Celebrating Distinguished Scientists and Peer-Reviewed Publications in Promega R&D

Promega R&D Scientists were recently honored for publishing papers and patents between 2019-2023

“We are a company that is built upon innovation, and R&D is one of the main drivers of that,” says Frank Fan, Director of Biology at Promega.

Promega Research and Development is focused on developing reliable tools that address the biggest problems facing life scientists. However, our R&D scientists do much more than just develop products. Promega scientists regularly pursue basic research to curate new skills and knowledge and collaborate extensively with researchers across academia and industry. This work fuels major advancements in areas like targeted genome editing, drug discovery, and genetic identity.

In June 2023, our Research and Development department gathered to recognize Promega scientists who have published peer-reviewed papers or patents. This was the first time the department had held this event since 2019, and in that time 71 scientists have published research in journals like Nature and Cell. 16 of those scientists published 10 or more times, and several were also invited to contribute review articles and book chapters.

In addition, Promega also recognized seven researchers with the title “Distinguished Scientist.” This award was intended to recognize scientists who are at the top of their game in both advancing and communicating science. Their work includes protein engineering, chemical biology, neuroscience and much more.

The Distinguished Scientists were selected for having an i10 index above 25 since 2018. This indicates that the scientist has more than 25 publications that have been cited 10+ times in the past five years, as measured by Google Scholar. As VP of R&D Poncho Meisenheimer said, “This award is truly from the scientific community. This is a recognition that your scientific peers see your work as valuable.”

Here is the list of Promega researchers recognized as Distinguished Scientists and some of their recent high-impact papers.

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Phage Therapy: Meeting the Challenge of Drug-Resistant Bacterial Infections

Global pandemics, such as COVID-19, have taught us to abhor viruses. The emergence of new, highly infectious viruses is—rightfully so—a cause for concern. However, despite the average human body harboring 380 trillion viruses, most of them simply coexist with us and are harmless. When it comes to an ancient lineage of viruses within the realm Duplodnaviria, researchers are even using them as weapons in the battle against infectious diseases.

In 1915, Frederick William Twort, an English bacteriologist at the University of London, reported the discovery of an unusual “ultramicroscopic virus” (1). Twort was culturing vaccinia virus as part of an experiment to determine if he could prepare smallpox vaccines in vitro. These vaccines, made in calves, were typically contaminated with Staphylococcus bacteria. When Twort plated the vaccines, he found small, clear areas on the agar plates where the bacteria would not grow, and these clear areas were the source of his ultramicroscopic virus. Two years later, a French-Canadian microbiologist, Félix d’Hérelle, independently discovered a similar phenomenon when culturing Shigella bacteria from fecal samples of patients with bacillary dysentery. He called the new virus “un bactériophage obligatoire” (2). Shortly after his discovery, he found that bacteriophages (phages) could be used as powerful agents to treat a variety of bacterial infections, and the field of phage therapy was born (3).

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Genome-Wide CRISPR Screening: Putting Death on Hold

We share this planet with approximately 8.7 million species of plants and animals. Within such a diverse environment, it’s only natural that many complex relationships have developed among different species. Some relationships are mutually beneficial, some are parasitic—and some are lethal.

Genome wide - crisper screening to help with toxic compounds to humans

Natural toxins and venoms are biologically active compounds produced by normal metabolic processes in an organism but are harmful to other organisms. Typically, toxins are encountered passively or ingested by the affected organisms, and have a specific mode of action and binding site within a cell. In contrast, venoms are introduced directly into the victim through a specialized delivery mechanism, and they may consist of a mixture of compounds that affect a range of cell types and tissues (1). Both types of poisons are produced for predation, defense, or to offer a competitive advantage (1).

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Cell Tracking Using HaloTag: Why are Scientists Chasing Cells?

Cells, commonly considered the smallest unit of life, provide structure and function for all living things (3).

Eye of a fruit fly, Drosophila melanogaster, scanning electron microscopy. Scientists used HaloTag for cell tracking during eye development.
Eye of a fruit fly, Drosophila melanogaster, scanning electron microscopy

Because cells contain the fundamental molecules of life, in some situations such as yeast, a single cell can be considered the complete organism. In other situations, for more complex multicellular organisms, a multitude of cells can mature and acquire different, specialized functions (3).

Cells developing specificity are undergoing differentiation, a process where a cell’s genes are either turned “on” or “off” resultant in a more specific cell type. As these differentiated cells start to exhibit their identity, they organize themselves into the tissues, organs, and organ systems integral to the functioning of a multicellular, developing organism. This process in which order and form is created within a developing organism is referred to as morphogenesis (5).

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PARP and DDR Pathways: Targeting the DNA Damage Response for Cancer Treatment

Our cells, and the DNA they contain, are under constant attack from external factors such as ionizing radiation, ultraviolet light and environmental toxins. Internal cellular processes can also generate metabolites, such as reactive oxygen species, that damage DNA. In most cases, DNA damage results in permanent changes to DNA molecules, including DNA mismatches, single-strand breaks (SSBs), double-strand breaks (DSBs), crosslinking, or chemical alteration of bases or sugars. If left unchecked, DNA damage can cause genome instability, mutations and aberrant transcription, and oncogenic transformation.

