A cellular protein, FGD3, boosts breast cancer chemotherapy, immunotherapy

The research team included, front row, from left: graduate student Junyao Zhu, biochemistry professor David Shapiro, and senior researcher Chengiian Mao; back row, from left: graduate students Abigail Spaulding, Xinyi Dai and Qianjin Jiang.
Photo Credit: Fred Zwicky

A naturally occurring protein that tends to be expressed at higher levels in breast cancer cells boosts the effectiveness of some anticancer agents, including doxorubicin, one of the most widely used chemotherapies, and a preclinical drug known as ErSO, researchers report. The protein, FGD3, contributes to the rupture of cancer cells disrupted by these drugs, boosting their effectiveness and enhancing anticancer immunotherapies.

The new findings were the happy result of experiments involving ErSO, an experimental drug that killed 95-100% of estrogen-receptor-positive breast cancer cells in a mouse model of the disease. ErSO upregulates a cellular pathway that normally protects cancer cells from stress, said University of Illinois Urbana-Champaign biochemistry professor David Shapiro, who led the new work with Illinois graduate student Junyao Zhu. But when that protective pathway is ramped up, the system goes awry.

How chromosomes separate accurately

Representation how separase recognizes the cohesin subunit SCC1 before chromosome segregation occurs.
Illustration Credit: © Margot Riggi

Cell division is a process of remarkable precision: during each cycle, the genetic material must be evenly distributed between the two daughter cells. To achieve this, duplicated chromosomes, known as sister chromatids, are temporarily linked by cohesin – a ring-shaped protein complex that holds them together until separation. Researchers at the University of Geneva (UNIGE), in collaboration with the National Cancer Institute (NCI) and the University of California, San Francisco (UCSF), have uncovered the mechanism by which separase – the molecular ‘‘scissors’’ responsible for this cleavage – recognizes and cuts cohesin. Their findings, published in Science Advances, shed new light on chromosome segregation errors that can lead to certain forms of cancer. 

Biochemistry: In-Depth Description

Image Credit: Scientific Frontline

Biochemistry is a branch of biology and chemistry that explores the chemical processes within and relating to living organisms. Its primary goal is to understand the chemical basis of life by studying the structure, function, and interactions of biological macromolecules.

This field seeks to answer fundamental questions about how collections of inanimate molecules interact to constitute, maintain, and perpetuate living organisms.

Nonsurgical treatment shows promise for targeted seizure control

Jerzy Szablowski
Photo Credit: Jeff Fitlow/Rice University

Rice University bioengineers have demonstrated a nonsurgical way to quiet a seizure-relevant brain circuit in an animal model. The team used low-intensity focused ultrasound to briefly open the blood-brain barrier (BBB) in the hippocampus, delivered an engineered gene therapy only to that region and later flipped an on-demand “dimmer switch” with an oral drug. The research shows that a one-time, targeted procedure can modulate a specific brain region without impacting off-target areas of the brain.

“Many neurological diseases are driven by hyperactive cells at a particular location in the brain,” said study lead Jerzy Szablowski, assistant professor of bioengineering and a member of the Rice Neuroengineering Initiative. “Our approach aims the therapy where it is needed and lets you control it when you need it, without surgery and without a permanent implant.”

Scientists Removed Amino Acids From the Diet of Lab Mice — and They Lost Weight

Legumes are a diverse group of plants from the Fabaceae family, including beans, peas, lentils, and peanuts, that grow in pods. They are a highly nutritious food, rich in protein, fiber, vitamins, and minerals, and are often considered a plant-based alternative to animal protein. Legumes also have the unique ability to fix nitrogen from the atmosphere, which benefits soil health.
Photo Credit: Shelley Pauls

It’s not pleasant to shiver from the cold, but for some, it has the appeal of making the body burn more energy as heat than when staying in a warmer environment. According to several studies, exposure to cold is a reliable way to boost energy expenditure in mice and humans. This process of burning energy through heat loss is called thermogenesis.

