Insights image for "The newborn Fmr1 knockout mouse: a novel model of excess ubiquinone and closed mitochondrial permeability transition pore in the developing heart"

Pediatr Res. 2021 Feb;89(3):707. doi: 10.1038/s41390-020-01144-4. Epub 2020 Sep 12.

Authors

Matthew Barajas¹, Aili Wang¹, Keren K Griffiths¹, Kenji Matsumoto², Rui Liu², Shunichi Homma², Richard J Levy³

Affiliations

¹ Department of Anesthesiology, Columbia University Medical Center, New York, NY, USA.
² Department of Medicine, Columbia University Medical Center, New York, NY, USA.
³ Department of Anesthesiology, Columbia University Medical Center, New York, NY, USA. RL2740@cumc.columbia.edu.

PMID: 32919395
DOI: 10.1038/s41390-020-01144-4

No abstract available

Publication types

Research Support, N.I.H., Extramural

MeSH terms

Animals
Fragile X Mental Retardation Protein / genetics*
Fragile X Syndrome / genetics
Heart / physiology*
Mice
Mice, Knockout
Mitochondrial Permeability Transition Pore / metabolism*
Ubiquinone / metabolism*

Substances

Fmr1 protein, mouse
Mitochondrial Permeability Transition Pore
Ubiquinone
Fragile X Mental Retardation Protein

Grants and funding

R01 NS112706/NS/NINDS NIH HHS/United States