1-dependent member of the adrenergic neuroblastoma core regulatory circuitry. Nature communications 73 31819055
2014 Transcriptional control of vertebrate neurogenesis by the proneural factor Ascl1. Frontiers in cellular neuroscience 67 25520623
2021 ASCL1 represses a SOX9+ neural crest stem-like state in small cell lung cancer. Genes & development 65 34016693
2006 Expression of oligodendroglial and astrocytic lineage markers in diffuse gliomas: use of YKL-40, ApoE, ASCL1, and NKX2-2. Journal of neuropathology and experimental neurology 59 17146289
2024 The neuroendocrine transition in prostate cancer is dynamic and dependent on ASCL1. Nature cancer 54 39394434
2016 miR-124-9-9* potentiates Ascl1-induced reprogramming of cultured Müller glia. Glia 54 26732729
2021 ASCL1, NKX2-1, and PROX1 co-regulate subtype-specific genes in small-cell lung cancer. iScience 49 34466783
2019 Analysis of DLL3 and ASCL1 in Surgically Resected Small Cell Lung Cancer (HOT1702). The oncologist 49 31068386
2018 The proneural gene ASCL1 governs the transcriptional subgroup affiliation in glioblastoma stem cells by directly repressing the mesenchymal gene NDRG1. Cell death and differentiation 48 30538287
2004 The Notch signaling cascade in neuroblastoma: role of the basic helix-loop-helix proteins HASH-1 and HES-1. Cancer letters 46 15013216
2014 Ascl1 controls the number and distribution of astrocytes and oligodendrocytes in the gray matter and white matter of the spinal cord. Development (Cambridge, England) 44 25249462
2023 Pioneer factor ASCL1 cooperates with the mSWI/SNF complex at distal regulatory elements to regulate human neural differentiation. Genes & development 43 36931659
2017 Epigenetic Editing of Ascl1 Gene in Neural Stem Cells by Optogenetics. Scientific reports 43 28181538
2013 ASCL1 and RET expression defines a clinically relevant subgroup of lung adenocarcinoma characterized by neuroendocrine differentiation. Oncogene 43 24037524
2011 Ascl1/Mash1 is a novel target of Gli2 during Gli2-induced neurogenesis in P19 EC cells. PloS one 43 21559470
2021 Molecular Mechanisms Underlying Ascl1-Mediated Astrocyte-to-Neuron Conversion. Stem cell reports 41 33577795
2013 Genome-wide expression analysis of Ptf1a- and Ascl1-deficient mice reveals new markers for distinct dorsal horn interneuron populations contributing to nociceptive reflex plasticity. The Journal of neuroscience : the official journal of the Society for Neuroscience 40 23616538
2012 Ascl1 (Mash1) knockout perturbs differentiation of nonneuronal cells in olfactory epithelium. PloS one 40 23284756
2002 Quantitative reverse transcription-polymerase chain reaction measurement of HASH1 (ASCL1), a marker for small cell lung carcinomas with neuroendocrine features. Clinical cancer research : an official journal of the American Association for Cancer Research 40 11948117
2016 Ascl1 Is Required for the Development of Specific Neuronal Subtypes in the Enteric Nervous System. The Journal of neuroscience : the official journal of the Society for Neuroscience 38 27076429
2022 Promoters of ASCL1- and NEUROD1-dependent genes are specific targets of lurbinectedin in SCLC cells. EMBO molecular medicine 37 35263037
2020 ASCL1 regulates neurodevelopmental transcription factors and cell cycle genes in brain tumors of glioma mouse models. Glia 37 32573857
2020 Developmental changes in the accessible chromatin, transcriptome and Ascl1-binding correlate with the loss in Müller Glial regenerative potential. Scientific reports 36 32788677
2019 Ascl1-induced Wnt11 regulates neuroendocrine differentiation, cell proliferation, and E-cadherin expression in small-cell lung cancer and Wnt11 regulates small-cell lung cancer biology. Laboratory investigation; a journal of technical methods and pathology 35 31231131
2015 Ascl1 phospho-status regulates neuronal differentiation in a Xenopus developmental model of neuroblastoma. Disease models & mechanisms 35 25786414
