One of the final pieces in the cell death and inflammation signalling pathway puzzle has been revealed
Peer-Reviewed Publication
Updates every hour. Last Updated: 30-Oct-2026 13:17 ET (30-Oct-2026 17:17 GMT/UTC)
An international research team has discovered that the protein HERC4 is a key component in the signalling pathways involved in programmed cell death, which is responsible for triggering inflammatory diseases. The discovery will potentially lead the way to new therapeutic approaches for chronic inflammatory bowel diseases, rheumatism and psoriasis, as well as for inflammation-related types of cancer / Publication in ‘Nature Structural and Molecular Biology’
Marine plastic debris can persist for long periods and gradually break down into microplastics that are difficult to remove. Researchers from Ritsumeikan University used a system dynamics model to examine how reducing marine plastic inputs and varying the timing and intensity of cleanup could affect plastic accumulation by 2050. The findings show that halting plastic inputs is essential but insufficient on its own. Earlier cleanup of legacy macroplastics can reduce accumulation, but at higher costs.
A new AI tool can identify aging patterns in blood stem cells by analyzing DAPI-stained nuclear images and chromatin architecture. It may accelerate the discovery and testing of cellular rejuvenation strategies.
Researchers have substantially expanded the known genomic diversity of Aoguangviridae, a family of marine viruses associated with the abundant archaeal order Poseidoniales. By increasing the non-redundant genome set from 59 to 227, the study revealed extensive previously unrecognized diversity and distinct ecological distribution patterns across the global ocean. The researchers also identified auxiliary metabolic genes and evidence of transcriptional activity, providing new insights into the potential ecological roles of these viruses and their interactions with archaeal hosts. The findings were published on 2 September in Ocean-Land-Atmosphere Research.
- Professor Juyoung Lee's team at the Graduate School of Engineering Biology combined DNA elements recognized by bacteria and yeast and used the resulting system to control the production of a green pigment in both microbes
- The design reduces the need to redesign gene expression systems for each microbe and is expected to be useful in biofoundries, where production routes are designed and tested
One of the differences between humans and the other great apes is that we commonly get chronic joint disease, while chimps and gorillas almost never do. At first glance, we seem to have struck a poor evolutionary bargain. Natural selection is supposed to weed out harmful traits, so why are we so much more prone to wear-and-tear disorders of the joints and spine than our evolutionary cousins? Osteoarthritis, for example, a major cause of disability and reduced quality of life, affects hundreds of millions worldwide. In a study published today in Nature, Israeli and Japanese researchers propose an answer based on the use of hybrid human-chimpanzee cells and other advanced techniques. They reveal that painful joints may be a hidden price we pay for traits that make us human.