ArticleThe EMBO journal1998
Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation.
Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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.
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Who cites it
53 citing papers in PubMed, 136 citations in OpenAlex.
- The roles of FGFR3 and c-MYC in urothelial bladder cancer.Discover oncology · 2024Review
- Review
- Review
- Article
- Emerging Contribution of PancRNAs in Cancer.Cancers · 2020Review
- The MYCL and MXD1 transcription factors regulate the fitness of murine dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 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
- Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis.Biochimica et biophysica acta · 2015Review
- Loss of MXD3 induces apoptosis of Reh human precursor B acute lymphoblastic leukemia cells.Blood cells, molecules & diseases · 2015Article
- Downregulation of Max dimerization protein 3 is involved in decreased visceral adipose tissue by inhibiting adipocyte differentiation in zebrafish and mice.International journal of obesity (2005) · 2014Article
- Article
- An overview of MYC and its interactome.Cold Spring Harbor perspectives in medicine · 2014Review
- Article
- Origin of bistability underlying mammalian cell cycle entry.Molecular systems biology · 2011Article
- TGFβ1 enhances MAD1 expression and stimulates promoter-bound Pol II phosphorylation: basic functions of C/EBP, SP and SMAD3 transcription factors.BMC molecular biology · 2011Article
- A humanized Smn gene containing the SMN2 nucleotide alteration in exon 7 mimics SMN2 splicing and the SMA disease phenotype.Human molecular genetics · 2010Article
- Mad3 negatively regulates B cell differentiation in the spleen by inducing Id2 expression.Molecular biology of the cell · 2010Article
- Keeping things quiet: roles of NuRD and Sin3 co-repressor complexes during mammalian development.The international journal of biochemistry & cell biology · 2009Review
- IKKalpha, a critical regulator of epidermal differentiation and a suppressor of skin cancer.The EMBO journal · 2008Review
- Specific requirement of the chromatin modifier mSin3B in cell cycle exit and cellular differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
The switch from transcriptionally activating MYC-MAX to transcriptionally repressing MAD1-MAX protein heterodimers has been correlated with the initiation of terminal differentiation in many cell types. To investigate the function of MAD1-MAX dimers during differentiation, we disrupted the Mad1 gene by homologous recombination in mice. Analysis of hematopoietic differentiation in homozygous mutant animals revealed that cell cycle exit of granulocytic precursors was inhibited following the colony-forming cell stage, resulting in increased proliferation and delayed terminal differentiation of low proliferative potential cluster-forming cells. Surprisingly, the numbers of terminally differentiated bone marrow and peripheral blood granulocytes were essentially unchanged in Mad1 null mice. This imbalance between the frequencies of precursor and mature granulocytes was correlated with a compensatory decrease in granulocytic cluster-forming cell survival under apoptosis-inducing conditions. In addition, recovery of the peripheral granulocyte compartment following bone marrow ablation was significantly enhanced in Mad1 knockout mice. Two Mad1-related genes, Mxi1 and Mad3, were found to be expressed ectopically in adult spleen, indicating that functional redundancy and cross-regulation between MAD family members may allow for apparently normal differentiation in the absence of MAD1. These findings demonstrate that MAD1 regulates cell cycle withdrawal during a late stage of granulocyte differentiation, and suggest that the relative levels of MYC versus MAD1 mediate a balance between cell proliferation and terminal differentiation.
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What OpenQuestion holds
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.