2014 EWS-WT1 oncoprotein activates neuronal reprogramming factor ASCL1 and promotes neural differentiation. Cancer research 35 24934812
2022 Cross-lineage potential of Ascl1 uncovered by comparing diverse reprogramming regulatomes. Cell stem cell 34 36206732
2020 ASCL1- and DLX2-induced GABAergic neurons from hiPSC-derived NPCs. Journal of neuroscience methods 34 32065989
2019 Ascl1 Regulates Electric Field-Induced Neuronal Differentiation Through PI3K/Akt Pathway. Neuroscience 34 30771509
2011 Phorbol-Ester Mediated Suppression of hASH1 Synthesis: Multiple Ways to Keep the Level Down. Frontiers in molecular neuroscience 33 21441980
2024 Neuroendocrine Differentiation in Prostate Cancer Requires ASCL1. Cancer research 32 39264686
2022 Elevated ASCL1 activity creates de novo regulatory elements associated with neuronal differentiation. BMC genomics 32 35366798
2021 Performance of DNA methylation analysis of ASCL1, LHX8, ST6GALNAC5, GHSR, ZIC1 and SST for the triage of HPV-positive women: Results from a Dutch primary HPV-based screening cohort. International journal of cancer 32 34558659
2018 Subcellular localisation modulates ubiquitylation and degradation of Ascl1. Scientific reports 29 29545540
2012 Insights into the achaete-scute homolog-1 gene (hASH1) in normal and neoplastic human lung. Lung cancer (Amsterdam, Netherlands) 29 21684625
2023 Ascl1 and Ngn2 convert mouse embryonic stem cells to neurons via functionally distinct paths. Nature communications 28 37660160
2022 ASCL1 phosphorylation and ID2 upregulation are roadblocks to glioblastoma stem cell differentiation. Scientific reports 28 35149717
2021 Heterogeneity of neurons reprogrammed from spinal cord astrocytes by the proneural factors Ascl1 and Neurogenin2. Cell reports 28 34289357
2021 MAPK pathway activation selectively inhibits ASCL1-driven small cell lung cancer. iScience 28 34712921
2010 ASCL1 regulates the expression of the CHRNA5/A3/B4 lung cancer susceptibility locus. Molecular cancer research : MCR 28 20124469
2024 Transcription factors ASCL1 and OLIG2 drive glioblastoma initiation and co-regulate tumor cell types and migration. Nature communications 27 39609428
2023 ASCL1-mediated ferroptosis resistance enhances the progress of castration-resistant prostate cancer to neurosecretory prostate cancer. Free radical biology & medicine 27 37355053
2020 Significance of achaete-scute complex homologue 1 (ASCL1) in pulmonary neuroendocrine carcinomas; RNA sequence analyses using small cell lung cancer cells and Ascl1-induced pulmonary neuroendocrine carcinoma cells. Histochemistry and cell biology 27 32170367
2018 An Integrative Analysis of Transcriptome and Epigenome Features of ASCL1-Positive Lung Adenocarcinomas. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer 27 30121393
2023 ASCL1 induces neurogenesis in human Müller glia. Stem cell reports 26 38039971
2022 Therapeutic targeting of BAP1/ASXL3 sub-complex in ASCL1-dependent small cell lung cancer. Oncogene 26 35194152
2024 ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts. Cancer research 25 38359163
2016 Oligodendrocyte development in the embryonic tuberal hypothalamus and the influence of Ascl1. Neural development 25 27863528
2021 Initiation of Otx2 expression in the developing mouse retina requires a unique enhancer and either Ascl1 or Neurog2 activity. Development (Cambridge, England) 24 34143204
2019 Inhibition of Glioma Development by ASCL1-Mediated Direct Neuronal Reprogramming. Cells 24 31212628
2020 Physical interactions between Gsx2 and Ascl1 balance progenitor expansion versus neurogenesis in the mouse lateral ganglionic eminence. Development (Cambridge, England) 23 32122989
2015 hASH1 is a specific immunohistochemical marker for lung neuroendocrine tumors. Human pathology 23 26596584
2000 Morphometric analysis of CC10-hASH1 transgenic mouse lung: a model for bronchiolization of alveoli and neuroendocrine carcinoma. Experimental lung research 23 11195458
