ArticleDevelopmental cell2017
The Super Elongation Complex Drives Neural Stem Cell Fate Commitment.
Article in Developmental cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Stabilization of AFF1 by PARylation ensures transcriptional restart after DNA damage.Nature chemical biology · 2026Article
- Spen and Nito prevent dedifferentiation of intermediate progenitors by maintaining Notch target expression in stem cells at low levels.Cell reports · 2026Article
- MeCP2 interacts with the super elongation complex to regulate transcription.Science advances · 2025Article
- Dual mitotic bookmarking by GAF and H3K27ac orchestrates differential propagation of cell fate memory in neural development.Nature communications · 2025Article
- From the Making of a Neural Lineage to the Making of a Tumor: Lessons from the "Simple" Drosophila Brain.Advances in experimental medicine and biology · 2025Review
- Notch induces transcription by stimulating release of paused RNA polymerase II.Genes & development · 2024Article
- Bridging cultures: Chinese elements in scientific illustrations.Chinese medicine · 2024Article
- Notch induces transcription by stimulating release of paused RNA Polymerase II.bioRxiv : the preprint server for biology · 2024Article
- The Biological Significance of AFF4: Promoting Transcription Elongation, Osteogenic Differentiation and Tumor Progression.Combinatorial chemistry & high throughput screening · 2024Review
- The mitochondrial ribosomal protein mRpL4 regulates Notch signaling.EMBO reports · 2023Article
- BM-MSCs overexpressing the Numb enhance the therapeutic effect on cholestatic liver fibrosis by inhibiting the ductular reaction.Stem cell research & therapy · 2023Article
- Modelling Cancer Metastasis inCells · 2023Review
- AFF4 regulates cellular adipogenic differentiation via targeting autophagy.PLoS genetics · 2022Article
- Transcription Pause and Escape in Neurodevelopmental Disorders.Frontiers in neuroscience · 2022Review
- Enhancer analysis of the Drosophila zinc finger transcription factor Earmuff by gene targeting.Hereditas · 2021Article
- Tumor models in various Drosophila tissues.WIREs mechanisms of disease · 2021Review
- Fzr/Cdh1 Promotes the Differentiation of Neural Stem Cell Lineages inFrontiers in cell and developmental biology · 2020Article
- CDK9: a signaling hub for transcriptional control.Transcription · 2019Review
- Faster, higher, stronger: timely and robust cell fate/identity commitment in stem cell lineages.Open biology · 2019Review
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8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Asymmetric stem cell division establishes an initial difference between a stem cell and its differentiating sibling, critical for maintaining homeostasis and preventing carcinogenesis. Yet the mechanisms that consolidate and lock in such initial fate bias remain obscure. Here, we use Drosophila neuroblasts to demonstrate that the super elongation complex (SEC) acts as an intrinsic amplifier to drive cell fate commitment. SEC is highly expressed in neuroblasts, where it promotes self-renewal by physically associating with Notch transcription activation complex and enhancing HES (hairy and E(spl)) transcription. HES in turn upregulates SEC activity, forming an unexpected self-reinforcing feedback loop with SEC. SEC inactivation leads to neuroblast loss, whereas its forced activation results in neural progenitor dedifferentiation and tumorigenesis. Our studies unveil an SEC-mediated intracellular amplifier mechanism in ensuring robustness and precision in stem cell fate commitment and provide mechanistic explanation for the highly frequent association of SEC overactivation with human cancers.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.