Ming-Feng Tsai
University of Virginia, VA·Biophysics
Mitochondria, the cell's power plants, constantly take in and release calcium ions. This traffic helps control energy production, cell-death pathways and calcium signals elsewhere in the cell.
- Fields
Biophysics
Physiology
Biochemistry
- Topics
mitochondria
Letm1
sodium-calcium exchanger
- Grants
- 1 known grant, through Feb 2029
What they work on
- Establish how MICU3, a neuron-specific subunit of the mitochondrial calcium uniporter, boosts the channel's calcium uptake, using biochemical, electrophysiological and structural methods.
- Identify the functional role of the MCUR1 subunit in the uniporter complex and characterize its molecular properties.
- Determine how small-molecule compounds inhibit or activate the mitochondrial calcium uniporter, to reveal new ways to control it with drugs.
- Measure the transport kinetics of the sodium/calcium exchanger NCLX in liposomes with defined sides, and test how it is blocked by drugs and regulated by oxidation of conserved cysteines.
- Test the hypothesis that Letm1 exchanges protons for calcium through the same swapping mechanism used by CLC proton/chloride exchangers, using liposome reconstitution and electrical recording.
More about the research
When it goes wrong, it can contribute to tissue damage after blood flow returns to oxygen-starved tissue, as well as to neurodegeneration, heart failure and cancer spread. Three proteins in the inner mitochondrial membrane handle this traffic, but how they work at the molecular level is still largely unclear.
Why it matters
Faulty mitochondrial calcium handling is linked to tissue injury after blood flow is restored, neurodegenerative disease, heart failure and cancer metastasis. Knowing exactly how these transport proteins work, and how small molecules turn them on or off, could guide future development of medicines for these conditions.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Michael Bround
Baylor College of Medicine, TX·Physiology·Early-career
Determine whether LETM1 drives proton/calcium exchange in heart mitochondria, using mice in which Letm1 is deleted from the heart to study heart function, mitochondrial function and how charged particles cross the mitochondrial membrane.
Lai-Hua Xie
Rutgers University-New Brunswick, NJ·Physiology
Determine whether the mitochondrial calcium uniporter (mCU), a channel admitting calcium into mitochondria, also carries iron into heart-cell mitochondria and drives calcium dysregulation, oxidative stress and iron-induced cardiac toxicity, in isolated myocytes and in vivo.
Shey-Shing Sheu
Thomas Jefferson University, PA·Physiology
Test whether hypertrophic stress raises levels of mitochondrial ryanodine receptor type 1 (mRyR1), a calcium channel, to boost mitochondrial calcium uptake and ATP production, using RyR1-overexpressing and other mouse models.
The school
University of Virginia: 43 labs on PI Pages, $814M a year on research, 413 research doctorates a year.
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