Toward understanding the role of mitochondrial complex II in the intraerythrocytic stages of Plasmodium falciparum: Gene targeting of the Fp subunit

2012 ◽  
Vol 61 (4) ◽  
pp. 726-728 ◽  
Author(s):  
Takeshi Q. Tanaka ◽  
Makoto Hirai ◽  
Yoh-ichi Watanabe ◽  
Kiyoshi Kita
Keyword(s):  
Plasmodium Falciparum ◽  
Gene Targeting ◽  
Mitochondrial Complex ◽  
Complex Ii

scholarly journals The Emerging Role of Succinate Dehyrogenase Genes (SDHx) in Tumorigenesis

2019 ◽  
Author(s):  
Elham Nazar ◽  
Fatemeh Khatami ◽  
Hiva Saffar ◽  
Seyed Mohammad Tavangar
Keyword(s):  
Normal Cell ◽  
Neoplastic Transformation ◽  
Genetic Alterations ◽  
Epigenetic Changes ◽  
Epigenetic Alterations ◽  
Mitochondrial Complex ◽  
Complex Ii ◽  
Hypoxic Conditions ◽  
Sdh Mutation

Transformation of a normal cell to cancerous one is dependent on the accumulation of several genetic and epigenetic alterations. One of the candidate driver genetic alterations can happen in succinate dehydrogenases (SDHx) coding gene include SDHA, SDHB, SDHC, SDHD, and SDHAF2.  The most important SDH mutation is in the SDHD gene, which encodes the smallest subunit of mitochondrial complex II (SDH). It has key function both in familial and non-familial hereditary paraganglioma/phaeochromocytoma syndrome (HPGL/PCC). SDHx genes mutations can have resulted in genetic and epigenetic changes like histone hypermethylation. These properties can lead to succinate-mediated inhibition of α-ketoglutarate-dependent dioxygenases. So hypoxic conditions can generate subsequent neoplastic transformation, and in this review, we are presenting the role of SDHx in several malignancies.

scholarly journals Complex effects of pH on ROS from mitochondrial complex II driven complex I reverse electron transport challenge its role in tissue reperfusion injury

2020 ◽  
Author(s):  
Alexander S. Milliken ◽  
Chaitanya A. Kulkarni ◽  
Paul S. Brookes
Keyword(s):  
Electron Transport ◽  
Complex I ◽  
Ischemia Reperfusion ◽  
Mitochondrial Complex ◽  
Complex Ii ◽  
Effects Of Ph ◽  
Cellular Necrosis ◽  
Reverse Electron Transport ◽  
The Impact

ABSTRACTGeneration of mitochondrial reactive oxygen species (ROS) is an important process in triggering cellular necrosis and tissue infarction during ischemia-reperfusion (IR) injury. Ischemia results in accumulation of the metabolite succinate. Rapid oxidation of this succinate by mitochondrial complex II (Cx-II) during reperfusion reduces the co-enzyme Q (Co-Q) pool, thereby driving electrons backward into complex-I (Cx-I), a process known as reverse electron transport (RET), which is thought to be a major source of ROS. During ischemia, enhanced glycolysis results in an acidic cellular pH at the onset of reperfusion. While the process of RET within Cx-I is known to be enhanced by a high mitochondrial trans-membrane ΔpH, the impact of pH itself on the integrated process of Cx-II to Cx-I RET has not been fully studied. Using isolated mitochondria under conditions which mimic the onset of reperfusion (i.e., high [ADP]). We show that mitochondrial respiration (state 2 and state 3) as well as isolated Cx-II activity are impaired at acidic pH, whereas the overall generation of ROS by Cx-II to Cx-I RET was insensitive to pH. Together these data indicate that the acceleration of Cx-I RET ROS by ΔpH appears to be cancelled out by the impact of pH on the source of electrons, i.e. Cx-II. Implications for the role of Cx-II to Cx-I RET derived ROS in IR injury are discussed.

scholarly journals Role of complex II in anaerobic respiration of the parasite mitochondria from Ascaris suum and Plasmodium falciparum

