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anti-Mouse (Murine) ATP5J Anticorps:
anti-Human ATP5J Anticorps:
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Human Polyclonal ATP5J Primary Antibody pour ICC, IF - ABIN4282288
Uhlén, Oksvold, Älgenäs, Hamsten, Fagerberg, Klevebring, Lundberg, Odeberg, Pontén, Kondo, Sivertsson: Antibody-based protein profiling of the human chromosome 21. dans Molecular & cellular proteomics : MCP 2012
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 signaling, thereby cancelling its benefit for cardiac function in mice.
CF6 plays a crucial role in the development of insulin resistance and hypertension
coupling factor 6 induces the development of systolic dysfunction and upregulation of nicotinamide adenine dinucleotide phosphate oxidase in the heart under the high-salt diet
identification of functional elements in bi-directional promoter
AKT2 and XIST expression was identified as a potential biomarker participating in the effect of ATP5J in colorectal cancer
CF6-induced increase in apoptotic cells was blocked by immature or mature IF1, being accompanied by protein kinase B (PKB) phosphorylation. IF1 antagonizes the pro-apoptotic action of CF6 by relief of intracellular acidification and resultant phosphorylation of PKB.
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.
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.
Mutation analysis revealed the T9176C mutation in the mtATPase 6 gene (OMIM 516060) and the mutation load was above 90% in the patients with Leigh syndrome.
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.
T8993G allele causes severe extrapyramidal dysfunction and Leigh disease but there is no correlation between the degree of enzyme deficiency and the severity of the phenotype.
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) expression via activation of c-Src kinase
Coupling factor 6 enhances Src-mediated responsiveness to angiotensin II in resistance arterioles and cells.
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