2021 Injury-induced ASCL1 expression orchestrates a transitory cell state required for repair of the neonatal cerebellum. Science advances 22 34878841
2020 ASCL1-regulated DARPP-32 and t-DARPP stimulate small cell lung cancer growth and neuroendocrine tumour cell proliferation. British journal of cancer 22 32499571
2005 Genetic association analyses of PHOX2B and ASCL1 in neuropsychiatric disorders: evidence for association of ASCL1 with Parkinson's disease. Human genetics 22 16021468
2023 Comparison of ASCL1, NEUROD1, and POU2F3 expression in surgically resected specimens, paired tissue microarrays, and lymph node metastases in small cell lung carcinoma. Histopathology 21 36715573
2022 Helicobacter pylori infection activates Wnt/β-catenin pathway to promote the occurrence of gastritis by upregulating ASCL1 and AQP5. Cell death discovery 21 35538066
2022 Ascl1 phospho-site mutations enhance neuronal conversion of adult cortical astrocytes in vivo. Frontiers in neuroscience 21 36061596
2022 The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma. Frontiers in cell and developmental biology 21 36263020
2019 hASH1 nuclear localization persists in neuroendocrine transdifferentiated prostate cancer cells, even upon reintroduction of androgen. Scientific reports 21 31836808
2018 Instructing neuronal identity during CNS development and astroglial-lineage reprogramming: Roles of NEUROG2 and ASCL1. Brain research 21 29510143
2013 Heterochronic misexpression of Ascl1 in the Atoh7 retinal cell lineage blocks cell cycle exit. Molecular and cellular neurosciences 21 23481413
2004 Human achaete-scute homologue (hASH1) mRNA level as a diagnostic marker to distinguish esthesioneuroblastoma from poorly differentiated tumors arising in the sinonasal tract. American journal of clinical pathology 21 15272537
2022 Histone H3.3 K27M chromatin functions implicate a network of neurodevelopmental factors including ASCL1 and NEUROD1 in DIPG. Epigenetics & chromatin 20 35590427
2022 ASCL1 regulates super-enhancer-associated miRNAs to define molecular subtypes of small cell lung cancer. Cancer science 20 35789143
2018 ASCL1 regulates proliferation of NG2-glia in the embryonic and adult spinal cord. Glia 19 29683222
2010 Hes1/Hes5 gene inhibits differentiation via down-regulating Hash1 and promotes proliferation in cervical carcinoma cells. International journal of gynecological cancer : official journal of the International Gynecological Cancer Society 19 21495212
2001 Downregulation of hASH1 is associated with the retinoic acid-induced differentiation of human neuroblastoma cell lines. Medical and pediatric oncology 19 11464865
2024 Transformation to small cell lung cancer is irrespective of EGFR and accelerated by SMAD4-mediated ASCL1 transcription independently of RB1 in non-small cell lung cancer. Cell communication and signaling : CCS 18 38233864
2023 ASCL1 is activated downstream of the ROR2/CREB signaling pathway to support lineage plasticity in prostate cancer. Cell reports 18 37552603
2022 Function of Proneural Genes Ascl1 and Asense in Neurogenesis: How Similar Are They? Frontiers in cell and developmental biology 18 35252201
2022 Molecular features and evolutionary trajectory of ASCL1+ and NEUROD1+ SCLC cells. British journal of cancer 18 36517551
2021 ASCL1 and DLL3 expressions and their clinicopathological implications in surgically resected pure small cell lung cancer: A study of 247 cases from the National Cancer Center of China. Thoracic cancer 18 34931456
2019 Expression of ventral telencephalon transcription factors ASCL1 and DLX2 in the early fetal human cerebral cortex. Journal of anatomy 18 30861584
2017 The Potential of Targeting Brain Pathology with Ascl1/Mash1. Cells 18 28832532
2015 A novel role for Ascl1 in the regulation of mesendoderm formation via HDAC-dependent antagonism of VegT. Development (Cambridge, England) 18 26700681

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