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Protein sensor for fatty acid buildup in mitochondria

nts. Most of the cell's energy-rich molecules called ATP are made in the mitochondria, and these ATP molecules serve as the "currency" with which the cell can "buy" all of the biochemical reactions that keep the cell alive and performing its functions. Virtually all cells have mitochondria, and disruption of their function can cause a variety of diseases.

"Our study showed the connection between the location of PanK2 in the mitochondria and its role in as a sensor of energy demand," said Yong-Mei Zhang, Ph.D., a researcher in the Infectious Diseases department at St. Jude and the report's senior author. "This is an ideal location for PanK2 because it can detect acylcarnitine as it enters the mitochondrion."

The importance of PanK2 is especially evident in individuals who have mutations in the PANK2 gene that give rise to PanK-associated neurodegeneration (PKAN), an inherited disease in which patients have intellectual impairment and difficulty in walking and speaking.

"The new understanding of PanK2 activity and its location in the cell suggests a potential treatment strategy for PKAN," said Roberta Leonardi, Ph.D., a postdoctoral fellow in the St. Jude Infectious Diseases department and first author of the PNAS article. "For example, reducing the level of fat in the diet and taking carnitine supplements might help PKAN patients cope with this debilitating disease."

"One of our challenges is how to develop an animal model of this disease that we can use to determine if reduced dietary fat and carnitine supplements offer hope in the treatment of PKAN in humans," said Suzanne Jackowski, Ph.D., a member of the Infectious Diseases department at St. Jude and a co-author of the report.


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Source:St. Jude Children's Research Hospital


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