Publications by authors named "Julia Weissbach"

The assessment of cancer patient care during the COVID-19 pandemic has been mainly reported from a physician's perspective. Patients with rare tumor entities such as neuroendocrine tumors (NET), which require a complex and specialized care infrastructure, were highly affected by the COVID-19 crisis. Using a structured questionnaire consisting of a general section on the disease and a special COVID-19 section to record medical care, vaccination behavior as well as social and psycho-emotional parameters were collected from NET patients.

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Background: Neurotrophic growth factors can stabilize the intestinal barrier by preventing the apoptosis of enteric glial cells (EGCs) and enterocytes. We reasoned that a selective 5-HT1A receptor agonist may have neuroprotective properties in the gut and that topical application of SR57746A might be an effective treatment strategy in inflammatory bowel disease (IBD).

Methods: The therapeutic potential of 5-HT1A receptor agonist SR57746A in IBD was evaluated in vitro (nontransformed NCM460 colonic epithelial cells, SW480 colorectal carcinoma cells) and in vivo (murine dextran sulfate sodium [DSS] colitis and CD4-T-cell transfer colitis).

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Compared to pancreatic adenocarcinoma (PDAC), pancreatic neuroendocrine tumors (PanNET) represent a rare and heterogeneous tumor entity. In addition to surgical resection, several therapeutic approaches, including biotherapy, targeted therapy or chemotherapy are applicable. However, primary or secondary resistance to current therapies is still challenging.

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Recently, we identified the homeodomain transcription factor Cut homeobox 1 (CUX1) as mediator of tumour de-differentiation and metastatic behaviour in human insulinoma patients. In insulinomas, CUX1 enhanced tumour progression by stimulating proliferation and angiogenesis in vitro and in vivo. In patients with non-functional pancreatic neuroendocrine tumours (PanNET), however, the impact of CUX1 remains to be elucidated.

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Article Synopsis
  • MRTF-A is a key protein for gene expression that relies on the dissociation of G-actin to function properly; JMY plays a crucial role in regulating MRTF-A by influencing actin dynamics.
  • Experiments showed that JMY not only increased MRTF-A's activity and nuclear presence but also indicated that deleting certain parts of JMY led to even higher MRTF-A activation, revealing an unexpected self-inhibitory mechanism.
  • The study concluded that JMY can enhance MRTF-SRF activity independently of F-actin by competing for actin binding and that its C-terminal region likely limits its own effectiveness through self-regulation.
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The myocardin-related transcription factors (MRTFs) are coactivators of serum response factor (SRF)-mediated gene expression. Activation of MRTF-A occurs in response to alterations in actin dynamics and critically requires the dissociation of repressive G-actin-MRTF-A complexes. However, the mechanism leading to the release of MRTF-A remains unclear.

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Compared to the cytoplasmic F-actin abundance in cells, nuclear F-actin levels are generally quite low. However, nuclear actin is present in certain cell types including oocytes and under certain cellular conditions including stress or serum stimulation. Currently, the architecture and polymerization status of nuclear actin networks has not been analyzed in great detail.

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Synopsis of recent research by authors named "Julia Weissbach"

  • - Julia Weissbach's recent research focuses on understanding the implications of neuroendocrine tumors (NET) in various contexts, particularly during the COVID-19 pandemic, and exploring innovative therapeutic strategies for inflammatory bowel disease (IBD).
  • - Her studies highlight patient perspectives during the pandemic, revealing how COVID-19 significantly disrupted the care infrastructures for patients with rare tumor types like NET, and emphasizing the need for enhanced patient-oriented care models.
  • - Additionally, Weissbach investigates the therapeutic potential of selective 5-HT1A receptor agonists in protecting gut epithelial cells and targeting histone deacetylases (HDACs) in pancreatic NET models, while also assessing the role of transcription factors like CUX1 in tumor progression and metastasis.

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