One Health in Action: Integrated Solutions for Animal Health Pathogens

For research use only

Introduction: Diagnostic Innovation for Zoonotic Threats

When a veterinarian detects influenza A in pigs, they’re not just protecting a herd; they’re helping safeguard public health through broad ongoing surveillance.

To support rapid, biosafe detection of Influenza A viruses (H5N1, H3N2, H1N1) in animal populations, Promega and Longhorn Vaccines and Diagnostics have partnered to create a workflow that doesn’t require BSL-3 containment. It’s scalable, field-ready, and designed with One Health in mind.

This work is part of our broader commitment to enabling real-time disease surveillance—across species and borders. Together with Longhorn, we’re building molecular diagnostics that meet the moment, and the future.

Want the technical details? Read the press release. 

Why It Matters: Influenza A and Diagnostic Bottlenecks

Influenza A viruses—including highly pathogenic strains like H5N1—pose a dual threat to animal health and human safety. Yet despite the urgency, many surveillance and research efforts stall at the lab bench. Why? Because working with zoonotic pathogens often requires high-containment (BSL-3) facilities—especially when dealing with real-world samples like cow milk, poultry swabs, or pig oral fluids.

To help overcome this barrier, Promega and Longhorn set out to design a complete diagnostic workflow that does more than just detect. It needed to:

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What Drives Muscle Fiber Shifts in Obesity and Type ll Diabetes?

Skeletal muscle is the body’s main consumer of glucose derived from food.

Muscle Fiber Types
Skeletal muscle is composed of two types of muscle fiber: Type I (slow-twitch) and Type II (fast-twitch).
Type I fibers contract slowly and can maintain contraction over long periods of time. They are rich in mitochondria and myoglobin and are well vascularized. These fibers rely mostly on aerobic metabolism to make the ATP that fuels cells. Type I muscle fibers are fatigue-resistant and efficient—great for supporting posture, distance running, cycling and any activity that needs steady output.

Type II fibers contract quickly, produce more force and power, but also fatigue more quickly. They have fewer mitochondria and less vasculature and rely more on anaerobic pathways like glycolysis (using glucose without oxygen).

Type I muscle fibers are smaller in diameter and generate less peak force but excel at endurance and heat management. Type II fibers are typically larger, produce more force and speed and handle explosive tasks like sprinting, jumping or heavy lifting.

Most muscles are a mix of fiber types, and genetics sets the starting ratio of Type l to Type ll, but fibers are adaptable. With aging and disuse, Type II fibers tend to atrophy more, which is one reason that power declines faster than endurance.

Another distinction important for this story: Type I fibers are more insulin-sensitive than Type II fibers. Additionally, these fiber types differ in different body types.

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Measure Engagement to Target Proteins within Complexes: Why Context Matters

This blog was written by guest contributor Tian Yang, Associate Product Manager, Promega, in collaboration with Kristin Huwiler, Manager, Small Molecule Drug Discovery, Promega.

For target-based drug discovery programs, biochemical assays using purified target proteins are often run for initial hit discovery, as these assays are target-specific, quantitative and amenable for high-throughput screens, allowing for precise characterization of target-compound interactions. However, proteins do not act in isolation inside the cells. Instead, proteins form complexes with other cellular components to drive cellular processes, signaling cascades, and metabolic pathways. Just as the interactions between a target protein and its binding partners can influence the target function, compound engagement with target proteins can vary depending on the protein complex formed.

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What Shelter Dogs Can Tell Us About Emerging Zoonotic Diseases

Why Are Zoonotic Diseases Becoming a Bigger Risk?

As of September 9, 2025, the Worldometer listed the human global population as 8.3 billion people (1). This population growth means that humans will be living and working in previously uninhabited or minimally disturbed environments, increasing interactions between humans, domestic animals, wildlife, and their pathogens. This intensifying human-animal interface heightens the risk of zoonotic disease transmission, where pathogens cross species barriers (from wildlife to domestic livestock or from wildlife to humans), potentially leading to outbreaks and even pandemics.

How Do Urbanization and Climate Change Amplify Zoonotic Threats?

Urbanization, habitat disruption, and climate change further exacerbate these risks by altering ecosystems and facilitating the spread and emergence of vector-borne and zoonotic diseases. Understanding and addressing these threats requires robust surveillance, effective diagnostics, and proactive strategies to prevent and mitigate disease emergence and spread.

In urban areas, public health officials are already using wastewater to monitor known pathogens and identify “hot spots” of activity to predict increases in illness within local populations (2). Animal shelters are another place where there is an opportunity to monitor for emerging infectious diseases that could affect domestic pet animals.

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Polyserine Targeting: A New Strategy Against Neurodegeneration

Neurodegenerative diseases like Alzheimer’s are marked by the accumulation of misfolded proteins that wreak havoc on neurons. One of the most notorious culprits is tau, a structural protein that, in its diseased form, clumps together into aggregates that spread throughout the brain. These aggregates interfere with normal cellular processes, leading to memory loss, behavioral changes, and other devastating symptoms. Preventing tau aggregation is therefore a key strategy for slowing the progression of these symptoms.