While scientists and pharmaceutical companies are exploring ways to trick the body into thinking it’s cold—so that it activates thermogenesis and burns energy without the need for ice baths or winter walks in a T-shirt—obesity researchers Philip Ruppert and Jan-Wilhelm Kornfeld from the Department of Biochemistry and Molecular Biology (BMB) set out to investigate another route:

A form of thermogenesis triggered by eating specialized diets rather than temperature.

Researchers decipher mechanism that prevents the loss of brown adipose tissue activity during ageing

From left to right, Tania Quesada-López, Francesc Villarroya, Albert Blasco-Roset, Marta Giralt, Alberto Mestres-Arenas, Joan Villarroya, Aleix Gavaldà-Navarro and Rubén Cereijo.
Photo Credit: Courtesy of University of Barcelona

As the body ages, brown adipose tissue activity decreases, fewer calories are burned, and this can contribute to obesity and certain chronic cardiovascular diseases that worsen with age. A study led by the University of Barcelona has identified a key molecular mechanism in the loss of brown fat activity during ageing. The study opens up new perspectives for designing strategies to boost the activity of this tissue and prevent chronic metabolic and cardiovascular diseases as the population ages.

The paper, published in the journal Science Advances, is led by Professor Joan Villarroya, from the Faculty of Biology and the Institute of Biomedicine of the UB (IBUB) — based at the Barcelona Science Park-UB  — and the CIBER Area for Physiopathology of Obesity and Nutrition  (CIBEROBN). Teams from the Albert Einstein College of Medicine in New York (United States) are also collaborating.

UQ scientists uncover secrets of yellow fever

Dr Summa Bibby
Photo Credit: The University of Queensland

University of Queensland researchers have captured the first high-resolution images of the yellow fever virus (YFV), a potentially deadly viral disease transmitted by mosquitoes that affects the liver.

They’ve revealed structural differences between the vaccine strain (YFV-17D) and the virulent, disease-causing strains of the virus.

Dr Summa Bibby from UQ’s School of Chemistry and Molecular Bioscience said despite decades of research on yellow fever, this was the first time a complete 3D structure of a fully mature yellow fever virus particle had been recorded at near-atomic resolution.

“By utilising the well-established Binjari virus platform developed here at UQ, we combined yellow fever’s structural genes with the backbone of the harmless Binjari virus and produced virus particles that could be safely examined with a cryo-electron microscope,” Dr Bibby said.

Scientists Produce Powerhouse Pigment Behind Octopus Camouflage

An octopus camouflages itself with the seafloor. UC San Diego scientists have discovered a new way to produce large amounts of xanthommatin, a natural pigment used in animal camouflage, in a bacterium for the first time.
Photo Credit: Charlotte Seid

Scientists at UC San Diego have moved one step closer to unlocking a superpower held by some of nature’s greatest “masters of disguise.”

Octopuses, squids, cuttlefish and other animals in the cephalopod family are well known for their ability to camouflage, changing the color of their skin to blend in with the environment. This remarkable display of mimicry is made possible by complex biological processes involving xanthommatin, a natural pigment.

Because of its color-shifting capabilities, xanthommatin has long intrigued scientists and even the military, but has proven difficult to produce and research in the lab — until now.

New switch for programmed cell death identified

During the analysis work: Prof. Franz Hagn (left) and Dr. Umut Günsel
Photo Credit: Astrid Eckert / TUM 

In the fight against disease, programmed cell death – also known as apoptosis – is a key protective function of the body. It breaks down cells that are damaged or have undergone dangerous changes. However, cancer cells often manage to override this mechanism. A research team at the Technical University of Munich (TUM) has now succeeded in identifying a new molecular switch in this process and elucidating how it works.

