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-dependent MLCS regulation on lysosomal trafficking, mitochondrial quality control and hypoxia-induced cell death. Please apply for this project using this link: https://www.sheffield.ac.uk/postgraduate/phd
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of Experimental Medicine and Therapy Research, in the laboratory of Dr. Melanie Werner-Klein (https://www.experimentelle-medizin.de/erforschung-der-metastasierung ), we are inviting applications for a highly
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Institut de Chimie des Substances Naturelles (ICSN), CNRS, UPR 2301 | Gif sur Yvette, le de France | France | 11 days ago
functions and regulate ferroptosis and cuproptosis, two forms of non-apoptotic cell death that have gained a strong interest in cancer research. Despite their importance, the mechanisms governing
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with producing rAAV and brings together experts from two leading Irish institutions, NIBRT and UCD, and APC-VLE Ltd. (https://approcess.com/services/cell-and-gene-therapies ) - a leading Irish industrial
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-leading cause for death globally and there is a high demand for novel approaches to understand and treat cancer. Only recently it has become clear that mechanical forces play an important role in cancer
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Investigating how DNA damage responses combat infections by the typhoid pathogen Salmonella enterica
cases / 129 000 deaths each year. Understanding how infection develops and how human host cells combat Salmonella will improve control strategies that are vital to typhoid elimination efforts. Typhoid
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, and cell lysates. The primary area of research focus is deregulated cell death and transcriptional pathways in cancer, with a major interest in overcoming chemoresistance through the development and
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death of the sensory hair cells that sit inside the cochlea, but the reasons why these cells die faster in some individuals remain incompletely understood. In everyday life we are repeatedly exposed
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Investigating Roles for C9orf72 in Regulating FIS1-mediated Cell Death and Survival School of Biosciences PhD Research Project Self Funded Dr C Guo, Dr Kurt de Vos Application Deadline
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the role of maladaptive innate immune pathways in neuronal stress and death, and (2) examine how innate immune activation contributes to microglial dysfunction and senescence in Alzheimer’s disease and