Welcome to Molecular and Integrative Physiology
In this post-genomic era, physiology is uniquely poised at the nexus between molecular function and whole animal integration with the goal of understanding how the functions of thousands of encoded proteins serve to bring about the highly coordinated behavior of cells and tissues underlying physiological functions in animals and how their dysfunction may lead to disease. Research and graduate training in the Department of Molecular & Integrative Physiology is focused on understanding the regulation and function of gene products at multiple levels of biological organization, from molecules and macromolecular complexes to cells, tissues, and whole organisms. With the tools of molecular genetics and modern systems biology, physiologists are at the forefront of dramatic advances currently occurring in life and biomedical sciences. Advanced training in molecular and integrative physiology will provide the necessary foundation to prepare for a career in this exciting area of functional biology.
Claudio Grosman, Head
MIP News
Using a suite of techniques both common and new to geology and biology, researchers, from left, M.D./Ph.D. student Jessica Saw, geologist and microbiologist Bruce Fouke, microscopy expert and plant biologist Mayandi Sivaguru and their colleagues made new discoveries about how kidney stones repeatedly grow and dissolve as they form inside the kidney.
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Molecular and integrative physiology professor Hee Jung Chung (left), postdoctoral fellow Eung Chang Kim (right), and their colleagues discovered that abnormal expression and phosphoinositide regulation of KCNQ/Kv7 potassium channels underlie neuronal hyperexcitability and injury in early-onset epileptic encephalopathy characterized by drug-resistant seizures and severe psychomotor retardation.
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The Kemper lab has recently published two high-profile papers on metabolic regulation in the Journal of Clinical Investigation and Nature Communications.
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Research scientist Kwan Young Lee, left, molecular and integrative physiology professor Nien-Pei Tsai and their colleagues discovered that an overabundance of the tumor suppressor protein p53 in neurons can lead to impaired regulation of neuronal excitability in a mouse model of Fragile X syndrome.
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