ArticleMolecular and cellular biology2007
A novel role of the Mad family member Mad3 in cerebellar granule neuron precursor proliferation.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 33 citations in OpenAlex.
- Massively parallel characterization and predictive modelling of neuronal regulatory variation.bioRxiv : the preprint server for biology · 2026Article
- Protective Effect of Dexmedetomidine against Hyperoxia-Damaged Cerebellar Neurodevelopment in the Juvenile Rat.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- Comparative transcriptional analyses of preclinical models and patient samples reveal MYC and RELA driven expression patterns that define the molecular landscape of IBC.NPJ breast cancer · 2022Article
- A Novel Gene Signature Associated With "E2F Target" Pathway for Predicting the Prognosis of Prostate Cancer.Frontiers in molecular biosciences · 2022Article
- MXD3 Promotes Obesity and the Androgen Receptor Signaling Pathway in Gender-Disparity Hepatocarcinogenesis.Cells · 2021Article
- Overexpression of MAX dimerization protein 3 (MXD3) predicts poor prognosis in clear cell renal cell carcinoma.Translational andrology and urology · 2021Article
- MXD3 as an Immunological and Prognostic Factor From Pancancer Analysis.Frontiers in molecular biosciences · 2021Article
- 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
- Signaling pathways in cerebellar granule cells development.American journal of stem cells · 2019Review
- 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
- Advances in biology of acute lymphoblastic leukemia (ALL) and therapeutic implications.American journal of blood research · 2018Review
- Novel Targeted Therapy for Precursor B Cell Acute Lymphoblastic Leukemia: anti-CD22 Antibody-MXD3 Antisense Oligonucleotide Conjugate.Molecular medicine (Cambridge, Mass.) · 2016Article
- Loss of MXD3 induces apoptosis of Reh human precursor B acute lymphoblastic leukemia cells.Blood cells, molecules & diseases · 2015Article
- Focus formation: a cell-based assay to determine the oncogenic potential of a gene.Journal of visualized experiments : JoVE · 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
- MXD3 regulation of DAOY cell proliferation dictated by time course of activation.BMC cell biology · 2014Article
- Developmental hypothyroxinemia and hypothyroidism reduce proliferation of cerebellar granule neuron precursors in rat offspring by downregulation of the sonic hedgehog signaling pathway.Molecular neurobiology · 2014Article
- An overview of MYC and its interactome.Cold Spring Harbor perspectives in medicine · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During development, Sonic hedgehog (Shh) regulates the proliferation of cerebellar granule neuron precursors (GNPs) in part via expression of Nmyc. We present evidence supporting a novel role for the Mad family member Mad3 in the Shh pathway to regulate Nmyc expression and GNP proliferation. Mad3 mRNA is transiently expressed in GNPs during proliferation. Cultured GNPs express Mad3 in response to Shh stimulation in a cyclopamine-dependent manner. Mad3 is necessary for Shh-dependent GNP proliferation as measured by bromodeoxyuridine incorporation and Nmyc expression. Furthermore, Mad3 overexpression, but not that of other Mad proteins, is sufficient to induce GNP proliferation in the absence of Shh. Structure-function analysis revealed that Max dimerization and recruitment of the mSin3 corepressor are required for Mad3-mediated GNP proliferation. Surprisingly, basic-domain-dependent DNA binding of Mad3 is not required, suggesting that Mad3 interacts with other DNA binding proteins to repress transcription. Interestingly, cerebellar tumors and pretumor cells derived from patched heterozygous mice express high levels of Mad3 compared with adjacent normal cerebellar tissue. Our studies support a novel role for Mad3 in cerebellar GNP proliferation and possibly tumorigenesis, and they challenge the current paradigm that Mad3 should antagonize Nmyc by competition for direct DNA binding via Max dimerization.
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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.