ArticleMolecular and cellular biology2005
Disruption of Sept6, a fusion partner gene of MLL, does not affect ontogeny, leukemogenesis induced by MLL-SEPT6, or phenotype induced by the loss of Sept4.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 61 citations in OpenAlex.
- Septin complexes: Ahead of the curve.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Maternal PRDM10 activates essential genes for oocyte-to-embryo transition.Nature communications · 2025Article
- SEPT9_i1 and Septin Dynamics in Oncogenesis and Cancer Treatment.Biomolecules · 2024Review
- Rare variants found in multiplex families with orofacial clefts: Does expanding the phenotype make a difference?American journal of medical genetics. Part A · 2023Article
- Clinical profile inFrontiers in medicine · 2022Article
- Congenital X-linked neutropenia with myelodysplasia and somatic tetraploidy due to a germline mutation in SEPT6.American journal of hematology · 2022Article
- UBC Mediated by SEPT6 Inhibited the Progression of Prostate Cancer.Mediators of inflammation · 2021Article
- Article
- A case of double-refractory multiple myeloma with both the IgH-MMSET fusion protein and the congenital abnormality t(11;22).International journal of hematology · 2019Article
- Septins in kidney: A territory little explored.Cytoskeleton (Hoboken, N.J.) · 2019Review
- Eya2, a Target Activated by Plzf, Is Critical forMolecular and cellular biology · 2017Article
- Functional Redundancy of Septin Homologs in Dendritic Branching.Frontiers in cell and developmental biology · 2017Article
- A CDC42EP4/septin-based perisynaptic glial scaffold facilitates glutamate clearance.Nature communications · 2015Article
- Septin dynamics are essential for exocytosis.The Journal of biological chemistry · 2015Article
- Sept6 is required for ciliogenesis in Kupffer's vesicle, the pronephros, and the neural tube during early embryonic development.Molecular and cellular biology · 2014Article
- Septin functions in organ system physiology and pathology.Biological chemistry · 2014Review
- Septins promote dendrite and axon development by negatively regulating microtubule stability via HDAC6-mediated deacetylation.Nature communications · 2013Article
- Septin 8 is an interaction partner and in vitro substrate of MK5.World journal of biological chemistry · 2012Article
- Article
- The role of the Parkinson's disease gene PARK9 in essential cellular pathways and the manganese homeostasis network in yeast.PloS one · 2012Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Septins are evolutionarily conserved GTP-binding proteins that can heteropolymerize into filaments. Recent studies have revealed that septins are involved in not only diverse normal cellular processes but also the pathogenesis of various diseases, including cancer. SEPT6 is ubiquitously expressed in tissues and one of the fusion partner genes of MLL in the 11q23 translocations implicated in acute leukemia. However, the roles of this septin in vivo remain elusive. We have developed Sept6-deficient mice that exhibited neither gross abnormalities, changes in cytokinesis, nor spontaneous malignancy. Sept6 deficiency did not cause any quantitative changes in any of the septins evaluated in this study, nor did it cause any additional changes in the Sept4-deficient mice. Even the depletion of Sept11, a close homolog of Sept6, did not affect the Sept6-null cells in vitro, thus implying a high degree of redundancy in the septin system. Furthermore, a loss of Sept6 did not alter the phenotype of myeloproliferative disease induced by MLL-SEPT6, thus suggesting that Sept6 does not function as a tumor suppressor. To our knowledge, this is the first report demonstrating that a disruption of the translocation partner gene of MLL in 11q23 translocation does not contribute to leukemogenesis by the MLL fusion gene.
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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.