ArticleMolecular and cellular biology2001
Targeted deletion of the S-phase-specific Myc antagonist Mad3 sensitizes neuronal and lymphoid cells to radiation-induced apoptosis.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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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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
29 citing papers in PubMed, 57 citations in OpenAlex.
- Review
- MXD3 Promotes Obesity and the Androgen Receptor Signaling Pathway in Gender-Disparity Hepatocarcinogenesis.Cells · 2021Article
- Review
- Article
- MXD3 as an onco-immunological biomarker encompassing the tumor microenvironment, disease staging, prognoses, and therapeutic responses in multiple cancer types.Computational and structural biotechnology journal · 2021Article
- Alternative Splicing of MXD3 and Its Regulation of MXD3 Levels in Glioblastoma.Frontiers in molecular biosciences · 2019Article
- The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis.Frontiers of medicine · 2018Review
- 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
- Embryonic stem cell-specific microRNAs contribute to pluripotency by inhibiting regulators of multiple differentiation pathways.Nucleic acids research · 2014Article
- 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
- An overview of MYC and its interactome.Cold Spring Harbor perspectives in medicine · 2014Review
- Article
- OX40 engagement stabilizes Mxd4 and Mnt protein levels in antigen-stimulated T cells leading to an increase in cell survival.European journal of immunology · 2011Article
- Mad3 negatively regulates B cell differentiation in the spleen by inducing Id2 expression.Molecular biology of the cell · 2010Article
- IKKalpha is a critical coregulator of a Smad4-independent TGFbeta-Smad2/3 signaling pathway that controls keratinocyte differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- A novel role of the Mad family member Mad3 in cerebellar granule neuron precursor proliferation.Molecular and cellular biology · 2007Article
- Inflammatory disease and lymphomagenesis caused by deletion of the Myc antagonist Mnt in T cells.Molecular and cellular biology · 2006Article
- RNF17, a component of the mammalian germ cell nuage, is essential for spermiogenesis.Development (Cambridge, England) · 2005Article
- The transcriptional repressor dMnt is a regulator of growth in Drosophila melanogaster.Molecular and cellular biology · 2005Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The Mad family comprises four basic-helix-loop-helix/leucine zipper proteins, Mad1, Mxi1, Mad3, and Mad4, which heterodimerize with Max and function as transcriptional repressors. The balance between Myc-Max and Mad-Max complexes has been postulated to influence cell proliferation and differentiation. The expression patterns of Mad family genes are complex, but in general, the induction of most family members is linked to cell cycle exit and differentiation. The expression pattern of mad3 is unusual in that mad3 mRNA and protein were found to be restricted to proliferating cells prior to differentiation. We show here that during murine development mad3 is specifically expressed in the S phase of the cell cycle in neuronal progenitor cells that are committed to differentiation. To investigate mad3 function, we disrupted the mad3 gene by homologous recombination in mice. No defect in cell cycle exit and differentiation could be detected in mad3 homozygous mutant mice. However, upon gamma irradiation, increased cell death of thymocytes and neural progenitor cells was observed, implicating mad3 in the regulation of the cellular response to DNA damage.
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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.