ArticleEMBO reports2014
Molecular basis of crosstalk between oncogenic Ras and the master regulator of hematopoiesis GATA-2.
Article in EMBO reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 38 citations in OpenAlex.
- Interleukin-1β as target to induce synthetic lethality in KRAS mutant biliary tract cancer.Clinical and molecular hepatology · 2026Article
- Dual mechanism of inflammation sensing by the hematopoietic progenitor genome.Science advances · 2025Article
- Restricting genomic actions of innate immune mediators on fetal hematopoietic progenitor cells.iScience · 2023Article
- Pathogenic human variant that dislocates GATA2 zinc fingers disrupts hematopoietic gene expression and signaling networks.The Journal of clinical investigation · 2023Article
- A CGA/EGFR/GATA2 positive feedback circuit confers chemoresistance in gastric cancer.The Journal of clinical investigation · 2022Article
- Article
- MNK Inhibition SensitizesCancer discovery · 2021Article
- Constructing and deconstructing GATA2-regulated cell fate programs to establish developmental trajectories.The Journal of experimental medicine · 2020Article
- Human GATA2 mutations and hematologic disease: how many paths to pathogenesis?Blood advances · 2020Review
- GATA2 +9.5 enhancer: from principles of hematopoiesis to genetic diagnosis in precision medicine.Current opinion in hematology · 2020Review
- Article
- Blood disease-causing and -suppressing transcriptional enhancers: general principles andBlood advances · 2019Review
- Single-nucleotide human disease mutation inactivates a blood-regenerative GATA2 enhancer.The Journal of clinical investigation · 2019Article
- Transcription factor mutations as a cause of familial myeloid neoplasms.The Journal of clinical investigation · 2019Review
- Human leukemia mutations corrupt but do not abrogate GATA-2 function.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Mechanisms of erythrocyte development and regeneration: implications for regenerative medicine and beyond.Development (Cambridge, England) · 2018Review
- PIASy antagonizes Ras-driven NSCLC survival by promoting GATA2 SUMOylation.Journal of Cancer · 2018Article
- Differential effects on gene transcription and hematopoietic differentiation correlate with GATA2 mutant disease phenotypes.Leukemia · 2018Article
- Integrating Enhancer Mechanisms to Establish a Hierarchical Blood Development Program.Cell reports · 2017Article
- GATA2 regulates the erythropoietin receptor in t(12;21) ALL.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Disease mutations provide unique opportunities to decipher protein and cell function. Mutations in the master regulator of hematopoiesis GATA-2 underlie an immunodeficiency associated with myelodysplastic syndrome and leukemia. We discovered that a GATA-2 disease mutant (T354M) defective in chromatin binding was hyperphosphorylated by p38 mitogen-activated protein kinase. p38 also induced multisite phosphorylation of wild-type GATA-2, which required a single phosphorylated residue (S192). Phosphorylation of GATA-2, but not T354M, stimulated target gene expression. While crosstalk between oncogenic Ras and GATA-2 has been implicated as an important axis in cancer biology, its mechanistic underpinnings are unclear. Oncogenic Ras enhanced S192-dependent GATA-2 phosphorylation, nuclear foci localization, and transcriptional activation. These studies define a mechanism that controls a key regulator of hematopoiesis and a dual mode of impairing GATA-2-dependent genetic networks: mutational disruption of chromatin occupancy yielding insufficient GATA-2, and oncogenic Ras-mediated amplification of GATA-2 activity.
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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.