Mapping to 1q23 of the human gene (NDUFS2) encoding the 49-kDa subunit of the mitochondrial respiratory Complex I and immunodetection of the mature protein in mitochondria

Procaccio, Vincent; Sury, Régis de; Martinez, Pascal; Depetris, Danielle; Rabilloud, Thierry; Lunardi, Joël; Issartel, Jean-Paul

doi:10.1007/s003359900803

Cited by 12 publications

(9 citation statements)

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“…1). Mit RLuc expression was nearly completely colocalized with the NDUFS2 and cytochrome c protein which are important components of the mitochondrial membrane respiratory chain (Procaccio et al 1998; Loeffen et al 2001; Waterhouse et al 2001) (Fig. 1, Supplemental Fig.…”

Section: Resultsmentioning

confidence: 99%

β₂- but not β₁-adrenoceptor activation modulates intracellular oxygen availability

Yan

Huo

et al. 2010

The Journal of Physiology

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β-Adrenoceptors (β-ARs) play a critical role in the regulation of cardiovascular function. Intracellular oxygen homeostasis is crucial for the survival of cardiomyocytes. However, it is still unclear whether β-AR activation can modulate intracellular oxygen. Here we used mitochondrial and cytosolic target Renilla luciferase to detect intracellular oxygen concentration. Pharmacological experiments revealed that β 2 -AR activation specifically regulates intracellular oxygen in cardiomyocytes and COS7 cells. This effect was abrogated by inhibitory G protein (G i ) inhibition, endothelial nitric oxide synthase (eNOS) blockade, and NO scavenging, implicating that the β 2 -AR-G i -eNOS pathway is involved in this regulation. β 2 -AR activation increased the AMP/ATP ratio, AMPK activity, ROS production and prolyl hydroxylase activity. These effects also contribute to the regulation of β 2 -AR signalling, thus providing an additional layer of complexity to enforce the specificity of β 1 -AR and β 2 -AR signalling. Collectively, the study provides novel insight into the modulation of oxygen homeostasis, broadens the scope of β 2 -AR function, and may have crucial implications for β 2 -AR signalling regulation.

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Section: Resultsmentioning

confidence: 99%

β₂- but not β₁-adrenoceptor activation modulates intracellular oxygen availability

Yan

Huo

et al. 2010

The Journal of Physiology

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“…3A). NDUFS2 is a known NADHubiquinone oxidoreductase 49 kDa subunit (42,43). NADH dehydrogenase contributes to site I of the mitochondrial electron transport chain (44).…”

Section: Discussionmentioning

confidence: 99%

Discovery of Predictive Biomarkers for Litter Size in Boar Spermatozoa*

Kwon

Rahman

Lee

et al. 2015

Molecular & Cellular Proteomics

124

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Conventional semen analysis has been used for prognosis and diagnosis of male fertility. Although this tool is essential for providing initial quantitative information about semen, it remains a subject of debate. Therefore, development of new methods for the prognosis and diagnosis of male fertility should be seriously considered for animal species of economic importance as well as for humans. In the present study, we applied a comprehensive proteomic approach to identify global protein biomarkers in boar spermatozoa in order to increase the precision of male fertility prognoses and diagnoses. We determined that L-amino acid oxidase, mitochondrial malate dehydrogenase 2, NAD (MDH2), cytosolic 5-nucleotidase 1B, lysozyme-like protein 4, and calmodulin (CALM) were significantly and abundantly expressed in high-litter size spermatozoa. We also found that equatorin, spermadhesin AWN, triosephosphate isomerase (TPI), Ras-related protein Rab-2A (RAB2A), spermadhesin AQN-3, and NADH dehydrogenase [ubiquinone] iron-sulfur protein 2 (NDUFS2) were significantly and abundantly expressed in low-litter size spermatozoa (>3-fold). Moreover, RAB2A, TPI, and NDUFS2 were negatively correlated with litter size, whereas CALM and MDH2 were positively correlated. This study provides novel biomarkers for the prediction of male fertility. To the best of our knowledge, this is the first work that shows significantly increased litter size using male fertility biomarkers in a field trial. Moreover, these protein markers may provide new developmental tools for the selection of superior sires as well as for the prognosis and diagnosis of male fertility.

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“…Decrease in subunits in patients' mitochondria was estimated by comparing the signal yielded by different dilutions of the patients' samples to the signal obtained for equivalent samples of control fibroblasts. Antibodies were raised in rabbit against peptides corresponding to the major complex I subunits (26,27) and the cytochrome c oxidase subunit II (COII). The anti-24 kDa bovine subunit antibody was a gift from M. Skehel and J. Walker (Medical Research Council, Cambridge, United Kingdom).…”

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confidence: 99%

Nuclear DNA origin of mitochondrial complex I deficiency in fatal infantile lactic acidosis evidenced by transnuclear complementation of cultured fibroblasts

Procaccio

Mousson²,

Beugnot³

et al. 1999

J. Clin. Invest.

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Mapping to 1q23 of the human gene (NDUFS2) encoding the 49-kDa subunit of the mitochondrial respiratory Complex I and immunodetection of the mature protein in mitochondria

Cited by 12 publications

References 0 publications

β₂- but not β₁-adrenoceptor activation modulates intracellular oxygen availability

β₂- but not β₁-adrenoceptor activation modulates intracellular oxygen availability

Discovery of Predictive Biomarkers for Litter Size in Boar Spermatozoa*

Nuclear DNA origin of mitochondrial complex I deficiency in fatal infantile lactic acidosis evidenced by transnuclear complementation of cultured fibroblasts

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Mapping to 1q23 of the human gene (NDUFS2) encoding the 49-kDa subunit of the mitochondrial respiratory Complex I and immunodetection of the mature protein in mitochondria

Cited by 12 publications

References 0 publications

β2- but not β1-adrenoceptor activation modulates intracellular oxygen availability

β2- but not β1-adrenoceptor activation modulates intracellular oxygen availability

Discovery of Predictive Biomarkers for Litter Size in Boar Spermatozoa*

Nuclear DNA origin of mitochondrial complex I deficiency in fatal infantile lactic acidosis evidenced by transnuclear complementation of cultured fibroblasts

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β₂- but not β₁-adrenoceptor activation modulates intracellular oxygen availability

β₂- but not β₁-adrenoceptor activation modulates intracellular oxygen availability