Restoring the healthy form of a protein could revive blood vessel growth in premature infants’ lungs

A blood vessel organoid.
Video Credit: Yunpei Zhang and Enbo Zhu, Mingxia Gu Lab

A UCLA-led research team has discovered a molecular switch that determines whether tiny blood vessels in premature infants’ lungs can regenerate after injury. A failure of this repair process is a hallmark of bronchopulmonary dysplasia, or BPD, a serious lung disease that affects babies born very early. It arises from a combination of premature birth, inflammation or infection, and exposure to the high levels of oxygen and breathing support that are necessary to keep these infants alive during a critical period of lung development.

The researchers found that in BPD, the blood vessel cells in the lungs begin producing a shortened, nonfunctional isoform — a version of a protein — called NTRK2, which has been extensively studied in the nervous system but not in the pulmonary vasculature. When this shortened isoform dominates, the lung cannot rebuild the delicate network of tiny blood vessels needed for healthy breathing.

Capturing the moment a cell shuts the door on free radicals

The moment a cell shuts the door on free radicals.
Illustration Credit: Catrin Jakobsson, Lund University

For the first time, researchers have been able to show how a cell closes the door to free radicals – small oxygen molecules that are sometimes needed, but that can also damage our cells. The study is published in Nature Communications and was led by Lund University. 

For our cells to function, they need to maintain a careful balance between beneficial and harmful oxygen molecules known as free radicals. One of the most important is hydrogen peroxide – the same substance found in disinfectants, but which our cells use in very small amounts to send important signals. However, in excessive concentrations, hydrogen peroxide can cause damage and even cell death.  

Climate shapes arms race between ants and their social parasites

The "slave-making ant" Temnothorax americanus (left) and its host Temnothorax longispinosus
Photo Credit: ©: Romain Libbrecht

The battle between ant hosts and their social parasites is strongly influenced by climate. Temperature and humidity shape how the ants behave, communicate, and even evolve — while host and parasite respond with very different genetic strategies. These are the findings of two recent studies in which researchers at Johannes Gutenberg University Mainz (JGU) and the Senckenberg Biodiversity and Climate Research Centre combined behavioral experiments with state-of-the-art genomic analyses. "Climate clearly explains the variation in host and parasite behavior better than parasite prevalence itself," says Professor Susanne Foitzik, senior author of both studies and chair of Behavioral Ecology and Social Evolution at JGU.

In the first study, published in the Journal of Evolutionary Biology, the team examined a parasite, the so-called "slave-making ant" Temnothorax americanus, and its host, the ant Temnothorax longispinosus. The social parasite invades host nests and steals their brood, which later grows up to work for the parasite colony – an extraordinary form of social parasitism. The researchers focused on how the ants' behavior and chemical communication vary across different climates. By comparing ten natural populations along a 1,000‑kilometer north-south gradient in the United States, they found that climate influenced the conflict more strongly than the local frequency of parasite colonies.

UCLA team discovers how to target ‘undruggable’ protein that fuels aggressive leukemia

B-lymphoblastic leukemia, a type of blood cancer.
Image Credit: Courtesy of the Rao Laboratory.

Researchers at the UCLA Health Jonsson Comprehensive Cancer Center have identified a small molecule that can inhibit a cancer-driving protein long considered impossible to target with drugs — a discovery that could open the door to a new class of treatments for leukemia and other hard-to-treat cancers. 

The compound, called I3IN-002, disrupts the ability of a protein known as IGF2BP3 to bind and stabilize cancer-promoting RNAs, a mechanism that fuels aggressive forms of acute leukemia. The study published in the journal Haematologica, found the molecule not only slowed leukemic cell growth but also triggered cancer cell death and reduced the population of leukemia-initiating cells that sustain the disease.

“This project has been more than a decade in the making,” said Dr. Dinesh Rao, professor of pathology and laboratory medicine at the David Geffen School of Medicine at UCLA and senior author of the study. “We discovered IGF2BP3 years ago as an important driver in acute leukemias, and for a long time there were no tools to target it. To finally show that we can inhibit this protein and disrupt its function in cancer cells is incredibly exciting.” 

A delicate balance between growth hormone and stem cells

Andrei Chagin, Institute of Medicine, Sahlgrenska Academy at the University of Gothenburg.
Photo Credit: Magnus Gotander

Researchers at the University of Gothenburg can now demonstrate previously unexplained processes behind growth therapy. It involves hormonal mechanisms at the cellular level, with focus on a sensitive balance between stem cells and growth hormone. 

