ArticleOncogene2000
Mlx, a new Max-like bHLHZip family member: the center stage of a novel transcription factors regulatory pathway?
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 88 citations in OpenAlex.
- MAX inactivation deregulates the MYC network and induces neuroendocrine neoplasia in multiple tissues.Science advances · 2025Article
- MLX phosphorylation stabilizes the ChREBP-MLX heterotetramer on tandem E-boxes to control carbohydrate and lipid metabolism.Science advances · 2025Article
- MLX phosphorylation stabilizes the ChREBP-MLX heterotetramer on tandem E-boxes to control carbohydrate and lipid metabolism.bioRxiv : the preprint server for biology · 2024Article
- Disruption of Multiple Overlapping Functions Following Stepwise Inactivation of the Extended Myc Network.Cells · 2022Article
- Regulation of Normal and Neoplastic Proliferation and Metabolism by the Extended Myc Network.Cells · 2022Review
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- SMaRT lncRNA controls translation of a G-quadruplex-containing mRNA antagonizing the DHX36 helicase.EMBO reports · 2020Article
- Partitioning of MLX-Family Transcription Factors to Lipid Droplets Regulates Metabolic Gene Expression.Molecular cell · 2020Article
- The MNT transcription factor autoregulates its expression and supports proliferation in MYC-associated factor X (MAX)-deficient cells.The Journal of biological chemistry · 2020Article
- Glucose-Sensing Transcription Factor MondoA/ChREBP as Targets for Type 2 Diabetes: Opportunities and Challenges.International journal of molecular sciences · 2019Review
- The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis.Frontiers of medicine · 2018Review
- Postimplantation Mga expression and embryonic lethality of two gene-trap alleles.Gene expression patterns : GEP · 2018Article
- The MYCN Protein in Health and Disease.Genes · 2017Review
- MNT and Emerging Concepts of MNT-MYC Antagonism.Genes · 2017Article
- Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis.Biochimica et biophysica acta · 2015Review
- Deregulated Myc requires MondoA/Mlx for metabolic reprogramming and tumorigenesis.Cancer cell · 2015Article
- Mga is essential for the survival of pluripotent cells during peri-implantation development.Development (Cambridge, England) · 2015Article
- An overview of MYC and its interactome.Cold Spring Harbor perspectives in medicine · 2014Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The Myc proto-oncogene family members have been identified as the cellular homologs of the transforming oncogene of avian retroviruses. They encode central regulators of mammalian cell proliferation and apoptosis, and they associate with the bHLHZip protein Max to bind specific DNA sequences and regulate the expression of genes important for cell cycle progression. The other family members, Mad1, Mxi1, Mad3, Mad4 and Rox (Mnt) antagonize their activities. The Mads and Rox compete with Myc in heterodimerizing with Max and in binding to the same specific target sequences. These Mads:Max and Rox:Max dimers repress transcription through binding to the mSIN3 corepressor protein and by tethering histone deacetylase-containing complexes to the DNA. In a screen for Rox interactors we isolated Mlx, a bHLHZip protein previously identified in a screen for Mad1 interactors. In the present work we extend the known dimerization partners of Mlx by demonstrating its ability to interact with Rox. Moreover, we show that contrary to previous reports Mlx is able to homodimerize and to bind E-box sequences at low concentration levels. The possible role of Mlx in an emerging regulatory pathway and acting parallel to the Max driven network is discussed.
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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.