Publications by authors named "Markus Brockmann"

Article Synopsis
  • The study investigates how proteins, crucial for biological functions, are regulated by genomic mutations in haploid human cells, linking genetic changes to protein activity at the single-cell level.
  • It explores various cellular processes and pathways, including transcription, protein regulation, signaling cascades like MAPK and AKT, and epigenetic modifications, using a sequencing-based method to identify genetic factors influencing protein states.
  • The findings reveal that KCTD5 negatively regulates the AKT signaling pathway, implicating it in cancer, and demonstrate its role in controlling GPCR signaling through the targeted degradation of specific protein subunits.
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Picornaviruses are a leading cause of human and veterinary infections that result in various diseases, including polio and the common cold. As archetypical non-enveloped viruses, their biology has been extensively studied. Although a range of different cell-surface receptors are bound by different picornaviruses, it is unclear whether common host factors are needed for them to reach the cytoplasm.

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Amplification of MYCN is a driver mutation in a subset of human neuroendocrine tumors, including neuroblastoma. No small molecules that target N-Myc, the protein encoded by MYCN, are clinically available. N-Myc forms a complex with the Aurora-A kinase, which protects N-Myc from proteasomal degradation.

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In human neuroblastoma, amplification of the MYCN gene predicts poor prognosis and resistance to therapy. In a shRNA screen of genes that are highly expressed in MYCN-amplified tumors, we have identified AURKA as a gene that is required for the growth of MYCN-amplified neuroblastoma cells but largely dispensable for cells lacking amplified MYCN. Aurora A has a critical function in regulating turnover of the N-Myc protein.

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