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Programme? Not funded by a EU programme Is the Job related to staff position within a Research Infrastructure? No Offer Description The postdoctoral researcher will be part of the Cellular senescence, Cancer
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mediating cellular senescence. Here a library of lentiviral vectors carrying miRNA target sequences, regulating expression of a reporter gene, will be used to identify and characterize senescence associated
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(https://doi.org/10.1101/2024.12.29.630686 ) reveal that senescence is important for mammary gland involution, a physiological wound healing process that is intimately linked to postpartum breast cancer
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Postdoctoral Researcher to join our AMED-PRIME-funded project from April 2026 to March 2028 (with a possible extension). This project focuses on human ribosomes and nucleoli in cellular senescence. By
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George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Târgu Mureș | Romania | 19 days ago
of autophagy and senescence to slow down cellular degeneration associated with ageing. Investigations into modulation of associated pathways particularly mTOR/AMPK, mitochondrial oxidative stress and
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throughput screening (HTS) and high-content screening (HCS) assays targeting pathways such as autophagy-lysosome, senescence, and epigenetics. The lab also targets Alzheimer¿s disease resilience factors
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Aging and Alzheimer's Disease A. La Spada: Mechanisms of Neurodegenerative Disease / Neurotherapeutics J. Lipkova: Artificial Intelligence in Medicine. https://octopath.org/ M. Rose: Neuronal Diversity
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that drive the entry into replicative senescence in budding yeast, ii) apply quantitative analyses to decipher the complexity of the physiological response to oxidative stress and starvation in yeast. The lab
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of maladaptive innate immune pathways in neuronal stress and death, and (2) examine how mito-nuclear retrograde signaling contributes to microglial dysfunction and senescence in Alzheimerâ™s disease and related
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of maladaptive innate immune pathways in neuronal stress and death, and (2) examine how mito-nuclear retrograde signaling contributes to microglial dysfunction and senescence in Alzheimer’s disease and related