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the development of genetic autoinflammatory diseases. Using techniques in cell biology, molecular biology and biophysics you will investigate how loss of function of the RNA editing enzyme ADAR1 causes the human
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), charging tRNA with tyrosine in the first step of protein biosynthesis. The Jordanova lab first described that dominant mutations in YARS1 cause CMT (Jordanova et al., Nat Genetics 2006) and linked
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first described that dominant mutations in YARS1 cause CMT (Jordanova et al., Nat Genetics 2006) and linked the enzyme’s non-canoncial functions to neurodegeneration. To gain better insights in disease
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lab first described that dominant mutations in YARS1 cause CMT (Jordanova et al., Nat Genetics 2006) and linked the enzyme’s non-canoncial functions to neurodegeneration. To gain better insights in
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is to integrate genetics, cell biology, genomics, and bio-computing to unravel plant biological processes and to further translate this knowledge into value for society. Please visit us at
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Autosomal dominant polycystic kidney disease (ADPKD) is the leading genetic cause of end-stage kidney disease, affecting over 12 million patients worldwide. Loss-of-function mutations in PKD1 (accounting
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nucleolar organization. We combine molecular genetics, cell biology, biochemistry, and high-resolution sequencing (short- and long-read) to understand how ribosome production is regulated in health and