Publications by authors named "J Boer"

Long AT repeat tracts form non-B DNA structures that stall DNA replication and cause chromosomal breakage. AT repeats are abundant in human common fragile sites (CFSs), genomic regions that undergo breakage under replication stress. Using an in vivo yeast model system containing AT-rich repetitive elements from human CFS FRA16D, we find that DNA polymerase zeta (Pol ζ) is required to prevent breakage and subsequent deletions at hairpin and cruciform forming (AT/TA)n sequences, with little to no role at an (A/T)28 repeat or a control non-structure forming sequence.

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The efficient conduction of mobile ions in halide perovskites is highly promising for artificial synapses (or memristive devices), devices with a conductivity that can be varied by applying a bias voltage. Here we address the challenge of downscaling halide perovskite-based artificial synapses to achieve low energy consumption and allow high-density integration. We fabricate halide perovskite artificial synapses in a back-contacted architecture to achieve microscale devices despite the high solubility of halide perovskites in polar solvents that are commonly used in lithography.

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The migration of mobile ions through the metal halide perovskite layer is still one of the main reasons for the poor stability of perovskite solar cells, LEDs, and photodetectors. To characterize mobile ions in the perovskite layer, time- and frequency-based electrical measurements are promising techniques. However, the presence of transport layers complicates their interpretation, limiting the information about mobile ions that can be extracted, and it is not clear how different features in frequency- and time-domain measurements relate to mobile ions.

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KMT2A-rearranged leukemias are a highly aggressive subset of acute leukemia, characterized by poor prognosis and frequent relapses despite intensive treatment. Menin inhibitors, which target the critical KMT2A-menin interaction driving leukemogenesis, have shown promise in early clinical trials. However, resistance to these inhibitors, often driven by menin mutations or alternative oncogenic pathways, remains a significant challenge.

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