The activation and deactivation of apoptosis is a promising field of research in basic biomedical research. The team led by Prof. Franz Hagn from the Chair of Structural Membrane Biochemistry at the TUM School of Natural Sciences has now discovered a new switch: "Many research teams worldwide are working on the exciting topic of apoptosis and its targeted control. The big advantage is that we are dealing with a highly efficient, evolutionarily developed regulatory mechanism. So, we don't have to invent something completely new, but can use the appropriate structural methods to learn from nature's optimized processes."

Researchers decipher a mechanism that determines the complexity of the glucocorticoid receptor

Above, from left to right, Pilar Montanyà-Vallugera, José Luis Torbado-Gardeazábal, Inés Montoya-Novoa and Montse Abella-Monleón. Below, from left to right, Alba Jiménez-Panizo, Pablo Fuentes-Prior, Eva Estébanez-Perpiñá and Andrea Alegre-Martí.
Photo Credit: Courtesy of University of Barcelona

Drugs to treat inflammatory and autoimmune diseases — such as asthma, psoriasis, rheumatoid arthritis or Chrousos syndrome — act mainly through the glucocorticoid receptor (GR). This essential protein regulates vital processes in various tissues, so understanding its structure and function at the molecular level is essential for designing more effective and safer drugs. Now, a study published in the journal Nucleic Acids Research (NAR) has revealed the mechanism of multimerization — the association of different molecules to form complex structures — of the glucocorticoid receptor, a process critical to its physiological function.

Deciphering how the GR forms oligomers — through the binding of several subunits — opens a crucial avenue for developing more selective drugs. These new drugs could modulate this association and thus minimize serious adverse effects, such as immunosuppression or bone loss.

Nanopore signals, machine learning unlocks new molecular analysis tool

Illustration of voltage-matrix nanopore profiling. The artistic rendering depicts proteins (colored shapes) being analyzed by solid-state nanopores under varying voltage conditions. By combining nanopore signals with machine learning, researchers can discriminate protein mixtures and detect changes in molecular populations.
Image Credit: ©2025 Sotaro Uemura, The University of Tokyo

Understanding molecular diversity is fundamental to biomedical research and diagnostics, but existing analytical tools struggle to distinguish subtle variations in the structure or composition among biomolecules, such as proteins. Researchers at the University of Tokyo have developed a new analytical approach, which helps overcome this problem. The new method, called voltage-matrix nanopore profiling, combines multivoltage solid-state nanopore recordings with machine learning for accurate classification of proteins in complex mixtures, based on the proteins’ intrinsic electrical signatures.

The study, published in Chemical Science, demonstrates how this new framework can identify and classify “molecular individuality” without the need for labels or modifications. The research holds promise of providing a foundation that could lead to more advanced and wider applications of molecular analysis in various areas, including disease diagnosis.

In a surprising discovery, scientists find tiny loops in the genomes of dividing cells

MIT experiments have revealed the existence of “microcompartments,” shown in yellow, within the 3D structure of the genome. These compartments are formed by tiny loops that may play a role in gene regulation.
Illustration Credit: Ed Banigan, edited by MIT News
(CC BY-NC-ND 4.0)

Before cells can divide, they first need to replicate all of their chromosomes, so that each of the daughter cells can receive a full set of genetic material. Until now, scientists had believed that as division occurs, the genome loses the distinctive 3D internal structure that it typically forms.

Once division is complete, it was thought, the genome gradually regains that complex, globular structure, which plays an essential role in controlling which genes are turned on in a given cell.

However, a new study from MIT shows that in fact, this picture is not fully accurate. Using a higher-resolution genome mapping technique, the research team discovered that small 3D loops connecting regulatory elements and genes persist in the genome during cell division, or mitosis.

“This study really helps to clarify how we should think about mitosis. In the past, mitosis was thought of as a blank slate, with no transcription and no structure related to gene activity. And we now know that that’s not quite the case,” says Anders Sejr Hansen, an associate professor of biological engineering at MIT. “What we see is that there’s always structure. It never goes away.”

