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Published in the Journal of the American Chemical Society, the research by scientists at King’s College London and their collaborators suggests that chromatin—the complex of DNA

DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

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Clinical trials are underway for a drug that could potentially prevent Alzheimer’s long before it kicks in. Researchers from Washington University School of Medicine are studying the effects of an experimental antibody called remternetug.

The drug was developed by pharmaceutical giant Eli Lilly. It is designed for genetically predisposed people to develop Alzheimer’s and its study focuses on young people aged 18 and up.

Remternetug targets amyloid beta, a protein that forms plaque in the brain. The presence of plaque is one of the key hallmarks of Alzheimer’s disease. Other recently approved drugs, like donanemab, also target amyloid plaque, since that seems to be what you attack if you want to chip away at Alzheimer’s.

Synthetic biologists from Yale were able to re-write the genetic code of an organism—a novel genomically recoded organism (GRO) with one stop codon—using a cellular platform that they developed enabling the production of new classes of synthetic proteins. These synthetic proteins, researchers say, offer the promise of innumerable medical and industrial applications that can benefit society and human health.

The creation of the landmark GRO, known as “Ochre”—which fully compresses redundant, or “degenerate” codons, into a single codon—is described in a new study published in the journal Nature. A codon is a sequence of three nucleotides in DNA or RNA that codes for a specific amino acid, which serves as the biochemical building blocks for proteins.

“This research allows us to ask fundamental questions about the malleability of genetic codes,” said Farren Isaacs, professor of molecular, cellular and at Yale School of Medicine and of biomedical engineering at Yale’s Faculty of Arts and Sciences, who is co-senior author of the paper. “It also demonstrates the ability to engineer the genetic code to endow multi-functionality into proteins and usher in a new era of programmable biotherapeutics and biomaterials.”

Every cell in the body normally has its fixed place as part of a tissue structure. Except for a few cell types, such as blood or immune cells. But cancer cells also cross established boundaries, grow into the surrounding tissue and multiply. And they can detach from the cell structure and spread via the blood or lymphatic vessels to other areas of the body, where they attach to new cells and form metastases.

The changes that undergo to metastasize are not yet fully understood. Rho (Ras-homologous) GTPases apparently play an important role. These proteins process signals within cells and regulate, among other things, growth, differentiation into the genetically predetermined cell type and cell migration.

Rho GTPases are molecular switches that switch between an active and an inactive state by binding to the phosphate compounds GTP and GDP. GTP corresponds to the ‘on’ position of the switch and starts the molecular biological processes, while GDP corresponds to the ‘off’ position and stops them.

Rice University researchers have revealed novel sequence-structure-property relationships for customizing engineered living materials (ELMs), enabling more precise control over their structure and how they respond to deformation forces like stretching or compression.

The study, published in a special issue of ACS Synthetic Biology, focuses on altering protein matrices, which are the networks of proteins that provide structure to ELMs. By introducing small genetic changes, the team discovered they could make a substantial difference in how these materials behaved. These findings could open doors for advancements in tissue engineering, drug delivery and even 3D printing of living devices.

“We are engineering cells to create customizable materials with unique properties,” said Caroline Ajo-Franklin, professor of biosciences and the study’s corresponding author. “While synthetic biology has given us tools to tweak these properties, the connection between genetic sequence, material structure and behavior has been largely unexplored until now.”

Phages are viruses that attack bacteria by injecting their DNA, then usurping bacterial machinery to reproduce. Eventually, they make so many copies of themselves that the bacteria burst. By looking at this process in a unique type of virus called a jumbo phage, scientists hope to learn how to make new antibiotics that can address the growing crisis of resistance.

The jumbo phage has more than four times the DNA of an average phage. It uses this to create a restricted space inside where it can copy its DNA while surrounded by a made of .

Researchers at UC San Francisco have discovered that the shield works via a set of “secret handshakes.” They allow only a specific set of useful proteins to pass through.

Professor Kwang-Hyun Cho’s research team of the Department of Bio and Brain Engineering at KAIST has captured the critical transition phenomenon at the moment when normal cells change into cancer cells and analyzed it to discover a molecular switch hidden in the genetic network that can revert cancer cells back into normal cells.

The team’s findings are published in the journal Advanced Science.

A critical transition is a phenomenon in which a sudden change in state occurs at a specific point in time, like water changing into steam at 100℃. This critical transition phenomenon also occurs in the process in which change into at a specific point in time due to the accumulation of genetic and .

The motivation behind the new study was to address these gaps in our understanding by leveraging the power of large-scale data. The researchers recognized that investigating the connection between genetic predisposition to dyslexia and brain structure in a very large sample could provide more robust and reliable insights than smaller, more traditional studies. They aimed to identify specific brain regions and white matter tracts that are associated with genetic risk for dyslexia, and to explore whether different genetic variants might influence distinct neural pathways.

“Thirty-five genetic variants that influence the chance of having dyslexia were already known from a very large study by the company 23andMe in the USA, carried out in over one million people. However, that study did not include brain MRI data. The new aspect of our study was to investigate the genetic variants in relation to brain structure in MRI data from thousands of people,” explained Clyde Francks (@clydefrancks), a professor at the Max Planck Institute for Psycholinguistics in Nijmegen and senior author of the study.

The researchers used two large datasets: the genetic data 23andMe and brain imaging data from over 30,000 adults in the UK Biobank. The 23andMe dataset helped identify genetic variants associated with dyslexia by comparing individuals who reported a dyslexia diagnosis to those who did not. These genetic variants were then used to calculate “polygenic scores” for individuals in the UK Biobank, reflecting their genetic predisposition to dyslexia.

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