ArticleOncogene2004
Mxi1-SRalpha: a novel Mxi1 isoform with enhanced transcriptional repression potential.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 17 citations in OpenAlex.
- Isoform-resolved mRNA profiling of ribosome load defines interplay of HIF and mTOR dysregulation in kidney cancer.Nature structural & molecular biology · 2022Article
- Mxi1-0 Promotes Hypoxic Pulmonary HypertensionFrontiers in genetics · 2022Article
- Article
- A mathematical model for short-term vs. long-term survival in patients with glioma.American journal of cancer research · 2014Article
- N-Myc differentially regulates expression of MXI1 isoforms in neuroblastoma.Neoplasia (New York, N.Y.) · 2013Article
- Alternative splicing regulates mouse embryonic stem cell pluripotency and differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- p73alpha isoforms drive opposite transcriptional and post-transcriptional regulation of MYCN expression in neuroblastoma cells.Nucleic acids research · 2008Article
- Induction of Mxi1-SR alpha by FOXO3a contributes to repression of Myc-dependent gene expression.Molecular and cellular biology · 2007Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mxi1 belongs to the Myc/Max/Mad network of proteins that have been implicated in the control of multiple aspects of cellular behavior. Previously, we had reported that the mouse mxi1 gene gives rise to two distinct transcript forms that can encode proteins with dramatically different functional abilities. The Mxi1-SR protein (here termed Mxi1-SRbeta) can interact with Sin3/histone deacetylase and function as a potent transcriptional repressor and growth suppressor, while the Mxi1-WR protein lacks these activities. Here, we describe a new mxi1-derived transcript form (termed mxi1-SRalpha) whose expression is governed by its own promoter, resulting in a spatiotemporally distinct expression profile from that of the highly related mxi1-SRbeta form. Moreover, the Mxi1-SRalpha protein product, with its unique Sin3 interacting domain, has a greater affinity than its Mxi1-SRbeta counterpart for the Sin3 adapter proteins as well as an enhanced potential for transcriptional repression in transient reporter assays. Our identification of this novel Mxi1 isoform that results from alternative 5' exon usage adds an additional layer of complexity to the Mad/Mxi1 family. In addition, our findings warrant re-evaluation of mxi1 expression patterns on the cellular level and its status in human cancer samples, with a renewed focus on the distinct isoforms.
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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.