The Many FACES of Lipid Research

Subcellular lipid distributions (magenta) in mitochondria (green) revealed using FACES and super-resolution structure illuminated microscopy.
Image Credit: William Moore

Lipids are fatty molecules that play critical roles in cell function, including membrane structure, energy storage and nutrient absorption. Most lipids are made in a cell organelle called the endoplasmic reticulum, but specific lipid types are shuttled around to different parts of the cell depending on their purpose. Each organelle serves a specific role in a cell and has its own unique mixture of lipids called a lipidome.

Scientists have long wanted to get a closer look at the movement of lipids around a cell, but because organelles are so close together – often only tens of nanometers apart – it’s tough to visualize with traditional light microscopy, which only has resolutions up to 250 nanometers.

Now researchers at the University of California San Diego have unveiled a new technology with the power to see cells in unprecedented detail. The tool, called fluorogen-activating coincidence encounter sensing (FACES), was developed in Associate Professor of Biochemistry & Molecular Biophysics Itay Budin’s lab. This work appears in Nature Chemical Biology.

Why women's brains face higher risk: scientists pinpoint X-chromosome gene behind MS and Alzheimer's

Image Credit: Scientific Frontline / AI generated

New research by UCLA Health has identified a sex-chromosome linked gene that drives inflammation in the female brain, offering insight into why women are disproportionately affected by conditions such as Alzheimer’s disease and multiple sclerosis as well as offering a potential target for intervention. 

The study published in the journal Science Translational Medicine, used a mouse model of multiple sclerosis to identify a gene on the X chromosome that drives inflammation in brain immune cells, known as microglia. Because females have two X chromosomes, as opposed to only one in males, they get a “double dose” of inflammation, which plays a major role in aging, Alzheimer’s disease and multiple sclerosis.  

When the gene, known as Kdm6a, and its associated protein were deactivated, the multiple sclerosis-like disease and neuropathology were both ameliorated with high significance in female mice.  

Cholesterol-lowering drugs could reduce the risk of dementia

Low cholesterol can reduce the risk of dementia, a new University of Bristol-led study with more than a million participants has shown.

The research, led by Dr Liv Tybjærg Nordestgaard while at the University of Bristol and the Department of Clinical Biochemistry at Copenhagen University Hospital – Herlev and Gentofte, found that people with certain genetic variants that naturally lower cholesterol have a lower risk of developing dementia.

The study, which is based on data from over a million people in Denmark, England, and Finland, has been published in the journal Alzheimer's & Dementia: The Journal of the Alzheimer's Association. 

Some people are born with genetic variants that naturally affect the same proteins targeted by cholesterol-lowering drugs, such as statins and ezetimibe. To test the effect of cholesterol-lowering medication on the risk of dementia, the researchers used a method called Mendelian Randomization — this genetic analysis technique allowed them to mimic the effects of these drugs to investigate how they influence the risk of dementia, while minimizing the influence of confounding factors like weight, diet, and other lifestyle habits.

Programmable proteins use logic to improve targeted drug delivery

Therapies that are sensitive to multiple biomarkers could allow medicines to reach only the areas of the body where they are needed. The diagram above shows three theoretical biomarkers that are present in specific, sometimes overlapping areas of the body. A therapy designed to find the unique area of overlap between the three will act on only that area.
Image Credit: DeForest et al./Nature Chemical Biology

Targeted drug delivery is a powerful and promising area of medicine. Therapies that pinpoint the exact areas of the body where they’re needed — and nowhere they’re not — can reduce the medicine dosage and avoid potentially harmful “off target” effects elsewhere in the body. A targeted immunotherapy, for example, might seek out cancerous tissues and activate immune cells to fight the disease only in those tissues.

The tricky part is making a therapy truly “smart,” where the medicine can move freely through the body and decide which areas to target.

