ArticleCancer cell2010
GSK-3 promotes conditional association of CREB and its coactivators with MEIS1 to facilitate HOX-mediated transcription and oncogenesis.
Article in Cancer cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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
83 citing papers in PubMed, 126 citations in OpenAlex.
- Menin Inhibition in Acute Myeloid Leukemia: Rewiring Leukemic Transcriptional Networks.International journal of molecular sciences · 2026Review
- Nonionotropic action of an acid-sensing ion channel inhibits leukemogenesis in the acidic bone marrow niche.The Journal of clinical investigation · 2025Article
- NUP214 in Acute Myeloid Leukemia.Cells · 2025Review
- Perturbing LSD1 and WNT rewires transcription to synergistically induce AML differentiation.Nature · 2025Article
- Elongation of very long chain fatty acids-3 (American journal of physiology. Gastrointestinal and liver physiology · 2023Article
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- Npm1 haploinsufficiency in collaboration with MEIS1 is sufficient to induce AML in mice.Blood advances · 2023Article
- Mammalian eIF4E2-GSK3β maintains basal phosphorylation of p53 to resist senescence under hypoxia.Cell death & disease · 2022Article
- Re-Expression of ERα and AR in Receptor Negative Endocrine CancersFrontiers in oncology · 2022Article
- Nuclear GSK-3β and Oncogenic KRas Lead to the Retention of Pancreatic Ductal Progenitor Cells Phenotypically Similar to Those Seen in IPMN.Frontiers in cell and developmental biology · 2022Article
- Proteasome Inhibitors Interrupt the Activation of Non-Canonical NF-κB Signaling Pathway and Induce Cell Apoptosis in Cytarabine-Resistant HL60 Cells.International journal of molecular sciences · 2021Article
- A Gene Expression Signature to Predict Nucleotide Excision Repair Defects and Novel Therapeutic Approaches.International journal of molecular sciences · 2021Article
- Lithium and Therapeutic Targeting of GSK-3.Cells · 2021Review
- Drug Repurposing for Targeting Acute Leukemia WithFrontiers in pharmacology · 2021Review
- Derivation of stable embryonic stem cell-like, but transcriptionally heterogenous, induced pluripotent stem cells from non-permissive mouse strains.Mammalian genome : official journal of the International Mammalian Genome Society · 2020Article
- Therapeutic Target Discovery Using High-Throughput Genetic Screens in Acute Myeloid Leukemia.Cells · 2020Review
- Review
- MBNL1 regulates essential alternative RNA splicing patterns in MLL-rearranged leukemia.Nature communications · 2020Article
- Crosstalk between MEIS1 and markers of different cell signaling pathways in esophageal squamous cell carcinoma.Molecular biology reports · 2020Article
- The role of exosomes and MYC in therapy resistance of acute myeloid leukemia: Challenges and opportunities.Molecular aspects of medicine · 2019Review
23 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Acute leukemias induced by MLL chimeric oncoproteins are among the subset of cancers distinguished by a paradoxical dependence on GSK-3 kinase activity for sustained proliferation. We demonstrate here that GSK-3 maintains the MLL leukemia stem cell transcriptional program by promoting the conditional association of CREB and its coactivators TORC and CBP with homedomain protein MEIS1, a critical component of the MLL-subordinate program, which in turn facilitates HOX-mediated transcription and transformation. This mechanism also applies to hematopoietic cells transformed by other HOX genes, including CDX2, which is highly expressed in a majority of acute myeloid leukemias, thus providing a molecular approach based on GSK-3 inhibitory strategies to target HOX-associated transcription in a broad spectrum of leukemias.
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Registered trials
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.