When children grow in length, it occurs from growth plates, a cartilage structure at both ends of the long bones found in the arms and legs. The growth plates contain special stem cells that continuously produce new cartilage cells, which are converted into bone tissue. 

In the case of growth disorders in children, with a height significantly below the average for their age and sex, injections of growth hormone are the most common treatment. In the development of growth hormone therapy, the University of Gothenburg has played a historically important role  

Previous research has shown that growth hormones act directly on the growth plate. However, it has been unclear which cells are targeted by growth hormones and how. 

How bacteria resist hostile attacks

Aggressor bacteria such as Acinetobacter baylyi (green) can rarely kill Pseudomonas aeruginosa (live cells in black, dying cells in cyan).
Image Credit: Alejandro Tejada-Arranz, Biozentrum, University of Basel

Some bacteria use a kind of molecular “speargun” to eliminate their rivals, injecting them with a lethal cocktail. Researchers at the University of Basel have now discovered that certain bacteria can protect themselves against these toxic attacks. But this defense comes with a surprising downside: it makes them more vulnerable to antibiotics. 

Countless bacterial species share cramped environments where competition for space and resources is fierce. Some rely on a molecular speargun to outcompete their opponents. One of them is Pseudomonas aeruginosa. It is widespread in nature but also notorious as a difficult-to-treat hospital pathogen. 

Pseudomonas can live peacefully in coexistence with other microbes. But when attacked by bacteria from a different species, it rapidly assembles its own nano-speargun – the so-called type VI secretion system (T6SS) – to inject its aggressor with a toxic cocktail. 

How can Pseudomonas strike back when it has already been hit by a deadly cocktail itself? The answer has now been uncovered by Professor Marek Basler’s team at the Biozentrum of the University of Basel and published in Nature Communications. 

Molecular Biology: In-Depth Description

Image Credit: Scientific Frontline / AI Generated

Molecular biology is the branch of biology that studies the molecular basis of biological activity. It focuses on the chemical and physical structure of biological macromolecules—specifically nucleic acids (DNA and RNA) and proteins—and how these molecules interact to regulate cell function, replication, and expression of genetic information. The primary goal of this field is to understand the intricate molecular machinery within a cell that governs life itself, from the synthesis of proteins to the regulation of gene expression.

Researchers identify kidney sensor that helps control fluid balance

Rose Hill, Ph.D., second from left,studies sensory nerves within the kidneys at OHSU. Her new study identified a protein that acts as a pressure sensor in the kidneys, which helps the body control fluids and blood pressure. With her are lab team members: Taylor Krilanovich, Lily Schainker and Janelle Doyle.
 Photo Credit: OHSU/Christine Torres Hicks

A new study has identified a critical “pressure sensor” inside the kidney that helps the body control blood pressure and fluid levels. The finding helps explain how the kidneys sense changes in blood volume — something scientists for decades have known occurs but didn’t have a mechanistic explanation.

Researchers at Oregon Health & Science University and collaborating institutions discovered that a protein called PIEZO2 acts as a mechanical sensor in the kidney. When blood volume changes, this protein helps trigger the release of renin, a hormone that starts a chain reaction known as the renin-angiotensin-aldosterone system, or RAAS. The system is one of the body’s main tools for keeping blood pressure stable and making sure the body has the right balance of salt and water.

Researchers identify key molecular mechanism in cell communication

Albert Lu (left) and Carles Enrich (right).
Photo Credit: Courtesy of University of Barcelona

A new study describes a key molecular mechanism that explains how cells exchange information through extracellular vesicles (EVs), small particles with great therapeutic potential. The results, published in the Journal of Extracellular Vesicles, reveal that the Commander protein complex, previously known for its role in membrane recycling, also coordinates the entry and internal destination of vesicles within the cell. This finding sheds light on the process of intercellular communication, which is fundamental to the development of new therapies and diagnostic tools.

The study was led by Professor Albert Lu, from the Faculty of Medicine and Health Sciences of the UB and the CELLEX Biomedical Research Centre (IDIBAPS-UB), and María Yáñez-Mó, from the Severo Ochoa Centre for Molecular Biology (CSIC-UAM). Carles Enrich, professor at the same faculty (IDIBAPS-UB), also participated. 

