- Rita Allen Foundation

All Scholars

Since 1976, the Rita Allen Foundation has awarded millions of dollars in grants to early-career biomedical scholars. These grants allow Rita Allen Foundation Scholars to establish labs and pursue research directions with above-average risk and promise. See below for a full list of Scholars, or read more about the Rita Allen Foundation Scholars program.

2026

Haopeng Xiao +
Stanford University

Haopeng Xiao

Assistant Professor, Department of Biochemistry and Stanford Cancer Institute

B.A./B.S., Peking University, China

Ph.D., Georgia Institute of Technology

While the concept of metabolite signaling has transformed the metabolism field, a systematic and mechanistic understanding of how proteins and metabolites are co-regulated remains lacking. We develop mass spectrometry– and machine learning–based approaches to define how metabolism regulates protein function in vivo and how disease rewires protein-metabolite relationships.

In parallel, we recognized that endogenous metabolite regulation of protein function is conceptually analogous to pharmacological modulation of proteins by small molecules. This insight motivated my lab to develop mass spectrometry–based technologies to study small molecule–protein interactions, redefine protein ligandability and druggability, and to train machine learning models based on these datasets to guide the design of small molecules that modulate protein function. Ultimately, we aim to leverage these models to develop translational therapeutics for aging, metabolic disease, and cancer.
Hannah Meyer +
Cold Spring Harbor Laboratory

Hannah Meyer

Assistant Professor, Simons Center for Quantitative Biology

B.S., Heidelberg University, Germany

M.Sc., Heidelberg University, Germany

Ph.D., Cambridge University, United Kingdom

The immune system exists in an intricate balance. Inappropriate response to the body’s own antigens leads to autoimmunity, but a lack of appropriate response to foreign invaders results in immunodeficiency. The thymus plays a key role in establishing this balance by presenting the body’s self-antigens to developing T cells in a process called central tolerance induction. The overarching objective of the Meyer lab research program is to understand T-cell tolerance induction in the human thymus and its functional consequences. Thus far, insights into human thymus function have been mostly descriptive. The Meyer lab seeks to significantly extend this understanding by conducting mechanistic and functional studies of human thymus physiology, leveraging in silico and statistical models, genomics, and advanced imaging technologies.
Eirene Markenscoff-Papadimitriou +
Cornell University

Eirene Markenscoff-Papadimitriou

Assistant Professor, Department of Molecular Biology and Genetics

B.A., Harvard College

Ph.D., University of California San Francisco

Neurons are unusual cells: We’re born with them and keep the same ones for life, with no possibility of replacement or regeneration. This creates unique pressures on how their genes are switched on and off. Many neuronal genes are extraordinarily long, stretching over 100,000 DNA nucleotides, which makes them hard for the cell to read. They also sit in a precarious spot in the genome, right at the border between “open” DNA that can be read, and tightly packed “silent” DNA. This puts them at constant risk of being silenced, especially during development, when such mistakes can have lifelong consequences.

My lab studies a family of genes that evolved from ancient “jumping genes,” or transposable elements, that we are finding help keep vulnerable neuronal genes readable and expressed in the developing brain. One example is POGZ, a gene evolved from a transposon 500 million years ago that is mutated in White-Sutton syndrome, a syndromic form of intellectual disability. We think these repurposed ancient genes act as protectors, shielding the long, fragile genes neurons depend on to build and wire the brain.
Michael J. Lacagnina +
Cincinnati Children’s Hospital Medical Center

Michael J. Lacagnina

Assistant Professor, Department of Anesthesia

B.S., Arizona State University

Ph.D., Duke University

Immune cells and sensory neurons are in constant communication to coordinate host defense, but how this cellular conversation shapes sensory processing in health and disease remains an open question. To this end, the Lacagnina Lab is dedicated to unraveling how neuroimmune signaling influences the development and maintenance of chronic pain. We are particularly interested in exploring the role of B cells and their release of autoantibodies in the etiology of neuropathic pain. While the importance of B cells in autoimmune disease is well established, their contribution to nerve-injury-induced pain is largely unexplored. We aim to overcome this knowledge gap by deciphering how B cells communicate with neurons, glial cells, and other immune cells across tissues to shape pain pathogenesis, and by leveraging these discoveries to inform rational design of effective pain immunotherapies.
Aakanksha Jain +
University of Washington

Aakanksha Jain

Assistant Professor, Immunology

B.Tech., National Institute of Technology, Warangal, India

Ph.D., University of Texas Southwestern Medical Center

Neuropathic pain has long been viewed as a disorder of the nervous system alone. However, growing evidence shows that the immune system plays a critical role in driving pain, yet efforts to target it remain limited by an incomplete understanding of neuroimmune interactions. Our research focuses on defining the cellular and molecular pathways through which immune cells regulate pain through their interactions with sensory neurons. In particular, we study T cells, which are best known for their roles in fighting infection and cancer and driving autoimmunity. We have found that T cells infiltrate damaged nerves and exhibit features strikingly similar to those seen in autoimmune diseases. These findings raise the possibility that nerve injury triggers an autoimmune-like response that contributes to chronic pain. We aim to apply principles from autoimmune disease research to understand mechanisms of neuropathic pain with the long-term goal of immune-based therapies for chronic pain.
Wendy Yue +
University of California, San Francisco

Wendy Yue

Assistant Professor, Physiology

Milton E. Cassel Scholar

B.S., University of Hong Kong

Ph.D., Johns Hopkins University, School of Medicine

Most brain blood vessels are sealed by a tight barrier that protects the brain from harmful substances circulating in the blood. However, this barrier also limits the passage of many potential medicines, making it difficult to treat neurological diseases. Not all brain regions follow this rule, however. A handful of specialized areas lack this conventional barrier because they need to sense chemical signals from the body and release hormones into the bloodstream to regulate vital functions. The walls of blood vessels in these regions contain unique molecular structures that allow selective exchange between blood and brain tissues. Yet, despite their importance, the molecular identity and working principles of these structures remain poorly understood. Wendy Yue’s lab at UCSF aims to determine what these structures are made of and what governs their selectivity, knowledge that could guide the rational design of drugs capable of reaching the brain.
Naomi R. Latorraca +
Columbia University

Naomi R. Latorraca

Assistant Professor, Department of Biochemistry and Molecular Biophysics

B.A./B.S., University of Pittsburgh

Ph.D., Stanford University

The 800 human G protein–coupled receptors (GPCRs) represent molecular targets for various human diseases, from cognitive disorders to autoimmunity and cancer. In canonical GPCR signaling, diffusible ligands bind GPCRs to turn on signaling networks within the cell. GPCRs also interact with proteins on neighboring cell membranes to organize cellular contacts, but whether and how these interactions regulate GPCR signaling remains poorly understood. Our long-term objective is to harness such interactions to develop novel GPCR-targeted therapeutics, focusing on two questions: first, how do transcellular modulators alter the signaling profile of a GPCR and its sensitivity to known drugs? Second, how do adhesive forces at cellular interfaces modulate GPCR signaling? We monitor conformational changes in membrane-bound receptors using single-molecule fluorescence and integrate these measurements with physics-based simulations of receptor activation and signaling assays. Collectively, these data will identify new strategies and targets for modulating GPCR signaling in the lab and the clinic.

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