Call for Applications: The 2018 Vilcek Prizes for Creative Promise in Biomedical Science Three $50,000 cash awards for young, foreign-born researchers Learn more about eligibility requirements and apply at Vilcek.org Deadline: May 31, 2017
Lab Animal, a Nature Research journal focusing on in vivo methods, research and technology with model organisms of human health & disease, presents a special Focus on reproducibility and translation of in vivo research with disease models.
A mouse recapitulating APOL1-associated kidney disease pp411 - 412 Cheryl A Winkler and George W Nelson doi:10.1038/nm.4318 In a recent study, researchers generated a mouse model expressing variant APOL1 that recapitulates human kidney disease. Variant APOL1 leads to caspase-1-dependent pyroptosis, which opens the door for the development of new druggable targets to treat APOL1-mediated kidney disease.
Poster on Molecular mechanisms of amyotrophic lateral sclerosis
This poster from Nature Reviews Neuroscience provides an overview of the molecular and cellular mechanisms that have been proposed to contribute to the pathogenesis of amyotrophic lateral sclerosis, which is the most common form of motor neuron disease.
EZH2 is a potential therapeutic target for H3K27M-mutant pediatric gliomas pp483 - 492 Faizaan Mohammad, Simon Weissmann, Benjamin Leblanc, Deo P Pandey, Jonas W Hojfeldt et al. doi:10.1038/nm.4293 Although mutant H3K27M histones inhibit PRC2 in diffuse intrinsic pontine gliomas, these tumors exhibit significant amounts of PRC2 activity. The repression of several genes, including INK4A, by residual EZH2 activity is required for tumor growth, and EZH2 inhibitors therefore represent potential therapies for these patients.
Therapeutic targeting of polycomb and BET bromodomain proteins in diffuse intrinsic pontine gliomas pp493 - 500 Andrea Piunti, Rintaro Hashizume, Marc A Morgan, Elizabeth T Bartom, Craig M Horbinski et al. doi:10.1038/nm.4296 Nucleosomes containing mutant K27M histones in diffuse intrinsic pediatric gliomas (DIPG) exclude PRC2 binding and recruit BET bromodomain proteins; however, residual PRC2-dependent repression of specific loci, is required for DIPG oncogenesis. These results provide a rationale for targeting these epigenetic regulators in patients.
HRDetect is a predictor of BRCA1 and BRCA2 deficiency based on mutational signatures pp517 - 525 Helen Davies, Dominik Glodzik, Sandro Morganella, Lucy R Yates, Johan Staaf et al. doi:10.1038/nm.4292 HRDetect represents a model integrating whole-genome sequencing mutation signatures associated with BRCA1 and BRCA2 deficiency. The implementation of this predictor across different tumor types identifies a larger proportion of patients displaying /`BRCAness/' than previously recognized; they might derive benefit from platinum and PARP-inhibitor therapies.
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