ArticleMolecular and cellular biology2019
Growth Factor Independence 1B-Mediated Transcriptional Repression and Lineage Allocation Require Lysine-Specific Demethylase 1-Dependent Recruitment of the BHC Complex.
Article in Molecular and cellular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- LSD1 Performs Demethylase-Independent and Context-Specific Roles in Ewing Sarcoma.Cancer research communications · 2026Article
- Scaling perturbations: beyond genome-scale CRISPR screens.bioRxiv : the preprint server for biology · 2026Article
- LSD1 Performs Demethylase-Independent and Context-Specific Roles in Ewing Sarcoma.bioRxiv : the preprint server for biology · 2025Article
- Single-cell transcriptome analysis profiles the enlarged subsets of myeloid-biased HSPCs with preleukemic characters in disuse osteoporosis mice.Cell & bioscience · 2025Article
- Gfi1 controls the formation of effector-like CD8Nature communications · 2025Article
- Community Diversity of Fungi Carried by Four Common Woodpeckers in Heilongjiang Province, China.Journal of fungi (Basel, Switzerland) · 2024Article
- GFI1B and LSD1 repress myeloid traits during megakaryocyte differentiation.Communications biology · 2024Article
- GSE1 links the HDAC1/CoREST co-repressor complex to DNA damage.Nucleic acids research · 2023Article
- The H2A.Z and NuRD associated protein HMG20A controls early head and heart developmental transcription programs.Nature communications · 2023Article
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- GFI1 Cooperates with IKZF1/IKAROS to Activate Gene Expression in T-cell Acute Lymphoblastic Leukemia.Molecular cancer research : MCR · 2022Article
- Lysine specific demethylase 1 is a molecular driver and therapeutic target in sarcoma.Frontiers in oncology · 2022Review
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- Proximity-dependent labeling methods for proteomic profiling in living cells: An update.Wiley interdisciplinary reviews. Developmental biology · 2021Review
- Proximity labeling in mammalian cells with TurboID and split-TurboID.Nature protocols · 2020Article
- A human cell atlas of fetal chromatin accessibility.Science (New York, N.Y.) · 2020Article
- Review
- Oct4-Mediated Inhibition of Lsd1 Activity Promotes the Active and Primed State of Pluripotency Enhancers.Cell reports · 2020Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Growth factor independence 1B (GFI1B) coordinates assembly of transcriptional repressor complexes comprised of corepressors and histone-modifying enzymes to control gene expression programs governing lineage allocation in hematopoiesis. Enforced expression of GFI1B in K562 erythroleukemia cells favors erythroid over megakaryocytic differentiation, providing a platform to define molecular determinants of binary fate decisions triggered by GFI1B. We deployed proteome-wide proximity labeling to identify factors whose inclusion in GFI1B complexes depends upon GFI1B's obligate effector, lysine-specific demethylase 1 (LSD1). We show that GFI1B preferentially recruits core and putative elements of the BRAF-histone deacetylase (HDAC) (BHC) chromatin-remodeling complex (LSD1, RCOR1, HMG20A, HMG20B, HDAC1, HDAC2, PHF21A, GSE1, ZMYM2, and ZNF217) in an LSD1-dependent manner to control acquisition of erythroid traits by K562 cells. Among these elements, depletion of both HMG20A and HMG20B or of GSE1 blocks GFI1B-mediated erythroid differentiation, phenocopying impaired differentiation brought on by LSD1 depletion or disruption of GFI1B-LSD1 binding. These findings demonstrate the central role of the GFI1B-LSD1 interaction as a determinant of BHC complex recruitment to enable cell fate decisions driven by GFI1B.
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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.