ArticleNeoplasia (New York, N.Y.)
Mxi1-0, an alternatively transcribed Mxi1 isoform, is overexpressed in glioblastomas.
Article in Neoplasia (New York, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- Single-cell profiling identifies a pro-tumoral VCAN positive macrophage subset and defines a prognostic signature in glioblastoma.Discover oncology · 2026Article
- Integrative analysis of Iso-Seq and RNA-seq reveals dynamic changes of alternative promoter, alternative splicing and alternative polyadenylation during Angiotensin II-induced senescence in rat primary aortic endothelial cells.Frontiers in genetics · 2023Article
- Mxi1-0 Promotes Hypoxic Pulmonary HypertensionFrontiers in genetics · 2022Article
- Article
- Mxi1 and mxi1-0 antagonize N-myc function and independently mediate apoptosis in neuroblastoma.Translational oncology · 2015Article
- N-Myc differentially regulates expression of MXI1 isoforms in neuroblastoma.Neoplasia (New York, N.Y.) · 2013Article
- LXR-α selectively reprogrammes cancer cells to enter into apoptosis.Molecular and cellular biochemistry · 2011Article
- Oesophageal adenocarcinoma is associated with a deregulation in the MYC/MAX/MAD network.British journal of cancer · 2008Article
- Induction of Mxi1-SR alpha by FOXO3a contributes to repression of Myc-dependent gene expression.Molecular and cellular biology · 2007Article
- A review of the past, present, and future directions of neoplasia.Neoplasia (New York, N.Y.) · 2005Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The c-Myc transcription factor regulates expression of genes related to cell growth, division, and apoptosis. Mxi1, a member of the Mad family, represses transcription of c-Myc-regulated genes by mediating chromatin condensation via histone deacetylase and the Sin3 corepressor. Mxi1 is a c-Myc antagonist and suppresses cell proliferation in vitro. Here, we describe the identification of Mxi1-0, a novel Mxi1 isoform that is alternatively transcribed from an upstream exon. Mxi1-0 and Mxi1 have different amino-terminal sequences, but share identical Max- and DNA-binding domains. Both isoforms are able to bind Max, to recognize E-box binding sites, and to interact with Sin3. Despite these similarities and in contrast to Mxi1, Mxi1-0 is predominantly localized to the cytoplasm and fails to repress c-Myc-dependent transcription. Although Mxi1-0 and Mxi1 are coexpressed in both human and mouse cells, the relative levels of Mxi1-0 are higher in primary glioblastoma tumors than in normal brain tissue. This variation in the levels of Mxi1-0 and Mxi1 suggests that Mxi1-0 may modulate the Myc-inhibitory activity of Mxi1. The identification of Mxi1-0 as an alternatively transcribed Mxi1 isoform has significant implications for the interpretation of previous Mxi1 studies, particularly those related to the phenotype of the mxi1 knockout mouse.
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