Hypothyroid phenotype is contributed by mitochondrial complex I inactivation due to translocated neuronal nitric-oxide synthase. [electronic resource]
Producer: 20060504Description: 4779-86 p. digitalISSN:- 0021-9258
- Animals
- Cyclin D1 -- metabolism
- Cytosol -- metabolism
- Electron Transport Complex I -- metabolism
- Electrons
- Electrophoresis, Polyacrylamide Gel
- HSP90 Heat-Shock Proteins -- metabolism
- Hypothyroidism -- metabolism
- Immunoblotting
- Immunoprecipitation
- Liver -- enzymology
- MAP Kinase Signaling System
- Male
- Microscopy, Immunoelectron
- Mitochondria -- metabolism
- Mitochondria, Liver -- metabolism
- Models, Chemical
- NG-Nitroarginine Methyl Ester -- pharmacology
- Nitric Oxide Synthase -- metabolism
- Nitric Oxide Synthase Type I -- metabolism
- Oxidants -- metabolism
- Oxygen -- metabolism
- Peroxynitrous Acid -- chemistry
- Phenotype
- Protein Isoforms
- Protein Transport
- RNA, Messenger -- metabolism
- Rats
- Rats, Wistar
- Reactive Oxygen Species -- metabolism
- Reverse Transcriptase Polymerase Chain Reaction
- Signal Transduction
- Subcellular Fractions -- metabolism
- Thyroid Hormones -- metabolism
- Transcription, Genetic
- p38 Mitogen-Activated Protein Kinases -- metabolism
No physical items for this record
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
There are no comments on this title.
Log in to your account to post a comment.