DNA nanospring measures cellular motor power

Experimental design for the force measurement of KIF1A.
An inert protein known as KIF5B serves as the anchor from which KIF1A pulls the nanospring. As with more familiar springs, the extended length correlates with the force being applied. But in this case, the DNA nanospring is also labeled with fluorescent molecules which give away how far it stretches to make visualization of KIF1A’s motile strength possible.
Image Credit: ©2025 Hayashi et al
(CC BY-ND 4.0)

Cells all require the transport of materials to maintain their function. In nerve cells, a tiny motor made of protein called KIF1A is responsible for that. Mutations in this protein can lead to neurological disorders, including difficulties in walking, intellectual impairment and nerve degradation. It’s known that mutations in KIF1A also result in a weakened motor performance, but this has been difficult to measure so far. Researchers including those from the University of Tokyo and the National Institute of Information and Communications Technology (NICT) in Japan have measured changes in the force of KIF1A using a nanospring, a tiny, coiled structure, made of DNA which could lead to improved diagnosis of diseases related to the protein’s mutations.

Cell death in microalgae resembles that in humans

Under the microscope, it is possible to see for the first time how microalgae undergo the same type of programmed cell death as animal cells. (Microalgae in purple and apoptotic bodies as small dots.)
 Image Credit: Luisa Fernanda Corredor Arias

For the first time, researchers at Umeå University have observed the same type of programmed cell death in microalgae as in humans. The discovery, published in Nature Communications, shows that this central biological process is older than previously thought.

“This is the first photosynthetic organism, and the first single-cell organism, shown to produce so called apoptotic bodies during cell death. This proves that apoptosis, a pathway of programmed cell death which was thought to be unique to animals, is more ancient and widespread than previously believed,” says Christiane Funk, Professor at the Department of Chemistry, Umeå University.

Cells can die naturally from age or disease, but organisms can also actively trigger the death of certain cells when needed. This is known as programmed cell death (PCD), a central biological system that allows the development of organs in our bodies and provides advantage during an organism’s life cycle. One example is the differentiation of fingers in a developing human embryo; others are the control of cell numbers or the elimination of non-functional cells.

Early changes during brain development may hold the key to autism and schizophrenia

Photo Credit: Michal Jarmoluk

Researchers at the University of Exeter have created a detailed temporal map of chemical changes to DNA through development and aging of the human brain, offering new insights into how conditions such as autism and schizophrenia may arise.

The team studied epigenetic changes – chemical tags on our DNA that control how genes are switched on or off. These changes are crucial in regulating the expression of genes, guiding brain cells to develop and specialize correctly.

One important mechanism, called DNA methylation, was examined in nearly 1,000 donated human brains, spanning life from just six weeks after conception through to 108 years of age. The researchers focused on the cortex, a region of the brain involved in high-level functions such as thought, memory, perception, and behavior. Correct development of the cortex during early life is important to support healthy brain function after birth.

Possible breakthrough in the development of effective biomaterials

Professor Dr. Shikha Dhiman from the Department of Chemistry of JGU
Photo Credit: © Ankit Sakhuja

When model cell membranes bind to biomaterials, it is not the binding strength but the speed of the receptors in the membranes that is crucial

Many hopes rested on so-called tissue engineering: With the help of stem cells, skin and other organs could be grown, thereby enabling better wound healing and better transplants. Although some of this is already a reality, the level expected around 20 years ago has not yet been achieved because the stem cells do not always bind to the required host material as they should in theory. An international research team led by chemist Professor Shikha Dhiman from Johannes Gutenberg University Mainz (JGU) has now found the reason for this: "Whether an interaction between model cell membrane and matrix material occurs depends not only on the strength of the interaction but also on the speed at which the binding partner molecules move. The understanding of this interaction that we have now gained is crucial for the development of effective biomaterials," says Dhiman. The team's results were recently published in the renowned scientific journal PNAS.