Renzi et al. identify creatine kinase B (CKB) as a metabolic sensor during white adipocyte differentiation. By modulating AKT, CKB fine-tunes insulin signaling and glycolysis to restrain ChREBP activation, thereby controlling de novo lipogenesis. This work links creatine metabolism to nutrient-responsive transcriptional regulation of lipid accumulation.
One specific state, referred to as State 4, emerged as a key point of difference between the two groups. This state was characterized by strong connections between the left and right hemispheres of the brain. It specifically involved robust communication between the temporal and parietal regions, which are areas often associated with language and sensory processing.
The data showed that children with autism spent considerably less time in State 4 compared to the typically developing children. They also transitioned into and out of this state less frequently. The reduced time spent in this high-connectivity state was statistically distinct.
The researchers then compared these brain patterns to clinical assessments of the children. They found a correlation between the brain data and the severity of autism symptoms. Children who spent the least amount of time in State 4 tended to have higher scores on standardized measures of autism severity.
Here, Qing Zhang & team show targeting kinesin family member KIF20A in vitro and in mice sensitizes stem-like TNBC cells to standard chemotherapy.
1Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
2Department of Breast and Endocrine Surgery, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
3Jinfeng Laboratory, Chongqing, China.
4Quantitative Biomedical Research Center, Peter O’Donnell Jr. School of Public Health, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Toledo, B., González-Titos, A., Hernández-Camarero, P. et al. Impact of pancreatic proenzymes on pancreatic ductal adenocarcinoma associated fibroblasts. Sci Rep 15, 43,750 (2025). https://doi.org/10.1038/s41598-025-24863-2
There has been significant discussion recently on the concept of the “virtual cell.” I want to summarize the key concepts regarding what the field wants from a virtual cell and the challenges we face. In particular, the current trajectory reminds me of the evolution of statistical genetics (GWAS) and Mendelian disorders—analogies that I believe point to the most likely path for the field’s development.
Until AlphaFold’s debut in November 2020, DeepMind had been best known for teaching an artificial intelligence to beat human champions at the ancient game of Go. Then it started playing something more serious, aiming its deep learning algorithms at one of the most difficult problems in modern science: protein folding. The result was AlphaFold2, a system capable of predicting the three-dimensional shape of proteins with atomic accuracy.
Its work culminated in the compilation of a database that now contains over 200 million predicted structures, essentially the entire known protein universe, and is used by nearly 3.5 million researchers in 190 countries around the world. The Nature article published in 2021 describing the algorithm has been cited 40,000 times to date. Last year, AlphaFold 3 arrived, extending the capabilities of artificial intelligence to DNA, RNA, and drugs. That transition is not without challenges—such as “structural hallucinations” in the disordered regions of proteins—but it marks a step toward the future.
To understand what the next five years holds for AlphaFold, WIRED spoke with Pushmeet Kohli, vice president of research at DeepMind and architect of its AI for Science division.
Restoring Sight For Those In Need — Dr. Edward J. Holland, M.D. & Robert Dempsey — Co-Founders — Holland Foundation For Sight Restoration
Dr. Edward Holland is a world-renowned leader in corneal transplantation and severe ocular surface disease, and is the Co-Founder of the Holland Foundation for Sight Restoration (HFSR — https://www.hollandfoundationforsight… is a 501©(3) nonprofit organization, dedicated to transforming the lives of individuals affected by these conditions, including limbal stem cell deficiency (LSCD) – a rare and devastating condition that can result in chronic pain, profound vision loss, and blindness.
Through this HFSR initiative, Centers of Excellence (COEs) focused on the advanced sight restoration procedures of Ocular Surface Stem Cell Transplantation (OSST) are being launched across the country. As part of its mission, the foundation is also committed to broadening education and training so that more physicians nationwide can learn and implement The Cincinnati ProtocolTM for the management of these patients.
Dr. Holland is also the Director of Cornea Services at Cincinnati Eye Institute (https://www.cincinnatieye.com/doctors…) and Professor of Ophthalmology at the University of Cincinnati (https://med.uc.edu/landing-pages/prof…).
Dr. Holland attended the Loyola-Stritch School of Medicine in Chicago and trained in Ophthalmology at the University of Minnesota. He completed a fellowship in cornea and external disease at the University of Iowa and then completed a second fellowship in ocular immunology at the National Eye Institute, National Institutes of Health in Bethesda, Maryland.
In the last few years, progress has been made in the fight against Alzheimer’s disease with a class of therapies called anti-amyloid antibodies (anti-Aβ). These monoclonal anti-Aβs are proteins made in a laboratory to stimulate the immune system to slow the progression of the disease by targeting amyloid plaques in the brain that are characteristic of Alzheimer’s.
Biomarkers, such as measures derived from PET scans that reflect amyloid plaques in the brain, were instrumental in FDA approval of anti-Aβ therapies, like lecanumab (Leqembi) and donanemab (Kisulna), and have been shown to reduce plaques in the brains of Alzheimer’s patients. Yet despite FDA approval, there is still a clinical need to better understand how to monitor the efficacy and safety of these treatments.
To this end, the Alzheimer’s Association convened a workgroup of scientists and clinicians with experience in Alzheimer’s disease, including clinical trials of anti-Aβ therapies and biomarkers, to propose a framework to characterize the response of patients receiving these treatments.
Our thoughts are specified by our knowledge and plans, yet our cognition can also be fast and flexible in handling new information. How does the well-controlled and yet highly nimble nature of cognition emerge from the brain’s anatomy of billions of neurons and circuits? A new study by researchers in The Picower Institute for Learning and Memory at MIT provides new evidence from tests in animals that the answer might be a theory called “Spatial Computing.”
First proposed in 2023 by Picower Professor Earl K. Miller and colleagues Mikael Lundqvist and Pawel Herman, Spatial Computing theory explains how neurons in the prefrontal cortex can be organized on the fly into a functional group capable of carrying out the information processing required by a cognitive task. Moreover, it allows for neurons to participate in multiple such groups, as years of experiments have shown that many prefrontal neurons can indeed participate in multiple tasks at once. The basic idea of the theory is that the brain recruits and organizes ad hoc “task forces” of neurons by using “alpha” and “beta” frequency brain waves (about 10–30 Hz) to apply control signals to physical patches of the prefrontal cortex. Rather than having to rewire themselves into new physical circuits every time a new task must be done, the neurons in the patch instead process information by following the patterns of excitation and inhibition imposed by the waves.
Think of the alpha and beta frequency waves as stencils that shape when and where in the prefrontal cortex groups of neurons can take in or express information from the senses, Miller said. In that way, the waves represent the rules of the task and can organize how the neurons electrically “spike” to process the information content needed for the task.