ArticleOncogene2003
MafA has strong cell transforming ability but is a weak transactivator.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Dual phenotype in a patient with adult-onset hyperinsulinism and diabetes caused by an activatingJournal of the Endocrine Society · 2026Article
- MAFB: a key regulator of myeloid commitment involved in hematological diseases.Cell death discovery · 2025Review
- The role and regulation of Maf proteins in cancer.Biomarker research · 2023Review
- ARMC5 is part of an RPB1-specific ubiquitin ligase implicated in adrenal hyperplasia.Nucleic acids research · 2022Article
- Second MAFA Variant Causing a Phosphorylation Defect in the Transactivation Domain and Familial Insulinomatosis.Cancers · 2022Article
- Review
- MAFb protein confers intrinsic resistance to proteasome inhibitors in multiple myeloma.BMC cancer · 2018Article
- Involvement of MAFB and MAFF in Retinoid-Mediated Suppression of Hepatocellular Carcinoma Invasion.International journal of molecular sciences · 2018Article
- NRL and CRX Define Photoreceptor Identity and Reveal Subgroup-Specific Dependencies in Medulloblastoma.Cancer cell · 2018Article
- Article
- Cribriform and intraductal prostate cancer are associated with increased genomic instability and distinct genomic alterations.BMC cancer · 2018Article
- Repression of COUP-TFI Improves Bone Marrow-Derived Mesenchymal Stem Cell Differentiation into Insulin-Producing Cells.Molecular therapy. Nucleic acids · 2017Article
- GSK3-mediated MAF phosphorylation in multiple myeloma as a potential therapeutic target.Blood cancer journal · 2014Article
- Yeast one-hybrid screen of a thymus epithelial library identifies ZBTB7A as a regulator of thymic insulin expression.Molecular immunology · 2013Article
- Loss of p53 exacerbates multiple myeloma phenotype by facilitating the reprogramming of hematopoietic stem/progenitor cells to malignant plasma cells by MafB.Cell cycle (Georgetown, Tex.) · 2012Article
- A novel molecular mechanism involved in multiple myeloma development revealed by targeting MafB to haematopoietic progenitors.The EMBO journal · 2012Article
- Reexpression of oncoprotein MafB in proliferative β-cells and Men1 insulinomas in mouse.Oncogene · 2012Article
- Insulin transactivator MafA regulates intrathymic expression of insulin and affects susceptibility to type 1 diabetes.Diabetes · 2010Article
- Phosphorylation within the MafA N terminus regulates C-terminal dimerization and DNA binding.The Journal of biological chemistry · 2010Article
- PML/RARalpha fusion protein transactivates the tissue factor promoter through a GAGC-containing element without direct DNA association.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The maf oncogene of the avian oncogenic retrovirus AS42 encodes a nuclear bZip protein, v-Maf, that recognizes sequences related to the AP-1 target site. The corresponding cellular protein, c-Maf belongs to a family of related bZip proteins together with MafA and MafB. In this paper, we compare the transactivation and cell transforming abilities of MafA and MafB along with two forms of the c-Maf protein. These proteins induce cellular transformation when expressed in chicken embryo fibroblasts. In reporter assays, MafA is a much less effective transactivator than the other Maf proteins, but unexpectedly shows the strongest activity in cell transformation. Chimeras of MafA and MafB correlate the strong cell transforming ability of MafA with its DNA-binding domain. The DNA-binding domain of MafA is also correlated with weak transactivation. Additional mutagenesis experiments show that transactivation and transformation by MafA are also controlled by phosphorylation of two conserved serine residues in the transactivation domain. Finally, we constructed MafA-estrogen receptor fusion molecules that show tightly hormone-dependent cell transforming ability. These regulatable constructs permit a kinetic characterization of target gene responses and facilitate discrimination between direct and indirect targets.
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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.