O18. Neuronal nitric oxide synthase trafficking into mitochondria involves the processing of the PDZ domain

Carreras, Marı́a Cecilia; Franco, María Clara; Molinas, María Florencia; González, Analía Silvia; Serra, María Pía; Finocchietto, Paola; Converso, Daniela P.; Poderoso, Juan José

doi:10.1016/j.niox.2008.06.019

Cited by 3 publications

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, the results indicated that mtNOS in mouse heart was the product encoded by the nNOS a gene. In this way, our current studies emphasize the importance of the processing of PDZ domain in nNOS translocation to mitochondria (18). This processing should explain the differences observed between cytosol and mitochondrial nNOS, after its translocation to the inner mitochondrial membrane.…”

Section: Mitochondrial Nitric Oxide Synthasesupporting

confidence: 66%

“…The mechanism of nNOS internalization into mitochondria is still unknown. We have recently observed that mtNOS is not detected in rat liver and brain mitochondria by anti-nNOS antibodies against the N-terminal region (aa 1-100, corresponding to the PDZ domain), while it is detected by antibodies against internal and C-terminal domains (12,18). These data suggest that the processing of cytosolic nNOS isoform during the import to rat liver and brain mitochondria requires the loss of the PDZ domain that could account for the reduction of their apparent molecular weight.…”

Section: Mitochondrial Nitric Oxide Synthasementioning

confidence: 99%

See 1 more Smart Citation

Mitochondrial Nitric Oxide Synthase: A Masterpiece of Metabolic Adaptation, Cell Growth, Transformation, and Death

Finocchietto

Franco

Holod

et al. 2009

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

Mitochondria are specialized organelles that control energy metabolism and also activate a multiplicity of pathways that modulate cell proliferation and mitochondrial biogenesis or, conversely, promote cell arrest and programmed cell death by a limited number of oxidative or nitrative reactions. Nitric oxide (NO) regulates oxygen uptake by reversible inhibition of cytochrome oxidase and the production of superoxide anion from the mitochondrial electron transfer chain. In this sense, NO produced by mtNOS will set the oxygen uptake level and contribute to oxidation-reduction reaction (redox)-dependent cell signaling. Modulation of translocation and activation of neuronal nitric oxide synthase (mtNOS activity) under different physiologic or pathologic conditions represents an adaptive response properly modulated to adjust mitochondria to different cell challenges.

show abstract

Section: Mitochondrial Nitric Oxide Synthasesupporting

confidence: 66%

Section: Mitochondrial Nitric Oxide Synthasementioning

confidence: 99%