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Coupling factor 6 overexpression induced salt-sensitive hypertension, complicated by systolic cardiac dysfunction, but its onset was delayed in females. Estrogen has an important role in the regulation of coupling factor 6-mediated pathophysiology.
Overexpression of coupling factor 6 attenuates exercise-induced physiological cardiac hypertrophy by downregulating Akt (show AKT1 Proteins) signaling, thereby cancelling its benefit for cardiac function in mice.
CF6 plays a crucial role in the development of insulin (show INS Proteins) resistance and hypertension
coupling factor 6 induces the development of systolic dysfunction and upregulation of nicotinamide adenine dinucleotide phosphate oxidase (show DUOX1 Proteins) in the heart under the high-salt diet
CF6-induced increase in apoptotic cells was blocked by immature or mature IF1 (show ATPIF1 Proteins), being accompanied by protein kinase B (PKB (show AKT1 Proteins)) phosphorylation. IF1 (show ATPIF1 Proteins) antagonizes the pro-apoptotic action of CF6 by relief of intracellular acidification and resultant phosphorylation of PKB (show AKT1 Proteins).
Over-expression of the ATP5J gene correlates with cell migration and 5-fluorouracil sensitivity in colorectal cancer.
The phenotypic range of retinal, peripheral and central nervous system disease expression is characterized in a single family with NARP syndrome from the ATPase 6 m.8993T>C mtDNA point mutation.
coupling factor 6 induces the development of systolic dysfunction and upregulation of nicotinamide adenine dinucleotide phosphate oxidase (show DUOX2 Proteins) in the heart under the high-salt diet
CF6 is a novel risk factor for ischemic heart disease in end-stage renal disease. Synergism of this peptide and asymmetric dimethylarginine might contribute to its occurrence presumably by inhibition of prostacyclin and nitric oxide production.
Plasma CF6 elevated in patients with acute myocardial infarction. At 3 days, plasma CF6 correlated positively with plasma creatinine kinase peak value and correlated negatively with left ventricular ejection fraction.
Membrane-bound ATP synthase functions as a receptor for CF6 and may have a previously unsuspected role in the genesis of hypertension by modulating the concentration of intracellular hydrogen.
Increased CF6 may be responsible in part for decreased prostacyclin observed in coronary heart disease, in particular after PTCA and stent therapy. Potential risk factor for coronary heart disease.
in vascular endothelial cells both CF6 (coupling factor 6) and Angiotensin II downregulate PECAM-1 (platelet/endothelial cell adhesion molecule (show PECAM1 Proteins)) expression via activation of c-Src kinase (show CSK Proteins)
Mitochondrial ATP synthase catalyzes ATP synthesis, utilizing an electrochemical gradient of protons across the inner membrane during oxidative phosphorylation. It is composed of two linked multi-subunit complexes: the soluble catalytic core, F1, and the membrane-spanning component, Fo, which comprises the proton channel. The F1 complex consists of 5 different subunits (alpha, beta, gamma, delta, and epsilon) assembled in a ratio of 3 alpha, 3 beta, and a single representative of the other 3. The Fo seems to have nine subunits (a, b, c, d, e, f, g, F6 and 8). This gene encodes the F6 subunit of the Fo complex, required for F1 and Fo interactions. Alternatively spliced transcript variants encoding different isoforms have been identified for this gene. A pseudogene exists on chromosome Yp11.
ATP synthase-coupling factor 6, mitochondrial
, ATP synthase, H+ transporting, mitochondrial F0 complex, subunit F6
, OXPHOS complex V coupling factor 6
, ATP synthase coupling factor VI
, ATPase subunit F6
, mitochondrial ATP synthase coupling factor 6
, coupling factor 6
, mitochondrial ATP synthase, coupling factor 6
, mitochondrial ATP synthase, subunit F6
, mitochondrial ATPase coupling factor 6
, proliferation-inducing protein 36