According to Albert Lu, “understanding how receptor cells capture and process extracellular vesicles is essential to understanding how our body communicates at the molecular level.” “Furthermore — he continues — this knowledge is key to harnessing the therapeutic and diagnostic potential of these vesicles, since their effectiveness depends on being able to direct them and have them captured by the appropriate target cells.” 

LJI scientists discover how T cells transform to defend our organs

The new study was led by Pandurangan Vijayanand, M.D., Ph.D., William K. Bowes Distinguished Professor at La Jolla Institute for Immunology
Photo Credit: Courtesy of La Jolla Institute for Immunology

We owe a lot to tissue resident memory T cells (TRM). These specialized immune cells are among the body’s first responders to disease. 

Rather than coursing through the bloodstream—as many T cells do—our TRM cells specialize in defending specific organs. They battle viruses, breast cancer, liver cancer, melanomas, and many other health threats. 

Pandurangan Vijayanand, M.D., Ph.D., William K. Bowes Distinguished Professor at La Jolla Institute for Immunology (LJI), has even shown that a greater density of TRM cells is linked to better survival outcomes in lung cancer patients.

What Is: Mitochondrion

Evolutionary Singularities and the Eukaryotic Dawn

The mitochondrion represents a biological singularity, a discrete evolutionary event that fundamentally partitioned life on Earth into two distinct energetic stratums: the prokaryotic and the eukaryotic. While colloquially reduced to the moniker of "cellular powerhouse," the mitochondrion is, in functional reality, a highly integrated endosymbiont that serves as the master regulator of eukaryotic physiology. It is the nexus of cellular respiration, the arbiter of programmed cell death, a buffer for intracellular calcium, and a hub for biosynthetic pathways ranging from heme synthesis to steroidogenesis. To comprehend the complexity of multicellular life, one must first dissect the intricate molecular sociology of this organelle.   

The origin of the mitochondrion is the subject of intense phylogenomic reconstruction. The prevailing consensus, the endosymbiotic theory, posits that the mitochondrion descends from a free-living bacterial ancestor—specifically a lineage within the Alphaproteobacteria—that entered into a symbiotic relationship with a host archaeal cell approximately 1.5 to 2 billion years ago. This was not a trivial acquisition but a transformative merger. The energetic capacity afforded by the internalization of a bioenergetic specialist allowed the host cell to escape the surface-area-to-volume constraints that limit prokaryotic genome size, facilitating the expansion of the nuclear genome and the development of complex intracellular compartmentalization. 

Genetic Engineering: Changing the Number of Chromosomes in Plants Using Molecular Scissors

For the first time, KIT researchers managed to reduce the number of chromosomes in a plant by fusing two chromosomes.
Illustration Credit: Michelle Rönspies – KIT

Higher yields, greater resilience to climatic changes or diseases – the demands on crop plants are constantly growing. To address these challenges, researchers at Karlsruhe Institute of Technology (KIT) are developing new methods in genetic engineering. In cooperation with other German and Czech researchers, they succeeded for the first time in leveraging the CRISPR/Cas molecular scissors for changing the number of chromosomes in the Arabidopsis thaliana model organism in a targeted way – without any adverse effects on plant growth. This discovery opens up new perspectives for plant breeding and agriculture.  

How the cheese-noodle principle could help counter Alzheimer's

Jinghui Luo is a researcher at the Center for Life Sciences at the Paul Scherrer Institute PSI. He studies accumulations of so-called amyloid proteins, which lead to nerve damage in the brain. His research aims to help mitigate neurodegenerative diseases such as Alzheimer's and Parkinson's in the long term.  Photo Credit: © Paul Scherrer Institute PSI/Markus Fischer

Researchers at the Paul Scherrer Institute PSI have clarified how spermine – a small molecule that regulates many processes in the body's cells – can guard against diseases such as Alzheimer's and Parkinson's: it renders certain proteins harmless by acting a bit like cheese on noodles, making them clump together. This discovery could help combat such diseases. The study has now been published in the journal Nature Communications.

Our life expectancy keeps rising – and as it does, age-related illnesses, including neurodegenerative diseases such as Alzheimer's and Parkinson's, become increasingly common. These diseases are caused by accumulations in the brain of harmful protein structures consisting of incorrectly folded amyloid proteins. Their shape is reminiscent of fibers or spaghetti. To date, there is no effective therapy to prevent or eliminate such accumulations. 

