Elucidating the role of ARID5A in central nervous system inflammation
Active Project Grant Awarded Last action
- Award ID
- F31NS149734
- Recipient
-
University Of California, San Diego UEI UYTTZT6G9DT1
- Awarding agency
-
National Institute of Neurological Disorders and Stroke
National Institutes of Health, Department of Health and Human Services
- Obligated
- $87,130
Award facts
- Assistance listing
- 93.853 Extramural Research Programs in the Neurosciences and Neurological Disorders
- Completion date 0% complete
- Originally
- Place of performance
- La Jolla, CA 92093, USA
Award details come from USAspending.gov.
Description
- Abstract
- Microglia are the resident immune cells of the central nervous system (CNS), playing essential roles in both tissue maintenance and injury response. In diseases like multiple sclerosis (MS), persistent microglial activation drives neuroinflammation, axonal injury, and neurodegeneration. Yet, the molecular mechanisms that maintain chronic microglial activation remain poorly defined, and no approved therapies directly target this compartment of disease. Although transcriptomic profiling has traditionally guided our understanding of inflammation, these approaches provide limited resolution over the rapid and reversible gene expression changes required for immune homeostasis. Post-transcriptional mechanisms, particularly those mediated by RNA-binding proteins (RBPS), enable more nuanced control of RNA fate. RBPS are emerging therapeutic targets in neurological disease in neurons, however, their function in microglial inflammation is largely unexplored. This proposal focuses on ARID5A, an RBP I have found to be upregulated in lesion-associated microglia in MS and experimental autoimmune encephalomyelitis (EAE), a model for MS. Preliminary studies show that ARID5A is required for sustained expression of interferon-stimulated genes in microglia, suggesting a central role in maintaining chronic CNS inflammation. This project will test the hypothesis that ARID5A enables microglia to sustain inflammatory gene expression by regulating RNA at multiple post-transcriptional checkpoints. I will define the cell autonomous role of ARID5A in microglial activation during CNS autoimmunity (aim 1), and how ARID5A controls protein output in inflammatory microglia using ribosome profiling (RIBO-SEQ) and RNA-SEQ in both primary mouse and human ipsc-derived microglia (aim 2). By uniting transcriptomic, translational, and regulatory profiling across complementary in vivo mouse and in vitro human systems, this work will define how dysregulated post-transcriptional control disrupts immune balance in microglia and contributes to chronic CNS inflammation. The complementary expertise of the YEO lab in RNA biology and the mendiola lab in neuroinflammation provides an ideal environment to execute this research plan and prepare me for a career as a physician-scientist in neuroimmunology and functional genomics.
Transactions
| Action | Obligated | Date |
|---|---|---|
| Amendment | $43,565 | |
| Amendment | $0 | |
| Original award | $43,565 |
Quick answers
Who received award F31NS149734?
F31NS149734 was awarded to University Of California, San Diego by National Institute of Neurological Disorders and Stroke (National Institutes of Health) on December 1, 2026.
How much is award F31NS149734 worth?
$87,130 has been obligated on F31NS149734.
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