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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

ATP synthase, H+ transporting, mitochondrial Fo complex, subunit F6

coupling factor 6, ATP synthase coupling factor 6, Atp5j
coupling factor 6 of the mitochondrial ATP synthase complex [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: ACID, ATPase, HAD, V1a, CAN
Papers on coupling factor 6
Mitochondrial coupling factor 6 upregulation in hypertension-induced cardiac hypertrophy.
New
Dai et al., Jinan, China. In Herz, Aug 2015
BACKGROUND: Mitochondrial coupling factor 6 (CF6) is a constriction factor in cardiac hypertrophy, whose mechanisms are not fully understood.
Maternal age and in vitro culture affect mitochondrial number and function in equine oocytes and embryos.
New
Stout et al., In Reprod Fertil Dev, May 2015
Effects of mare age (TFAM), mtDNA polymerase ? subunit B (mtPOLB) and mitochondrial single-stranded DNA-binding protein (SSB)), energy production (ATP synthase-coupling factor 6, mitochondrial-like (ATP-synth_F6)) and oxygen free radical scavenging (glutathione peroxidase 3 (GPX3)) were investigated in oocytes before and after in vitro maturation (IVM), and in early embryos.
Opposite phenotypes of muscle strength and locomotor function in mouse models of partial trisomy and monosomy 21 for the proximal Hspa13-App region.
New
Hérault et al., Illkirch-Graffenstaden, France. In Plos Genet, Mar 2015
Thus, we demonstrated how the Hspa13-App interval controls metabolic and mitochondrial phenotypes in muscles certainly as a consequence of change in dose of Gabpa, Nrip1, and Atp5j.
Coupling factor 6 attenuates CXCR4 expression through the HIF-1α and c-Src pathways and promotes endothelial apoptosis and inflammation.
Okumura et al., Hirosaki, Japan. In Hypertens Res, 2014
We investigated the effect of coupling factor 6 (CF6), a novel proton import activator, on CXCR4 signaling and its molecular mechanism.
Estrogen represses hepatocellular carcinoma (HCC) growth via inhibiting alternative activation of tumor-associated macrophages (TAMs).
Shen et al., Nanjing, China. In J Biol Chem, 2012
E2 functioned as a suppressor for macrophage alternative activation and tumor progression by keeping estrogen receptor β (ERβ) away from interacting with ATP5J (also known as ATPase-coupling factor 6), a part of ATPase, thus inhibiting the JAK1-STAT6 signaling pathway.
Estrogen attenuates coupling factor 6-induced salt-sensitive hypertension and cardiac systolic dysfunction in mice.
GeneRIF
Okumura et al., Hirosaki, Japan. In Hypertens Res, 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 inhibiting PI3K/Akt signaling in mice.
GeneRIF
Okumura et al., Hirosaki, Japan. In J Hypertens, 2012
Overexpression of coupling factor 6 attenuates exercise-induced physiological cardiac hypertrophy by downregulating Akt signaling, thereby cancelling its benefit for cardiac function in mice.
Coupling factor 6-induced activation of ecto-F1F(o) complex induces insulin resistance, mild glucose intolerance and elevated blood pressure in mice.
GeneRIF
Okumura et al., Hirosaki, Japan. In Diabetologia, 2012
CF6 plays a crucial role in the development of insulin resistance and hypertension
[Effect of obstructive sleep apnea- hypopnea syndrome on hypertension and metabolism disorder].
Jia et al., Qingdao, China. In Lin Chuang Er Bi Yan Hou Ke Za Zhi, 2010
There were 32 moderate or severe OSAHS patients and 20 healthy persons were selected to be measured the mitochondrial coupling factor 6 (CF6) with radio-immunity method.
Overexpression of coupling factor 6 causes cardiac dysfunction under high-salt diet in mice.
GeneRIF
Okumura et al., Hirosaki, Japan. In J Hypertens, 2010
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
Cardioprotection leads to novel changes in the mitochondrial proteome.
Murphy et al., Bethesda, United States. In Am J Physiol Heart Circ Physiol, 2010
Levels of cytochrome-c oxidase subunits Va and VIb, ATP synthase-coupling factor 6, and cytochrome b-c1 complex subunit 6 were increased while cytochrome c was decreased with PC and GSK Inhib VIII.
Novel pro-atherogenic molecule coupling factor 6 is elevated in patients with stroke: a possible linkage to homocysteine.
Okumura et al., Hirosaki, Japan. In Ann Med, 2009
Coupling factor 6 (CF6) is regulated by nuclear factor kappa B (NF-kappaB) signaling which is activated by Hcy.
Coupling factor 6-induced prostacyclin inhibition is enhanced in vascular smooth muscle cells from spontaneously hypertensive rats.
GeneRIF
Okumura et al., Hirosaki, Japan. In J Hypertens, 2009
suppresses prostacyclin generation in resistance arteriole vascular smooth muscle cells, which is enhanced in spontaneously hypertensive rats by the overproduction of CF6 and the hyperresponsiveness to CF6
Upregulation of soluble vascular endothelial growth factor receptor type 1 by endogenous prostacyclin inhibitor coupling factor 6 in vascular endothelial cells: a role of acidosis-induced c-Src activation.
Okumura et al., Hirosaki, Japan. In Hypertens Res, 2009
We recently showed that endogenous prostacyclin inhibitor coupling factor 6 (CF6) forces the clockwise rotation of F(1) motor of plasma membrane adenosine triphosphate synthase and induces intracellular acidosis and c-Src activation.
[Effect of rosiglitazone on tumor necrosis factor-alpha-induced nuclear factor-kappaB and coupling factor 6 expressions in human umbilical vein endothelial cells].
Liu et al., Guangzhou, China. In Nan Fang Yi Ke Da Xue Xue Bao, 2008
OBJECTIVE: To investigate the effect of rosiglitazone on the expression of nuclear factor-kappaB (NF-kappaB) and coupling factor 6 (CF6) induced by tumor necrosis factor-alpha (TNF-alpha) in cultured human umbilical vein endothelial cells (HUVEC).
Plasma level of mitochondrial coupling factor 6 increases in patients with coronary heart disease.
Tang et al., Beijing, China. In Circ J, 2007
BACKGROUND: The aim of the present study was to investigate alterations in the plasma level of coupling factor 6 (CF6), a novel endogenous inhibitor of prostacyclin, in patients with coronary heart disease.
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