Ping Zhou
Weill Medical College of Cornell University, NY·Neuroscience
When blood flow to part of the brain is cut off, as in a stroke, neurons starved of oxygen begin to die. Mitochondria, the compartments that supply a cell's energy, sit at the center of whether a stressed neuron lives or dies.
- Fields
Neuroscience
Biochemistry
Medicine & Clinical Research
- Topics
prohibitin
S-nitrosylation
nitric oxide
- Grants
- 1 known grant, through May 2027
What they work on
- Test whether S-nitrosylation, the attachment of nitric oxide to a cysteine on the mitochondrial protein prohibitin (PHB), is required for PHB to protect neurons, using knock-in mice whose PHB cannot be nitrosylated in models of ischemic brain injury.
- Determine the mechanisms by which nitric oxide regulates PHB function, comparing normal mice with mutant knock-in mice carrying a PHB protein that lacks its sole cysteine residue.
- Examine how loss of PHB nitrosylation alters mitochondrial structure and function in the brain after ischemia, to establish whether disturbed nitrosylation contributes to neuronal injury and pathology.
More about the research
Prohibitin (PHB) is a mitochondrial protein that cells cannot do without: mice lacking it die as embryos, and no disease-causing mutation has been found in its coding region, suggesting the protein must stay intact. Work from this team has shown that PHB can protect the brain against ischemic injury, the damage caused by lost blood supply, through a mitochondria-based mechanism. How PHB's protective activity gets switched on, and how it goes wrong in disease, is still largely unknown, since the protein is stable at both the RNA and protein level.
Why it matters
Stroke and other neurological diseases tied to faulty mitochondria leave many patients with lasting brain damage. Showing how nitric oxide controls prohibitin's protective activity could point toward treatments aimed at mitochondria, which may eventually help patients at risk of stroke and related conditions. The work also adds basic understanding of what decides whether a stressed neuron survives or dies.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Elizabeth Jonas
Yale University, CT·Neuroscience
Test whether mice carrying a low-leak mutant ATP synthase c-subunit are protected from delayed hippocampal CA1 neuron death after transient global ischemia induced by two-vessel occlusion in aged animals.
Shermali Gunawardena
University at Buffalo, NY·Neuroscience
Test whether the N-terminal region of α-synuclein, the Parkinson's-linked protein, controls how mitochondria break into smaller pieces, using transgenic Drosophila carrying N-terminal deletions.
Cameron Mccarthy
University of South Carolina-Columbia, SC·Physiology
Test whether loss of OGT, the enzyme that adds O-GlcNAc sugar tags to proteins, protects parenchymal arterioles from dysfunction before stroke in mice made diabetic with a high-fat diet and low-dose streptozotocin.
The school
Weill Medical College of Cornell University: 35 labs on PI Pages, $1.6B a year on research, 59 research doctorates a year.
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