UC San Diego researchers discover the enzyme SPRK1’s role in reorganizing the paternal genome during the first moments of fertilization — a finding that might help explain infertility cases of unknown cause.
From a simple blood draw, microbial DNA may reveal who has cancer and which type, even at early stages.
A comparison of normal and germ-free mice revealed that as much as 70 percent of a mouse’s gut chemistry is determined by its gut microbiome. Even in distant organs, such as the uterus or the brain, approximately 20 percent of molecules were different in the mice with gut microbes.
UC San Diego and IBM researchers reveal a new understanding of how our microbiomes change as we age, setting the stage for future research on the role microbes play in accelerating or decelerating the aging process and influencing age-related diseases.
UC San Diego researchers use 3D human gut organoids to reveal the molecular system that keeps intestinal linings sealed, demonstrate how the system breaks down and how it can be strengthened with the diabetes drug metformin.
UC San Diego School of Medicine researchers identified several genetic switches, or transcription factors, that determine whether or not liver cells produce collagen — providing a new therapeutic target for liver fibrosis.
Two different UC San Diego research teams identified the same molecule — αvβ5 integrin — as Zika virus’ key to brain cell entry. They found ways to take advantage of the integrin to both block Zika virus from infecting cells and turn it into something good: a way to shrink brain cancer stem cells.
UC San Diego School of Medicine researchers have discovered how a new immune system works to protect bacteria from phages, viruses that infect bacteria — new information that could be leveraged to improve treatment of multidrug-resistant bacterial infections by refining phage therapy.
In a UC San Diego study, rats with spinal cord injuries experienced a three-fold increase in motor activity when treated with neural progenitor cells that had been pre-conditioned with a modified form of tPA, a drug commonly used to treat non-hemorrhagic stroke.
People with cystic fibrosis who carry genetic variants that lower RNF5 gene expression have more mutant CFTR protein on cell surfaces. Even if the CFTR protein isn’t fully functional, it’s better than none, and may explain why some with cystic fibrosis are less prone to infection than others.