2002 ◽  
Vol 1553 (1-2) ◽  
pp. 123-139 ◽  
Author(s):  
Kiyoshi Kita ◽  
Hiroko Hirawake ◽  
Hiroko Miyadera ◽  
Hisako Amino ◽  
Satoru Takeo
Keyword(s):  
Plasmodium Falciparum ◽  
Ascaris Suum ◽  
Anaerobic Respiration ◽  
Complex Ii

scholarly journals A role of mitochondrial complex II defects in genetic models of Huntington's disease expressing N-terminal fragments of mutant huntingtin

2013 ◽  
Vol 22 (19) ◽  
pp. 3869-3882 ◽  
Author(s):  
Maria Damiano ◽  
Elsa Diguet ◽  
Carole Malgorn ◽  
Marilena D'Aurelio ◽  
Laurie Galvan ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Genetic Models ◽  
Mutant Huntingtin ◽  
Mitochondrial Complex ◽  
Complex Ii

scholarly journals Ubiquinone-binding site mutagenesis reveals the role of mitochondrial complex II in cell death initiation

2015 ◽  
Vol 6 (5) ◽  
pp. e1749-e1749 ◽  
Author(s):  
K Kluckova ◽  
M Sticha ◽  
J Cerny ◽  
T Mracek ◽  
L Dong ◽  
...  
Keyword(s):  
Cell Death ◽  
Binding Site ◽  
Mitochondrial Complex ◽  
Complex Ii ◽  
Site Mutagenesis ◽  
Ubiquinone Binding

scholarly journals Ndufs4 ablation decreases synaptophysin expression in hippocampus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Subrata Kumar Shil ◽  
Yoshiteru Kagawa ◽  
Banlanjo Abdulaziz Umaru ◽  
Fumika Nanto-Hara ◽  
Hirofumi Miyazaki ◽  
...  
Keyword(s):  
Nadh Dehydrogenase ◽  
Leigh Syndrome ◽  
Mitochondrial Respiratory Chain ◽  
Mitochondrial Activity ◽  
Mitochondrial Complex ◽  
Neuronal Function ◽  
Mouse Hippocampus ◽  
Extracellular Regulated Kinase ◽  
Presynaptic Protein

AbstractAltered function of mitochondrial respiratory chain in brain cells is related to many neurodegenerative diseases. NADH Dehydrogenase (Ubiquinone) Fe-S protein 4 (Ndufs4) is one of the subunits of mitochondrial complex I and its mutation in human is associated with Leigh syndrome. However, the molecular biological role of Ndufs4 in neuronal function is poorly understood. In this study, upon Ndufs4 expression confirmation in NeuN-positive neurons, and GFAP-positive astrocytes in WT mouse hippocampus, we found significant decrease of mitochondrial respiration in Ndufs4-KO mouse hippocampus. Although there was no change in the number of NeuN positive neurons in Ndufs4-KO hippocampus, the expression of synaptophysin, a presynaptic protein, was significantly decreased. To investigate the detailed mechanism, we silenced Ndufs4 in Neuro-2a cells and we observed shorter neurite lengths with decreased expression of synaptophysin. Furthermore, western blot analysis for phosphorylated extracellular regulated kinase (pERK) revealed that Ndufs4 silencing decreases the activity of ERK signalling. These results suggest that Ndufs4-modulated mitochondrial activity may be involved in neuroplasticity via regulating synaptophysin expression.

scholarly journals The Central Role of cAMP in Regulating Plasmodium falciparum Merozoite Invasion of Human Erythrocytes

2014 ◽  
Vol 10 (12) ◽  
pp. e1004520 ◽  
Author(s):  
Amrita Dawn ◽  
Shailja Singh ◽  
Kunal R. More ◽  
Faiza Amber Siddiqui ◽  
Niseema Pachikara ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Human Erythrocytes ◽  
Merozoite Invasion ◽  
Falciparum Merozoite
Sign in / Sign up

Export Citation Format

Share Document