Publications by authors named "M Leitges"

Cell immortalization, a hallmark of cancer development, is a process that cells can undergo on their path to carcinogenesis. Spontaneously immortalized mouse embryonic fibroblasts (MEFs) have been used for decades; however, changes in the global transcriptome during this process have been poorly described. In our research, we characterized the poly-A RNA transcriptome changes after spontaneous immortalization.

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  • Researchers studied the role of PKD3, a member of the Protein kinases D family, in T cell responses, particularly how it differs from the better-understood PKD2.
  • Using a mouse model that overexpresses PKD3 in T cells, they found an increase in central memory T cells, though this was not fully explained by lab tests and seemed tied to developmental changes during thymic development.
  • Ultimately, they concluded that PKD3 plays a subtle role in shaping the development of central memory and CD8 T cells, but it doesn't significantly affect overall immune responses in specific tests.
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Protein kinases D (PKDs) are implicated in T cell receptor (TCR) signaling. Of the two T cell-expressed isoforms PKD2 and PKD3, however, only the former one is rather well understood in this immune cell type. Recently, we have observed a putative hyper-phenotype of T cells from conventional PKD3-knockout mice, which we explained as a secondary effect due to a skewed T cell compartment from naïve towards effector/memory T cells already under steady state conditions.

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  • PKD3 is involved in T cell receptor signaling and its exact role in T lymphocyte activation remains unclear.
  • Researchers analyzed PKD3 expression and immune responses in PKD3-knockout mice through various methods like RT-PCR and flow cytometry.
  • The study found that PKD3-deficient mice have enhanced T follicular helper cell generation and increased interleukin-2 production, indicating a more activated T cell phenotype in vivo, but it does not affect the differentiation of naïve CD4 T cells in vitro.
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  • PKCι is identified as an oncogene involved in lung and ovarian cancer, and is important for pancreatic cancer cell growth and maintenance.
  • The study examines the effects of removing PKCι specifically in the pancreas, finding that this leads to increased immune cell infiltration, DNA damage, and cell death, while reducing the sensitivity to pancreatitis.
  • Disrupting PKCι in pancreatic cells promotes early tumor formation but prevents further progression to a more aggressive cancer stage, highlighting its role in autophagy and cancer development.
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