The key to regeneration has been inside you all along, new research suggests.
Category: biotech/medical
Copper-induced cell death stimulates antitumor immune cell responses
A preclinical study from researchers at The University of Texas MD Anderson Cancer Center, published today in Cell, details a connection between the immune system and cuproptosis, a type of copper-induced cell death. The findings suggest a new approach to help overcome resistance to immunotherapy.
The study, led by Boyi Gan, Ph.D., professor of Experimental Radiation Oncology, demonstrates that cancer cells undergoing cuproptosis release signals that activate the immune system. Significantly, this study is among the first to demonstrate that cuproptosis can actively engage the immune system and enhance responses to immunotherapy. In preclinical models, a combination approach of cuproptosis-inducing treatment along with anti-PD-L1 immunotherapy significantly slowed tumor growth.
“This study reveals a previously unrecognized partnership between the immune system and cuproptosis,” Gan said. “Importantly, because the cuproptosis-inducing agents used in our studies already have clinical experience and favorable safety profiles, these findings may offer a practical path toward developing new combination treatments for patients whose cancers no longer respond to immunotherapy.”
The Revolving Door of Adenovirus Cell Entry: Not All Pathways Are Equal
An interesting review on adenoviral cell entry and trafficking. Its discussion of how species B adenoviruses tolerate lower endosomal pH and accumulate in later-endosomal compartments before escaping were particularly intriguing. Link.
Adenoviruses represent exceptional candidates for wide-ranging therapeutic applications, from vectors for gene therapy to oncolytics for cancer treatments. The first ever commercial gene therapy medicine was based on a recombinant adenovirus vector, while most recently, adenoviral vectors have proven critical as vaccine platforms in effectively controlling the global coronavirus pandemic. Here, we discuss factors involved in adenovirus cell binding, entry, and trafficking; how they influence efficiency of adenovirus-based vectors; and how they can be manipulated to enhance efficacy of genetically modified adenoviral variants. We focus particularly on endocytosis and how different adenovirus serotypes employ different endocytic pathways to gain cell entry, and thus, have different intracellular trafficking pathways that subsequently trigger different host antiviral responses.
Opposing protein pathways steer skin stem cells toward renewal or repair
Two proteins with opposing functions orchestrate the development and maintenance of healthy skin, Stanford Medicine researchers have found. Modulating their activity with topical drugs could reduce inflammation, aid wound healing and slow or halt the growth of skin cancer, the researchers believe. The findings are published in the journal Science.
The proteins are part of a family called ubiquitin-like proteins. Ubiquitination controls the targeted destruction and disposal of unneeded proteins in a cell. But in the skin, certain ubiquitin-like proteins instead switch on or off wide swaths of genes involved in cellular growth and development, the study found. In particular, they trigger progenitor (stem) cells in the lower layer of the skin to either mature and migrate to the skin surface or to self-renew.
“These two ubiquitin-like protein systems are remarkably dedicated and opposite in their functions,” said Paul Khavari, MD, Ph.D., chair of dermatology at the Stanford School of Medicine and senior author of the study. “One promotes the stem-cell state while the other drives differentiation. It’s like having two opposing forces that determine a cell’s fate.”
Iron accumulation in the brain may contribute to neurodegeneration
Neurodegenerative diseases affect tens of millions of people worldwide. Among these, Alzheimer’s and Parkinson’s diseases are the most common; in the United States alone, the Alzheimer’s Disease Association and Parkinson’s Foundation report roughly 7 million people with Alzheimer’s and another million with Parkinson’s. An intriguing clue lies in the tangled mystery of neurodegeneration that scientists are working to solve: iron accumulation.
Scientists have noticed that iron can slowly build up inside neurons. Early in life, this iron accumulation appears to have little effect on neuronal function. However, later in life, it can contribute to a slow neuronal demise. Salk Institute researchers studied nerve cells to figure out whether and how this iron accumulation relates to neurodegenerative diseases. They found that the excess iron stuck in neurons lowers the cells’ defenses, making them more vulnerable to stressors and other cellular insults through a process they named chronoferroptosis.
The study, published in Cell Death Discovery on June 18, 2026, points to iron accumulation as a key target in the effort to predict, prevent and treat neurodegenerative diseases.
First 3D views of human cone opsins reveal how daylight vision reacts so fast
The retina of the human eye contains 6–7 million cone cells. These cells contain light-sensitive proteins known as cone opsins. They enable us to perceive our surroundings in detail in daylight. They allow us to see the world in thousands of colors: red strawberries, green leaves, the blue sky. They also enable us to see all the objects around us clearly. And they allow us to perceive fast movements, such as the rush of a train or the flight of a dragonfly.
Often, however, these all-rounders of daylight vision are also involved in retinal diseases. Impairment of cone receptor function, caused by genetic mutations or other degenerative processes, can lead to disorders such as color blindness and age-related macular degeneration (AMD), a disease affecting the central retina and causing progressive vision loss.
In a new study, Polina Isaikina and Sarah L. Schmidt, two researchers from the Center for Life Sciences at PSI, have succeeded for the first time in determining the three-dimensional structure of human cone opsins in their dark state and showing how their molecular architecture enables their rapid activation by light.
Preventing the next pandemic using AI-designed vaccines
For most of human history, infectious diseases were the main causes of morbidity and mortality. Advances in sanitation, antibiotics, vaccines, and public health dramatically shifted that balance, particularly in high-income countries, where life expectancy has increased by nearly 40 years over the past century. Yet the COVID-19 pandemic provided a stark reminder that infectious threats can still reshape societies almost overnight. Between 2019 and 2021 alone, life expectancy in the US fell by more than two years, and recent modelling suggests there is roughly a 50 percent chance of another COVID-scale pandemic occurring within the next 25 years.
Historically, the vaccine development model has been largely reactive and variant-driven, but the industry is now actively shifting toward proactive and universal vaccinology to get ahead of evolving pathogens. Recent results from a first-in-human clinical trial led by the University of Cambridge and its spin-out DIOSynVax, published in the Journal of Infection, provide early clinical evidence of this shift, demonstrating the safety of an AI-designed “super-antigen” intended to provide broad viral coverage.
Teaching AI to Invent Enzymes Nature Never Imagined
Evolution is an extraordinary engine for enzymatic diversity, yet the chemistry it has explored remains a narrow slice of what DNA can encode. Deep generative models can design new proteins that bind ligands, but none have created enzymes without pre-specifying catalytic residues.
In this webinar, Chenghao Liu and Jarrid Brooks from the Arnold Lab at Caltech will introduce DISCO (DIffusion for Sequence-structure CO-design). This multimodal model co-designs protein sequence and 3D structure around arbitrary biomolecules, as well as inference-time scaling methods that optimize objectives across both modalities. Conditioned solely on reactive intermediates, DISCO designs diverse heme enzymes with novel active-site geometries. These enzymes catalyze new-to-nature carbene-transfer reactions, including alkene cyclopropanation, spirocyclopropanation, B-H, and C(sp^3)-H insertions, with high activities exceeding those of engineered enzymes. Random mutagenesis of a selected design further confirmed that enzyme activity can be improved through directed evolution. By providing a scalable route to evolvable enzymes, DISCO broadens the potential scope of genetically encodable transformations.