It seems that PARKIN selectively binds to damaged mitochondria only,completely removing them.
Personally, I can't help thinking that occasional Nilotinib use may be most benificial as a means of mitochondrial quality control when using mitochondrial protectors like C60oo.
I am currently off of C60oo in anticipation of taking a dose, followed by C60oo again about 8-24? hours later.
Thoughts?
PINK1- and Parkin-mediated mitophagy at a glance
Mitophagy is the selective engulfment of mitochondria by autophagosomes and their subsequent catabolism by lysosomes (see Poster). Starvation induces a less-selective form of autophagy in which cytosol and a variety of organelles are engulfed into autophagosomes, which leads to their degradation in order to supply nutrients to compensate for the loss of external supplies. It was initially found that mitochondria are selectively engulfed by autophagosomes following a loss in membrane potential (Lemasters et al., 1998), suggesting that mitophagy mediates selective removal of damaged mitochondria. This idea has been supported by recent knockout mouse models, where loss-of-function of ATG7, which functions in the autophagy pathway, results in an accumulation of defective mitochondria in certain tissues (Komatsu et al., 2005; Wu et al., 2009). Among the first events in quality control by mitophagy is the distinction between damaged mitochondria and healthy mitochondria. Following their identification by PINK1, defective mitochondria are engulfed in double-membraned autophagosomes that fuse with lysosomes, thereby merging their contents and allowing hydrolytic degradation (reviewed by Kim et al., 2007). In addition to quality control, mitophagy occurs to regulate mitochondrial number (Zhang et al., 2009b) and eliminate mitochondria during the development of specialized cells or tissues such as reticulocytes (Kundu et al., 2008; Mortensen et al., 2010; Zhang et al., 2009a). Overexpression of Parkin has been found to induce the complete removal of mitochondria from cells by mitophagy when mitochondria lose their membrane potential (Narendra et al., 2008). As Parkin has also been found to selectively bind only to damaged mitochondria it has been suggested that Parkin might mediate a quality control pathway of mitophagy.
http://jcs.biologist...ntent/125/4/795
Here's a summary of the group buy for those that agree with me and may be interested:
http://www.longecity...1-month-supply/
Edited by Logic, 15 March 2016 - 09:56 PM.
