Author pages are created from data sourced from our academic publisher partnerships and public sources.
Share This Author
Complex III Releases Superoxide to Both Sides of the Inner Mitochondrial Membrane*
It is demonstrated that Complex I-dependent superoxide is exclusively released into the matrix and that no detectable levels escape from intact mitochondria, fitting well with the proposed site of electron leak at Complex I.
Tumor Evolution of Glioma-Intrinsic Gene Expression Subtypes Associates with Immunological Changes in the Microenvironment.
Genomic Classification of Cutaneous Melanoma
FoxOs cooperatively regulate diverse pathways governing neural stem cell homeostasis.
Trends in oxidative aging theories.
Denervation-induced skeletal muscle atrophy is associated with increased mitochondrial ROS production.
- F. Muller, Wook Song, H. Van Remmen
- BiologyAmerican journal of physiology. Regulatory…
- 1 September 2007
Enhanced generation of mitochondrial ROS may be a common factor in the mechanism underlying denervation-induced atrophy in aging, mice lacking CuZn-SOD, and in the neurodegenerative disease, amyotrophic lateral sclerosis.
Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy.
An inhibitor of oxidative phosphorylation exploits cancer vulnerability
Treatment with IACS-010759 robustly inhibited proliferation and induced apoptosis in models of brain cancer and acute myeloid leukemia (AML) reliant on OXPHOS, likely owing to a combination of energy depletion and reduced aspartate production that leads to impaired nucleotide biosynthesis.
Whole-genome and multisector exome sequencing of primary and post-treatment glioblastoma reveals patterns of tumor evolution.
This study used whole-genome sequencing and whole-exome sequencing of multiple sectors from primary and paired recurrent GBM tumors to reconstruct the genomic profile of residual, therapy resistant tumor initiating cells and found that genetic alteration of the p53 pathway is a primary molecular event predictive of a high number of subclonal mutations in glioblastoma.
Oncogenic NRAS signaling differentially regulates survival and proliferation in melanoma
A gradient model of oncogenic NRAS signaling in which the output is gated, resulting in the decoupling of discrete downstream biological phenotypes as a result of incomplete inhibition is suggested, offering a new framework to identify nonobvious coextinction target(s) for combined pharmacological inhibition in NRAS-mutant melanomas.