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Gene Review

ATP5J  -  ATP synthase, H+ transporting,...

Homo sapiens

Synonyms: ATP synthase-coupling factor 6, mitochondrial, ATP5, ATP5A, ATPM, ATPase subunit F6, ...
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Disease relevance of ATP5J


High impact information on ATP5J


Biological context of ATP5J

  • At 3 days, the plasma level of CF6 correlated positively with the plasma CK peak value and correlated negatively with left ventricular ejection fraction [2].
  • The hydrolysis activity of ATP to ADP was increased by 1.6-fold by CF6 at 10(-7) M, and efrapeptin at 10(-5) M, an inhibitor of ATP synthase, blocked it [3].
  • Transfection experiments with deletional and mutational CF6 promoter constructs, and with dominant negative mutant IkappaB kinase alpha (K44M) demonstrated that shear-induced CF6 transcription was dependent on nuclear factor-kappa B (NF-kappaB) activation [6].
  • Thus, the biologically active site probably resides at the C-terminal portion of CF-6 peptides [7].
  • Accordingly, intravenous administration of CF-6, pCF-6, rat CF-6, and rat pCF-6 produced a modest but statistically significant increase in blood pressure and heart rate in urethane anesthetized rats, whereas the N-terminal rat pro-coupling factor-6, (24-52)-NH(2) and (33-52)-NH(2) caused no significant pressor response [7].

Anatomical context of ATP5J

  • Previous studies have shown that mitochondrial coupling factor 6 (CF6) is an endogenous peptide that inhibits prostacyclin (PGI2) synthesis in vascular endothelial cells [2].
  • Incubation of human umbilical vein endothelial cells (HUVECs) with an excess of free CF6 reduced by 50% the immunoreactivity for the antibody to beta-subunit of ATP synthase at the cell surface, but unaffected that for the alpha-subunit antibody [3].
  • Treatment of ECV-304 and HUVEC with TNF-alpha enhanced the release of CF6 in a dose-dependent manner concomitantly with the decrease in CF6 content in the mitochondria at 24 h [8].
  • We investigated the intracellular signaling mechanism for shear-induced release of CF6 in HUVEC and the effects of troglitazone and 15-deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2), both peroxisome proliferator-activated receptor (PPAR)-gamma ligands, on it [6].
  • Immunofluorescence microscopy of both ECV 304 and HUVECs confirmed the surface-associated immunoreactivity of anti-CF6 antibody on the plasma membrane [9].

Associations of ATP5J with chemical compounds

  • We investigated cross-sectionally the association between coupling factor 6 (CF6), an endogenous inhibitor of prostacyclin synthesis, and cardiovascular events in 95 hemodialysis patients [1].
  • Plasma CF6 level was positively correlated with serum creatinine level (r=0.36, P < 0.01) and was reduced after dialysis (P < 0.05) [1].
  • At 24 h after onset of AMI, the plasma CF6 levels correlated positively with plasma total cholesterol levels and low-density lipoprotein levels [2].
  • Coupling factor 6 (CF6), a component of adenosine triphosphate (ATP) synthase, is circulating and functions as an endogenous vasoconstrictor by inhibiting cytosolic phospholipase A2 [3].
  • Arachidonic acid release was suppressed by CF6, and it was reversed by efrapeptin at 10(-5) M or beta-subunit antibody or ADP at 10(-7) M [3].

Other interactions of ATP5J

  • Coupling factor 6 (F6) is a component of mitochondrial ATP synthase which is required for the interactions of the catalytic and proton-translocating segments [10].

Analytical, diagnostic and therapeutic context of ATP5J

  • RESULTS: Plasma levels of CF6 and ADMA were threefold higher in hemodialysis patients than in control individuals, and there was a positive correlation between these two compounds (r=0.25, P < 0.05) [1].
  • METHODS: Plasma CF6 level was measured by radioimmunoassay, whereas plasma ADMA level by high-performance liquid chromatography (HPLC) [1].
  • At 7 days after the onset of AMI, the plasma CF6 levels of patients who received no reperfusion were significantly higher than those of patients who received a successful reperfusion [2].
  • METHODS AND RESULTS: The release and gene expression of CF6 in HUVEC were enhanced by shear stress at 25 dyn/cm2, measured by radioimmunoassay and real-time RT-PCR, respectively [6].
  • Flow cytometry analysis revealed that the cell surface-associated CF6 was significantly increased at 24 h after TNF-alpha in a dose-dependent manner [8].


  1. Plasma concentration of coupling factor 6 and cardiovascular events in patients with end-stage renal disease. Osanai, T., Nakamura, M., Sasaki, S., Tomita, H., Saitoh, M., Osawa, H., Yamabe, H., Murakami, S., Magota, K., Okumura, K. Kidney Int. (2003) [Pubmed]
  2. Plasma mitochondrial coupling factor 6 in patients with acute myocardial infarction. Ding, W.H., Chu, S.Y., Jiang, H.F., Cai, d.a. .Y., Pang, Y.Z., Tang, C.S., Qi, Y.F. Hypertens. Res. (2004) [Pubmed]
  3. Intracellular signaling for vasoconstrictor coupling factor 6: novel function of beta-subunit of ATP synthase as receptor. Osanai, T., Magota, K., Tanaka, M., Shimada, M., Murakami, R., Sasaki, S., Tomita, H., Maeda, N., Okumura, K. Hypertension (2005) [Pubmed]
  4. Effect of vasoconstrictor coupling factor 6 on gene expression profile in human vascular endothelial cells: enhanced release of asymmetric dimethylarginine. Tanaka, M., Osanai, T., Murakami, R., Sasaki, S., Tomita, H., Maeda, N., Satoh, K., Magota, K., Okumura, K. J. Hypertens. (2006) [Pubmed]
  5. Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes. Zima, A.V., Kocksk??mper, J., Blatter, L.A. J. Physiol. (Lond.) (2006) [Pubmed]
  6. Troglitazone and 15-deoxy-delta(12,14)-prostaglandin J2 inhibit shear-induced coupling factor 6 release in endothelial cells. Tomita, H., Osanai, T., Toki, T., Sasaki, S., Maeda, N., Murakami, R., Magota, K., Yasujima, M., Okumura, K. Cardiovasc. Res. (2005) [Pubmed]
  7. Total synthesis of human and rat coupling factor-6 amide and pressor effects in the rat. Chang, J.K., Scruggs, P., Yang, J., Ouyang, M., Duetzmann, A., Dun, N.J. Regul. Pept. (2003) [Pubmed]
  8. Tumor necrosis factor alpha as an endogenous stimulator for circulating coupling factor 6. Sasaki, S., Osanai, T., Tomita, H., Matsunaga, T., Magota, K., Okumura, K. Cardiovasc. Res. (2004) [Pubmed]
  9. Mitochondrial coupling factor 6 is present on the surface of human vascular endothelial cells and is released by shear stress. Osanai, T., Okada, S., Sirato, K., Nakano, T., Saitoh, M., Magota, K., Okumura, K. Circulation (2001) [Pubmed]
  10. Human mitochondrial ATP synthase: cloning cDNA for the nuclear-encoded precursor of coupling factor 6. Javed, A.A., Ogata, K., Sanadi, D.R. Gene (1991) [Pubmed]
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