PARP DDR pathway for drug discovery

Fortunately, our cells have also evolved multiple pathways to repair damaged DNA, collectively known as the DNA damage response (DDR). The type of repair mechanism depends on the nature of the damage, and whether the damage occurs in mitochondrial or nuclear DNA. These mechanisms have been reviewed extensively (1,2). Recently, considerable attention has focused on pathways for repairing SSBs and DSBs, mediated by the ADP-ribosylating enzyme known as poly (ADP-ribose) polymerase 1, or PARP-1.

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T Cells Newly Discovered Role in Alzheimer’s and Related Diseases Could Offer Another Therapeutic Approach

Alzheimer’s disease is a devastating, progressive degenerative brain condition that starts with mild   dementia symptoms like memory issues and gradually worsens to the point where you can no longer communicate or care for yourself. For anyone with personal experience with it, Alzheimer’s looms like a specter over the natural process of aging.

In the beginning phase of Alzheimer’s, abnormal plaques of the protein, amyloid-β, develop. These protein clumps can accumulate for decades with no detectable impact on cognitive ability or brain health. Eventually, a second protein, tau, begins to gather and form intercellular, fibrous, tangles. It is with the formation of these tau tangles that symptoms first appear. The combined presence of these extracellular plaques and intercellular tangles are the hallmarks of Alzheimer’s disease.

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Conversations: Nerve-Tumor Crosstalk in the Tumor Microenvironment

Cancer cells are characterized by features such as metabolic reprogramming and uncontrolled proliferation all of which are supported by underlying genomic instability, inflammation and the tumor microenvironment.

Cancer cells can be distinguished from normal cells by a variety of features including their ability to inappropriately activate signals for cell proliferation, evade growth suppression from contact inhibition or tumor suppressor activity, evade cell death signals, replicate DNA continually, induce angiogenesis, invade new tissues, reprogram their metabolism to provide energy for rapid proliferation, and evade immune detection (1) . Several biological processes are responsible for these features including genomic instability, inflammation, and the creation of a tumor microenvironment.

The tumor microenvironment is the network of non-malignant cells, connective tissue and blood vessels that surround and infiltrate the tumor. These surrounding “normal” cells interact with each other and the cancer cells and are important players in tumorigenesis. One cell type that is often found in the tumor microenvironment are nerve cells. In fact, cancer cells often express proteins that encourage nerve growth into the tumor microenvironment such as growth factors and axon-guidance molecules (2). Crosstalk between nerve cells and tumor cells can facilitate development of several cancer types (2) including pancreatic, head and neck, oral, prostate, and colorectal cancers.

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Monoclonal Antibody (mAb) Therapy to Delay the Onset of Type 1 Diabetes

On November 18, 2022, the US Food and Drug Administration (FDA) announced the approval of the first drug to delay the onset of stage 3 type 1 diabetes (T1D). The monoclonal antibody (mAb) drug, teplizumab, was approved for use in adults and pediatric patients 8 years and older.

3D illustration of a monoclonal antibody

The road to approval has been a bumpy one for the manufacturer, Provention Bio. In 2020, the FDA rejected the application for teplizumab due to several concerns, including the small size of the clinical trial. With the current approval, based on new clinical trial results, Provention Bio confirmed a co-promotion agreement with Sanofi US. The agreement included a $35 million Sanofi equity investment in the company.

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New Vaccine for Honeybees Could Take the Sting Out of Devastating American Foulbrood Disease

Our world is a complex, interdependent system, and invertebrate pollinators such as honeybees play a pivotal role in its survival. Threats to populations numbers of pollinators like honeybees can be equated to threats to the overall health and survival of the ecosystem in which they live. Of the over 20,000 known bee species, one—the western honeybee (Apis mellifera)—acts as the single most frequent pollinator for crops worldwide (1). Found on every continent except Antarctica, the western honeybee owes its status as a top pollinator to its widespread geographic distribution, generalist foraging behavior and competence as pollinators (1).

Deadly American Foulbrood Disease

Honeybees are the most economically valuable pollinators and are threatened by several pathogens (2). Perhaps the biggest threat to honeybee colony health and survival is the bacterial disease, American Foulbrood (AFB; (3). Caused by the spore-forming, Gram+ bacteria, Paenibacillus larvae, the highly contagious AFB disease affects the young brood of colonies.  When newly hatched larvae are fed spore-contaminated food, the spores germinate and replicate causing septicemia and death. P. larvae spores are incredibly resilient and can remain viable for decades (3). Each infected larva can produce over 1 billion new spores.  Thus, a colony can produce large numbers of spores with just a few cases of symptomatic brood (4).

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suPAR: A New Approach to Treating Cardiovascular Disease

Cardiovascular disease (CVD), continues to be the leading cause of death in the United States and worldwide. Many patients with CVD have signs of chronic kidney disease (CKD), and those with CKD are often times disproportionately affected by CVD.

This interconnectedness was further explored in a recent study published in the Journal of Clinical Investigation that identified a new immune target, suPAR, as a protein that causes kidney disease and atherosclerosis, the most common form of CVD. Unlike traditional approaches to treating CVD such as controlling blood pressure and lowering cholesterol, this breakthrough research offers a new approach to treatment from an entirely different perspective.

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