A gene called gasdermin E, which is downregulated in many cancers, aids cells in dying in an unexpected way, and may also suppress tumor growth.
Scientists have uncovered a process in cells that prevents DNA from becoming tangled, which resembles a method used to control climbers' ropes.
Obesity can break down our protective blood brain barrier resulting in problems with learning and memory, scientists report.
NTU Singapore scientists have developed a sustainable way to demonstrate a new genetic modification that can increase the yield of natural oil in seeds by up to 15% in laboratory conditions.
What will a three-degree-warmer world look like? When experiencing stress or damage from various sources, plants use chloroplast-to-nucleus communication to regulate gene expression and help them cope. Now, Salk Institute researchers have found that GUN1 -- a gene that integrates numerous chloroplast-to-nucleus retrograde signaling pathways -- also plays an important role in how proteins are made in damaged chloroplasts, which provides a new insight into how plants respond to stress.
Identifying a protein that plays a key role in cancer cell growth is a first step toward the development of a targeted cancer therapy. It is especially promising when this protein is dispensable for the growth of normal cells. Their discovery that UNC45A fits these criteria has researchers, led by Dr. Ahmed Chadli, of the Georgia Cancer Center at Augusta University, excited about potential new cancer therapeutic strategies involving the inhibition of UNC45A.
Research by a Barrow Neurological Center scientist on mechanisms of dysfunctional RNA processing in ALS and frontaltemporal dementia (FTD) was published in the April issue of Acta Neuropathologica. The research was conducted by Dr. Rita Sattler and her graduate student Stephen Moore in her laboratory at the Department of Neurobiology at Barrow Neurological Institute, which is dedicated to understanding the mechanisms of disease in ALS, FTD and related neurodegenerative diseases.
Since the CRISPR genome editing technology was invented in 2012, it has shown great promise to treat a number of intractable diseases. However, scientists have struggled to identify potential off-target effects in therapeutically relevant cell types, which remains the main barrier to moving therapies to the clinic. Now, a group of scientists at the Gladstone Institutes and the Innovative Genomics Institute (IGI), with collaborators at AstraZeneca, have developed a reliable method to do just that.
New evidence points to a key role for a molecular switch called VGLL3 in autoimmune diseases, and the major gap in incidence between women and men. Building on past research showing that women have more VGLL3 in their skin cells than men, a team studied it further in mice. They show that having too much VGLL3 in skin cells pushes the immune system into overdrive, leading to an autoimmune response and symptoms similar to lupus.
Named after the dark stripes that form inside potatoes after they are cut and fried, zebra chip disease is a potentially devastating affliction that can result in yield losses up to 100% for farmers. Swisher et al. identified a new haplotype, designated haplotype F, that causes zebra chip symptoms in potato. Prior to this discovery, 'only haplotypes A and B were known to cause zebra chip symptoms in potato,' explains Swisher.