ArticleMolecular and cellular biology2015
SRSF2 Is Essential for Hematopoiesis, and Its Myelodysplastic Syndrome-Related Mutations Dysregulate Alternative Pre-mRNA Splicing.
Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 96 citations in OpenAlex.
- TargetingGenes & development · 2026Article
- Vulnerability of SRSF2-mutated chronic myelomonocytic leukemia to perturbation of the cGAS-STING pathway.Blood advances · 2026Article
- Splicing regulatory dynamics for precision analysis and treatment of heterogeneous leukemias.Science translational medicine · 2025Article
- Looping forward: exploring R-loop processing and therapeutic potential.FEBS letters · 2025Review
- Essential role of Dhx16-mediated ribosome assembly in maintenance of hematopoietic stem cells.Leukemia · 2024Article
- Alternative Splicing: A Potential Therapeutic Target in Hematological Malignancies.Hematology reports · 2024Review
- Function of serine/arginine-rich splicing factors in hematopoiesis and hematopoietic malignancies.Cancer cell international · 2024Review
- SRSF2 plays an unexpected role as reader of mMolecular cell · 2023Article
- Towards understandings of serine/arginine-rich splicing factors.Acta pharmaceutica Sinica. B · 2023Review
- Association of Myelofibrosis Phenotypes with Clinical Manifestations, Molecular Profiles, and Treatments.Cancers · 2023Review
- Cpeb1b-mediated cytoplasmic polyadenylation ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- RUNX1 deficiency cooperates with SRSF2 mutation to induce multilineage hematopoietic defects characteristic of MDS.Blood advances · 2022Article
- Article
- The Role of RNA-Binding Proteins in Hematological Malignancies.International journal of molecular sciences · 2022Review
- Emerging roles of spliceosome in cancer and immunity.Protein & cell · 2022Review
- Genome-wide screening identifies cell-cycle control as a synthetic lethal pathway with SRSF2P95H mutation.Blood advances · 2022Article
- Altered pathways and targeted therapy in double hit lymphoma.Journal of hematology & oncology · 2022Review
- ZRSR1 co-operates with ZRSR2 in regulating splicing of U12-type introns in murine hematopoietic cells.Haematologica · 2022Article
- Single-cell architecture and functional requirement of alternative splicing during hematopoietic stem cell formation.Science advances · 2022Article
- Review
8 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Myelodysplastic syndromes (MDS) are a group of neoplasms characterized by ineffective myeloid hematopoiesis and various risks for leukemia. SRSF2, a member of the serine/arginine-rich (SR) family of splicing factors, is one of the mutation targets associated with poor survival in patients suffering from myelodysplastic syndromes. Here we report the biological function of SRSF2 in hematopoiesis by using conditional knockout mouse models. Ablation of SRSF2 in the hematopoietic lineage caused embryonic lethality, and Srsf2-deficient fetal liver cells showed significantly enhanced apoptosis and decreased levels of hematopoietic stem/progenitor cells. Induced ablation of SRSF2 in adult Mx1-Cre Srsf2(flox/flox) mice upon poly(I):poly(C) injection demonstrated a significant decrease in lineage(-) Sca(+) c-Kit(+) cells in bone marrow. To reveal the functional impact of myelodysplastic syndromes-associated mutations in SRSF2, we analyzed splicing responses on the MSD-L cell line and found that the missense mutation of proline 95 to histidine (P95H) and a P95-to-R102 in-frame 8-amino-acid deletion caused significant changes in alternative splicing. The affected genes were enriched in cancer development and apoptosis. These findings suggest that intact SRSF2 is essential for the functional integrity of the hematopoietic system and that its mutations likely contribute to development of myelodysplastic syndromes.
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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.