D
Douglas C. Wallace
Researcher at Children's Hospital of Philadelphia
Publications - 495
Citations - 77420
Douglas C. Wallace is an academic researcher from Children's Hospital of Philadelphia. The author has contributed to research in topics: Mitochondrial DNA & Mitochondrion. The author has an hindex of 134, co-authored 475 publications receiving 72035 citations. Previous affiliations of Douglas C. Wallace include University of California & Stanford University.
Papers
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Journal ArticleDOI
Spectrum of pathogenic mtDNA mutations in Leber’s hereditary optic neuropathy families from Siberia
N. V. Volodko,M. A. L’vova,Elena B. Starikovskaya,Olga Derbeneva,I. Yu. Bychkov,Irina E. Mikhailovskaya,I. V. Pogozheva,F. F. Fedotov,G. V. Soyan,Vincent Procaccio,Douglas C. Wallace,Rem I. Sukernik +11 more
TL;DR: It is suggested that phylogenetically ancient mutations could have provided their carriers with the adaptive advantages upon the development of Central and Northern Europe at the end of the last glaciation, thereby, contributing to the preservation of weekly pathogenic LHON mutations, appearing at specific genetic background.
Proceedings ArticleDOI
Scanning Microwave Microscopy of Vital Mitochondria in Respiration Buffer
TL;DR: In this article, a scanning microwave microscopy (SMM) of vital mitochondria in respiration buffer is demonstrated using an electrophysiologically relevant liquid (hence conducting) environment.
Book ChapterDOI
Mitochondrial Myopathies: Genetic Aspects
TL;DR: This chapter discusses the genetic aspects of mitochondrial myopathies, which are the major producers of cellular adenosine triphosphate (ATP) by the process of oxidative phosphorylation (OXPHOS).
Journal ArticleDOI
Profiling genes related to mitochondrial function in mice treated with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
TL;DR: Since mitochondrial dysfunction plays an important role in the pathogenesis of dopaminergic neurodegeneration in Parkinson's disease, the expression of genes related to mitochondrial function in the substantia nigra of mice treated with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is determined using a cDNA array.
Journal ArticleDOI
Heteroplasmic mutations of the mitochondrial genome cause paradoxical effects on mitochondrial functions
Chengkang Zhang,Vincent Huang,Mariella Simon,Lokendra Kumar Sharma,Weiwei Fan,Richard H. Haas,Douglas C. Wallace,Yidong Bai,Taosheng Huang +8 more
TL;DR: The results suggest that the phenotype caused bymtDNA mutations may depend on the availability of the nutrients, and this gene‐environment interaction may contribute to the complexity of pathogenesis and clinical phenotypes caused by mtDNA mutation.