Transcriptional profiling for understanding the basis of mitochondrial involvement in disease and toxicity using the mitochondria-specific MitoChip.
It is well documented that mitochondrial dysfunction significantly contributes to a number of degenerative diseases, metabolic disorders, and drug- and chemical-induced toxicities. Thus far, information gained by several molecular and biochemical techniques used to delineate the mechanism of impaired mitochondrial activity underlying different diseases and various toxicities is still limited due to their low throughput potential. Here, we describe the development of mitochondria-specific mouse oligonucleotide microarray and its potential to define mechanisms of disease progression and drug toxicities associated with mitochondrial dysfunction at both nuclear and mitochondrial genome level.
Desai
Varsha G
VG
Center for Functional Genomics, Division of Systems Toxicology, National Center for Toxicological Research, U.S. Food and Drug Administration, 3900 NCTR Road, HFT-130, Jefferson, AR 72079, USA. varsha.desai@fda.hhs.gov
Fuscoe
James C
JC
D000818:Animals; D004272:DNA, Mitochondrial / Q000378:metabolism*; D018450:Disease Progression; D005260:Female; D020869:Gene Expression Profiling / Q000379:methods*; D019259:Lamivudine / Q000494:pharmacology; D051379:Mice; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods*; D018894:Reverse Transcriptase Inhibitors / Q000494:pharmacology; D015215:Zidovudine / Q000494:pharmacology
D004272:DNA, Mitochondrial; D018894:Reverse Transcriptase Inhibitors; D019259:Lamivudine; D015215:Zidovudine