Publications by authors named "Christina Schuelein-Voelk"

The contribution of deubiquitylating enzymes (DUBs) to β-Catenin stabilization in intestinal stem cells and colorectal cancer (CRC) is poorly understood. Here, and by using an unbiassed screen, we discovered that the DUB USP10 stabilizes β-Catenin specifically in APC-truncated CRC in vitro and in vivo. Mechanistic studies, including in vitro binding together with computational modelling, revealed that USP10 binding to β-Catenin is mediated via the unstructured N-terminus of USP10 and is outcompeted by intact APC, favouring β-catenin degradation.

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Article Synopsis
  • - The MYCN oncoprotein works with another protein called MAX to attach to active gene promoters, and it also connects with the nuclear exosome, indicating its role in RNA processing.
  • - Research shows that MYCN forms large complexes with the exosome and various RNA-binding proteins, binding to RNA through a specific region known as MYCBoxI, which helps process many intronic RNA transcripts in cells.
  • - Disrupting the exosome alters MYCN's position from gene promoters to intronic RNAs, leading to a shift in its role from activating genes to being replaced by a repressor (MNT/MXD6), which can limit its ability to influence cell growth while being crucial for neuroblastoma cell
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The ATPase p97 (also known as VCP, Cdc48) has crucial functions in a variety of important cellular processes such as protein quality control, organellar homeostasis, and DNA damage repair, and its de-regulation is linked to neuromuscular diseases and cancer. p97 is tightly controlled by numerous regulatory cofactors, but the full range and function of the p97-cofactor network is unknown. Here, we identify the hitherto uncharacterized FAM104 proteins as a conserved family of p97 interactors.

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  • Disruption of ribosomal biogenesis and protein synthesis contributes to cancer development, making it a promising target for therapy.
  • Loss of the tumor suppressor APC in colorectal cancer leads to increased expression of RNA polymerase I, enhancing ribosomal DNA transcription and promoting tumor growth.
  • The inhibitor CX5461 disrupts this process, causing irreversible growth arrest and differentiation in cancer cells, and shows potential as a therapeutic strategy when combined with senolytic agents in experimental models.
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Community-acquired (CA) Staphylococcus aureus cause various diseases even in healthy individuals. Enhanced virulence of CA-strains is partly attributed to increased production of toxins such as phenol-soluble modulins (PSM). The pathogen is internalized efficiently by mammalian host cells and intracellular S.

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