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double strand breaks (DSBs) are toxic DNA lesions that can arise from cell intrinsic and extrinsic sources and can lead to genome rearrangements in cancer. In eukaryotic cells, DSBs are formed, detected
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study the role of progeria genes, which lead to premature ageing, in frog (Xenopus) embryos. We have recently shown that epignetic clock is applicable to frogs as it is in humans (Zoller et al., 2023
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PhD position: Repair of DNA double strand breaks by break-induced replication repair pathway (m/f/d)
them together. Importantly, the defective DSB repair can lead to cancer, immunological deficiencies, accelerated ageing and severe developmental abnormalities. Besides HR and NHEJ, cells can also use
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and a disturbance of oligodendrocytes. In order to cross the BBB, the T cells must be reactivated. It is currently unknown which kind of APCs are involved in this process. A specific cell population we
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discovered (Musheev et al., 2022). This reversible process may be crucial for regulating DNA repair, replication, and transcription, further underscoring the importance of understanding these epigenetic
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-Syndrome, Nicolaides-Baraitser-Syndrom or Autism spectrum disorder. They manifest as brain abnormalities, intellectual disabilities and other physical aberrations. The molecular and cellular consequences