The work has important implications for understanding how human cancer cells develop resistance to natural product-based chemotherapies.
The Morgridge Institute for Research has developed a portable, shareable light sheet microscope. The project can be mailed to a lab anywhere in the world, configured remotely by Morgridge engineers, and run one to three months of experiments.
Scientists seeking to unlock secrets of cellular aging have identified a gene that triggers senescence, a phenomenon in which cells stop dividing. The gene, called CD36, is unusually active in older, senescent cells. Heightening CD36 activity also caused young, healthy cells to stop dividing, with the effect also spreading to nearby cells in the same petri dish.
Tissue-engineered articular cartilage (AC) for repairing cartilage damaged by trauma or disease can be made to more closely mimic natural AC if mechanical stimulation of particular magnitude and duration is applied during the development process.
A new synthetic enzyme, crafted from DNA rather than protein, flips lipid molecules within the cell membrane, triggering a signal pathway that could be harnessed to induce cell death in cancer cells. This is the first such synthetic enzyme to outperform its natural counterpart -- and it does so by three orders of magnitude.
A zebrafish view of the world has been forensically analysed by researchers at the University of Sussex to reveal that how they see their surroundings changes hugely depending on what direction they are looking.
How does your brain decide what to do in a threatening situation? A new paper published in Nature describes a mechanism by which the brain classifies the level of a threat and decides when to escape.
A discovery about how human cells are 'triggered' to undergo an inflammatory type of cell death could have implications for treating cancer, stroke and tissue injury, and immune disorders. A research team from the Walter and Eliza Hall Institute in Melbourne identified the molecular trigger in human cells that drives necroptosis, and implicated defects in this molecular trigger as potentially playing a role in cancer development.
When cells grow and divide to ensure a biological function, DNA must be unwound from its typical tightly packed form and copied into RNA to create proteins. When this process goes awry, the result could be diseases such as cancers. University of North Carolina School of Medicine researchers have discovered that a protein called Spt6 facilitates RNA degradation so that cells have just the right amount of RNA for the creation of proteins.
A surprising form of cell-to-cell communication in glioblastoma promotes global changes in recipient cells, including aggressiveness, motility, and resistance to radiation or chemotherapy. Paradoxically, the sending cells in this signaling are glioblastoma cells undergoing programmed cell death. The apoptotic cancer cells release extracellular vesicles. These vesicle, or exosomes, carry components that alter RNA splicing in the recipient glioblastoma cells, and this altered splicing promotes therapy resistance and aggressive migration.