Scientists observe metabolic activity of individual lipid droplets in real time

LipiPB Red shows longer fluorescence lifetimes in stable lipid droplets (red) and shorter lifetimes as they undergo degradation (blue). This probe revealed that lipid droplets sequentially degrade, where lipolysis precedes lipophagy.
Image Credit: Issey Takahashi, Nagoya University

A research team has developed a fluorescent probe that allows scientists to visualize how individual lipid droplets break down inside living cells in real time. The probe changes its fluorescence properties depending on the chemical composition of each droplet, which allows researchers to observe not only their location within cells, but also their metabolic activity during lipid breakdown. The findings, published in the Journal of the American Chemical Society, may contribute to the development of new strategies to treat metabolic diseases such as obesity and diabetes, as well as cancers associated with abnormal lipid metabolism. 

“Lipid droplets are cellular organelles that not only store excess lipids but also play critical roles in lipid metabolism. However, understanding how individual droplets function has been challenging,” Professor Shigehiro Yamaguchi, from the Institute of Transformative Bio-Molecules (ITbM) at Nagoya University, explained. 

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. 

Thyroid gland new possible target for prostate cancer treatment

Lukas Kenner, visiting professor at the Department of Molecular Biology.
Photo Credit: Medizinische Universität Wien

A hormone produced in the thyroid gland can play a key role in the development of prostate cancer. This is shown in a new study by an international research group led by Umeå University, Sweden, and the Medical University of Vienna, Austria. By blocking a receptor for the hormone, the growth of tumor cells in the prostate was inhibited. In the long term, the discovery may open up a new way of attacking certain types of aggressive prostate cancer.

"The results indicate that the receptor in question is a driving force in the growth of cancer. Substances that block it could thus be a target for future drugs against prostate cancer," says Lukas Kenner, visiting professor at Umeå University and the one who has led the study that is published in Molecular Cancer.

The receptor in question is called thyroid hormone receptor Beta, TRβ. It binds the thyroid hormone triiodothyronine, T3. In laboratory experiments, the activation of T3 has led to a sharp increase in the number of prostate cancer cells. However, when the receptor TRβ was inhibited with the help of an active substance, NH-3, significantly reduced the growth of cancer cells. NH-3 is a substance that is only used in research to block TRβ.

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.

What Is: Hormones

The "Chemical Messenger"
The Endocrine System and Chemical Communication
Image Credit: Scientific Frontline

The Silent Orchestrators

Hormones are the silent orchestrators of the human body. They are the unseen chemical messengers that, in infinitesimally small quantities, conduct the complex symphony of life. These powerful molecules control and regulate nearly every critical function, from our mood, sleep, and metabolism to our growth, energy levels, and reproductive functions.

At its most fundamental level, a hormone is a chemical substance produced by a gland, organ, or specialized tissue in one part of the body. It is then released—typically into the bloodstream—to travel to other parts of the body, where it acts on specific "target cells" to coordinate function.

The power of this system, which has identified over 50 distinct hormones in humans, lies in its exquisite specificity. Although hormones circulate throughout the entire body, reaching every cell, they only affect the cells that are equipped to listen. This is governed by the "lock and key" principle: target cells possess specific "receptors," either on their surface or inside the cell, that are shaped to bind only to a compatible hormone. This report will delve into the world of these powerful molecules, exploring the intricate system that creates them, the chemical language they speak, and the profound, lifelong impact they have on our daily health and well-being.

OHSU researchers develop promising drug for aggressive breast cancer

New research reveals a drug developed by scientists at Oregon Health & Science University may develop into a new treatment for an especially aggressive form of breast cancer.
Photo Credit: Oregon Health & Science University

A new molecule developed by researchers at Oregon Health & Science University offers a promising avenue to treat intractable cases of triple-negative breast cancer — a form of cancer that is notoriously aggressive and lacks effective treatments.

In a study published today in the journal Cell Reports Medicine, researchers describe the effect of a molecule known as SU212 to inhibit an enzyme that is critical to cancer progression. The research was conducted in a humanized mouse model.

“It’s an important step forward to treat triple-negative breast cancer,” said senior author Sanjay V. Malhotra, Ph.D., co-director of the Center for Experimental Therapeutics in the OHSU Knight Cancer Institute. “Triple-negative breast cancer is an aggressive form of cancer and there are no effective drugs available right now.”

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.