ArticleOncogene2005
The MYO1F, unconventional myosin type 1F, gene is fused to MLL in infant acute monocytic leukemia with a complex translocation involving chromosomes 7, 11, 19 and 22.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Identification of a novelHaematologica · 2026Article
- Myosin Class I Genes Follow a Cell Type-Specific Transcription Pattern in Human Haematopoietic Cell Lines.International journal of molecular sciences · 2026Article
- MYO1F in neutrophils is required for the response to immune checkpoint blockade therapy.The Journal of experimental medicine · 2025Article
- Lysosome-related genes predict acute myeloid leukemia prognosis and response to immunotherapy.Frontiers in immunology · 2024Article
- Class I Myosins, molecular motors involved in cell migration and cancer.Cell adhesion & migration · 2022Article
- The role of motor proteins in photoreceptor protein transport and visual function.Ophthalmic genetics · 2022Article
- MYO1F regulates antifungal immunity by regulating acetylation of microtubules.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Long-Tailed Unconventional Class I Myosins in Health and Disease.International journal of molecular sciences · 2020Review
- Myo1f, an Unconventional Long-Tailed Myosin, Is a New Partner for the Adaptor 3BP2 Involved in Mast Cell Migration.Frontiers in immunology · 2019Article
- Cyclooxygenase and lipoxygenase gene expression in the inflammogenesis of breast cancer.Inflammopharmacology · 2018Article
- Bioinformatic prediction and functional characterization of human KIAA0100 gene.Journal of pharmaceutical analysis · 2017Article
- Myosin-I molecular motors at a glance.Journal of cell science · 2016Review
- Analysis of an independent tumor suppressor locus telomeric to Tp53 suggested Inpp5k and Myo1c as novel tumor suppressor gene candidates in this region.BMC genetics · 2015Article
- Rare MLL-ELL fusion transcripts in childhood acute myeloid leukemia-association with young age and myeloid sarcomas?Experimental hematology & oncology · 2015Article
- The role of phosphoinositide-regulated actin reorganization in chemotaxis and cell migration.British journal of pharmacology · 2014Review
- Non-muscle myosins in tumor progression, cancer cell invasion, and metastasis.Cytoskeleton (Hoboken, N.J.) · 2014Review
- Cell-based analysis of structure-function activity of threonine aspartase 1.The Journal of biological chemistry · 2011Article
- GermlineCancer genomics & proteomicsArticle
- RareCancer genomics & proteomicsReview
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We analysed a complex translocation involving chromosomes 7, 11, 19 and 22 in infant acute monocytic leukemia, and identified that the MLL gene on 11q23 was fused to the unconventional myosin type 1F, MYO1F, gene on 19p13.2-13.3. MYO1F consists of at least 28 exons and was predicted to encode a 1098-amino-acid with an N-terminal head domain containing both ATP-binding and actin-binding sequences, a neck domain with a single IQ motif, and a tail with TH1, TH2 and SH3 domains. Northern blot analysis of RNAs prepared from multiple tissues showed that the expression of approximately 4-kb transcripts appeared constant in most tissues examined. However, MYO1F was expressed in only three of 22 leukemic cell lines. The MLL-MYO1F fusion protein contains almost the entire MYO1F, however, C-terminal MYO1F has neither the transactivation domain nor the dimerization domain found in various MLL fusion partners. Further analysis of this novel type of MLL fusion protein would provide new insights into leukemogenesis. MYO1F is the fourth partner gene of MLL on 19p13. At the cytogenetic level, it may be difficult to distinguish MLL-ENL, MLL-ELL, MLL-EEN and MLL-MYO1F fusions created by t(11;19)(q23;p13), and it is likely that cases of t(11;19) lacking a known fusion gene may result in this gene fusion.
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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.