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Insight into mithramycin disruption of ETS transcription leads to improved understanding of more selective analogs.
Structure
May 2021
Molecular Targets Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA; Natural Products Branch, Developmental Therapeutics Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, Frederick, MD 21702, USA. Electronic address:
Fusion products with the ETS family of transcription factors play critical roles in the etiology of several cancers. In this issue of Structure, Hou et al. (2020) provide insight into allosteric mechanisms by which mithramycin and its analogs perturb protein-DNA interactions in higher-order complexes at a DNA enhancer site.
View Article and Find Full Text PDFTRPV1 expression regulation… A further step in defining its biology: commentary for K. Zavala et al. "The anticancer antibiotic mithramycin-A inhibits TRPV1 expression in dorsal root ganglion neurons" [Neurosci. Lett. (2014) doi:10.1016/j.neulet.2014.01.021].
Neurosci Lett
August 2014
Department of Anesthesiology, University of California, San Diego, United States. Electronic address:
A high-frequency regulatory polymorphism in the p53 pathway accelerates tumor development.
Cancer Cell
September 2010
Department of Genetics, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
MDM2, a negative regulator of p53, is elevated in many cancers that retain wild-type p53. A single nucleotide polymorphism (SNP) in the human MDM2 promoter increases the affinity of Sp1 resulting in elevated MDM2 levels. We generated mice carrying either the MDM2(SNP309T) or the MDM2(SNP309G) allele to address the impact of MDM2(SNP309G) on tumorigenesis.
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