Selected Publications
For detailed publication lists please refer to each research group
Publication by Kristin Seltmann et al.: Transport of CLCA2 to the nucleus by extracellular vesicles controls keratinocytes survival and migration.
Seltmann et al. discovered that the transmembrane protein CLCA2 is transported to the nucleus of keratinocytes via extracellular vesicles (EVs). Nuclear CLCA2 promotes expression of Wnt target genes and is required for the suppression of keratinocyte migration and for survival of these cells under hyperosmotic stress conditions.
Publication by Paul Hiebert et al.: A lysyl oxidase-responsive collagen peptide illuminates collagen remodeling in wound healing.
Hiebert et al. used a collagen peptide sensor to visualize lysyl oxidase-dependent collagen formation and remodeling during wound healing. The probe selectively detects newly produced or remodeling collagen, but not matured collagen fibers, and can be applied for in vivo wound imaging and for discerning differential remodeling in mice with altered collagen dynamics.
Publication by Lena Cords et al.: Cancer-associated fibroblast phenotypes are associated with patient outcome in non-small cell lung cancer.
Cords and colleagues report a spatial resolved single-cell imaging mass cytometry analysis of cancer-associated fibroblasts (CAFs) in a non-small cell lung cancer (NSCLC) cohort of 1’070 patients. Their data identify phenotypic and spatial features of CAFs that are associates with patient outcome in NSCLC.
Publication by Nikolau et al.: Inflammation-induced TRIM21 represses hepatic steatosis by promoting the ubiquitination of lipogenic regulators.
Authors identify TRIM21 as a negative regulator of liver steatosis in nonalcoholic steatohepatitis (NASH) and provides mechanistic insights into an immunometabolic crosstalk that limits fatty acid synthesis and fructose metabolism during metabolic stress. Thus, providing new insights for therapeutic opportunity to treat NASH.
Publication by Gurri et al.: NRF3 suppresses squamous carcinogenesis, involving the unfolded protein response regulator HSPA5.
Gurri et al. found that the NRF3 protein is downregulated or even absent in invasively growing cancer cells of non-melanoma skin cancer (NMSC) patients. NRF3-deficient cancer cells showed enhanced malignancy due to the upregulation of the unfolded protein response regulator HSPA5, which was found as potential NRF3 interactor. Pharmacological inhibition or knock-down of HSPA5 rescued the malignant features of NRF3-deficient cells, suggesting HSPA5 as promising target for the treatment of NMSC.