ArticleProceedings of the National Academy of Sciences of the United States of America2005
Deregulation of common genes by c-Myc and its direct target, MT-MC1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 26 citations in OpenAlex.
- MARCH1, transcriptionally regulated by POU2F2, facilitates acute myeloid leukemia progression via inducing MYCT1 degradation.Oncogene · 2025Article
- Article
- Differential transcriptomic changes in the central nervous system and urinary bladders of mice infected with a coronavirus.PloS one · 2022Article
- Myc and ChREBP transcription factors cooperatively regulate normal and neoplastic hepatocyte proliferation in mice.The Journal of biological chemistry · 2018Article
- YY1 directly suppresses MYCT1 leading to laryngeal tumorigenesis and progress.Cancer medicine · 2017Article
- Transmembrane domain is crucial to the subcellular localization and function of Myc target 1.Journal of cellular and molecular medicine · 2016Article
- The Quest for Targets Executing MYC-Dependent Cell Transformation.Frontiers in oncology · 2016Review
- Tamoxifen induces a pluripotency signature in breast cancer cells and human tumors.Molecular oncology · 2015Article
- Proteotranscriptomic Profiling of 231-BR Breast Cancer Cells: Identification of Potential Biomarkers and Therapeutic Targets for Brain Metastasis.Molecular & cellular proteomics : MCP · 2015Article
- Th-MYCN mice with caspase-8 deficiency develop advanced neuroblastoma with bone marrow metastasis.Cancer research · 2013Article
- Promoter hypermethylation-induced transcriptional down-regulation of the gene MYCT1 in laryngeal squamous cell carcinoma.BMC cancer · 2012Article
- Gene signatures in wound tissue as evidenced by molecular profiling in the chick embryo model.BMC genomics · 2010Article
- Widespread genomic instability mediated by a pathway involving glycoprotein Ib alpha and Aurora B kinase.The Journal of biological chemistry · 2010Article
- Gene profiling of the erythro- and megakaryoblastic leukaemias induced by the Graffi murine retrovirus.BMC medical genomics · 2010Article
- Modularity of the oncoprotein-like properties of platelet glycoprotein Ibalpha.The Journal of biological chemistry · 2009Article
- Transformation, genomic instability and senescence mediated by platelet/megakaryocyte glycoprotein Ibalpha.Oncogene · 2008Article
- c-Myc-mediated genomic instability proceeds via a megakaryocytic endomitosis pathway involving Gp1balpha.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- A distance difference matrix approach to identifying transcription factors that regulate differential gene expression.Genome biology · 2007Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
In addition to its role in cancer, the c-Myc oncoprotein controls many normal cellular processes as a consequence of its function as a basic helix-loop-helix leucine zipper transcription factor. Determining which of the myriad genes under c-Myc control are relevant for these various roles is thus a major challenge. mt-mc1 is a direct c-Myc target gene whose overexpression recapitulates multiple c-Myc phenotypes, including transformation. Using transcriptional profiling, we now show that MT-MC1-overexpressing myeloid cells misregulate a total of 47 distinct transcripts, a large proportion of which are involved in signal transduction and/or cancer. Analysis of these genes reveals a consensus promoter structure consisting of multiple, often closely spaced c-Myc binding sites and three additional Wilm's tumor and Egr1-like motifs. More than one-third of MT-MC1 target genes are also clustered on six cancer-associated chromosomal loci. Most surprisingly, all of the transcripts examined also are regulated by c-Myc. Finally, an estrogen receptor-MT-MC1 fusion protein was used to establish that all examined transcripts were regulated directly by the chimeric protein. Our results thus indicate that MT-MC1 target genes largely comprise a subset of those regulated by c-Myc. We propose that the properties imparted by MT-MC1 are the result of its control of a small and select c-Myc target gene population.
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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.