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.
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.
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.
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
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.
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).
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.