What if we could recruit molecular “helpers” to stop tau from accumulating?

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A New View of Protein Degradation with HiBiT and Live Cell Imaging

Targeted protein degradation (TPD) is an emerging drug discovery strategy that offers an entirely different approach to tackle disease-relevant proteins, including classic “undruggable” targets. Instead of inhibiting protein function, small molecules like PROTACs and molecular glues co-opt the cell’s own ubiquitin-proteasome system to eliminate specific proteins altogether. But as this targeted approach gains traction, it also challenges existing methods for validating compound activity.  

How do you confirm that degradation is happening in a biologically-relevant system? Can you validate protein degradation in real-time?  

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Exploring How NEAT1 Shapes Granulosa Cell Function

Granulosa Cells

Granulosa cells (GCs), which surround and support developing oocytes, play a critical role in estrogen production, follicle maturation and overall ovarian health (3). Their ability to regulate hormone production and cell survival makes them a central focus in studies of ovarian biology.

A recent study investigated how the long non-coding RNA (lncRNA) NEAT1 regulates GC function and mapped a pathway that links NEAT1 expression to cell proliferation, apoptosis and hormone production (1).

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At the Forefront of Biologics Characterization: Insights from Promega R&D Scientists 

As biologics grow more complex, so do the tools required to understand, validate, and ensure their quality. From monoclonal antibody cocktails to antibody-drug conjugates (ADCs) and cell therapies, developers are navigating new frontiers in potency, purity, and functional characterization. 

Promega’s R&D scientists have been actively contributing to this evolving dialogue through respected industry platforms like BioCompare and BEBPA. Through ongoing collaboration with industry experts, Promega scientists are developing innovative assays and strategies that address the complex challenges of biologics development and quality assurance. 

This article highlights key takeaways from five recent publications featuring Promega experts and collaborators, with insights spanning from early research to quality assurance in manufacturing. 

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Cellular Selectivity Profiling: Unveiling Novel Interactions and More Accurate Compound Specificity

This blog was written by guest contributor Tian Yang, Associate Product Manager, Promega, in collaboration with Kristin Huwiler, Manager, Small Molecule Drug Discovery, Promega.

Determining the selectivity of a compound is critical during chemical probe or drug development. In the case of chemical probes, having a clearly defined mechanism of action and specific on-target activity are needed for a chemical probe to be useful in delineating the function of a biological target of interest in cells. Similarly, optimizing a drug candidate for on-target potency and reducing off-target interactions is important in the drug development process (1,2). A thorough understanding of the selectivity profile of a drug can facilitate drug repurposing, by enabling approved therapeutics to be applied to new indications (3). Interestingly, small molecule drugs do not necessarily require the same selectivity as a chemical probe, since some drugs may benefit from polypharmacology to achieve their desired clinical outcome.

Selectivity profiling panels based on biochemical methods have commonly been used to assess compound specificity for established target classes in drug discovery and chemical probe development. Biochemical assays are target-specific and often quantitative, enabling direct measurements of compound affinities for targets of interest and facilitate comparison of compound engagement to a panel of targets. As an example, several providers offer kinase selectivity profiling services using different assay formats and kinase panels comprised of 100 to 400 kinases (4). However, just as biochemical target engagement does not always translate to cellular activity, selectivity profiles based on biochemical platforms may not reflect compound selectivity in live cells (5).

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Is Your Lab Environment Messing with Your Results? How to Spot the Signs Early

This blog was contributed by guest Avi Aggarwal, 2025 summer intern at Promega.

If you’ve ever scratched your head over inconsistent experimental results, especially ones that seem to fluctuate for no obvious reason—you’re not alone. Sometimes the problem isn’t your pipetting, your reagents, or even your protocol. It might be the room itself.

Changes in temperature, humidity, or even invisible dust particles can quietly throw off your results. Something as simple as moving your thermocycler under an air vent or setting up a plate reader where sunlight hits it in the afternoon could cause subtle but significant issues.

Scientist removes samples from liquid nitrogen tank, affecting the immediate laboratory environment.
Any number of things can affect the laboratory environment, from opening a cryo tank to moving an instrument under an air vent.

Our Project to Learn How Subtle Environmental Changes Can Affect Sensitive Lab Equipment

We spent some time developing an environmental anomaly detection framework aimed at helping scientists understand how subtle environmental changes can affect sensitive lab equipment and experimental results. Our team set out to monitor real-world lab conditions using temperature and humidity sensors, including live testing with a GloMax® Discover platform and Sensirion SHT45 sensors. We also worked with open-source environmental datasets to simulate a variety of lab-like conditions, such as daily cycles, sudden temperature spikes, and slow humidity drifts.

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