Bacterial pathogens developed several strategies to overcome defense systems of eukaryotic hosts. Within the infection process they need to attach to and cross through epithelial layers, escape from the innate and adaptive immune response, and find a physiological niche to survive. For this purpose bacteria developed toxins that specifically target central eukaryotic proteins, for example actin or Rho GTPases as regulators of the actin cytoskeleton. Some bacterial toxins catalyze a covalent modification of Rho GTPases to keep these molecular switches in a constitutive active or inactive state. This leads to rearrangement of the actin cytoskeleton. Toxin-treated cells show typical morphological changes depending on substrate specificity and action of the toxins. In this chapter I describe methods to illustrate how bacterial toxins may help to study the involvement of Rho GTPases in physiological and pathophysiological processes.
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http://dx.doi.org/10.1007/978-1-4939-8612-5_10 | DOI Listing |
FASEB J
December 2024
State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, College of Veterinary Medicine Jilin University, Center of Infectious Diseases and Pathogen Biology, Department of Infectious Diseases, First Hospital of Jilin University, Changchun, China.
Salmonella enterica serovar Typhimurium (S. Typhimurium) poses a serious threat to human and animal health, and there is an urgent need to develop new therapeutic agents. In our in vivo study, ginsenoside Ro (Ro) reduced the mortality rate of S.
View Article and Find Full Text PDFIn Saccharomyces cerevisiae cells, the bulk of mitochondrial DNA (mtDNA) replication is mediated by the replicative high-fidelity DNA polymerase γ. However, upon UV irradiation low-fidelity translesion polymerases: Polη, Polζ and Rev1, participate in an error-free replicative bypass of UV-induced lesions in mtDNA. We analysed how translesion polymerases could function in mitochondria.
View Article and Find Full Text PDFCell Mol Life Sci
December 2024
State Key Laboratory of Reproductive Medicine and Offspring Health, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Nanjing Medical University/Jiangsu Province Hospital/Jiangsu Women and Children Health Hospital, Nanjing, 210036, China.
The reproductive lifespan of female mammals is determined by the size of the primordial follicle pool, which comprises oocytes enclosed by a layer of flattened pre-granulosa cells. Oocyte differentiation needs acquiring organelles and cytoplasm from sister germ cells in cysts, but the mechanisms regulating this process remain unknown. Previously helicase for meiosis 1 (HFM1) is reported to be related to the development of premature ovarian insufficiency.
View Article and Find Full Text PDFPLoS One
December 2024
Department of Pediatrics, the First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Butyric acid (BA) can potentially enhance the function of the intestinal barrier. However, the mechanisms by which BA protects the intestinal mucosal barrier remain to be elucidated. Given that the Ras homolog gene family, member A (RhoA)/Rho-associated kinase 2 (ROCK2)/Myosin light chain kinase (MLCK) signaling pathway is crucial for maintaining the permeability of the intestinal epithelium, we further investigated whether BA exerts a protective effect on epithelial barrier function by inhibiting this pathway in LPS-induced Caco2 cells.
View Article and Find Full Text PDFCell Rep
December 2024
Department of Pharmacology, University of Colorado School of Medicine, Aurora, CO 80045, USA; University of Colorado Cancer Center, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA. Electronic address:
Metastasis to vital organs remains the leading cause of cancer-related deaths, emphasizing an urgent need for actionable targets in advanced-stage cancer. The role of mitochondrial Rho GTPase 2 (MIRO2) in prostate cancer growth was recently reported; however, whether MIRO2 is important for additional steps in the metastatic cascade is unknown. Here, we show that knockdown of MIRO2 ubiquitously reduces tumor cell invasion in vitro and suppresses metastatic burden in prostate and breast cancer mouse models.
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