It was realized very early on that the enzyme diacylglycerol kinase (DAGK) is active in bicelles, while activity is lost in micelles.
The cytoprotective activity of these triterpenoids is dependent on activation of Nrf2, since such activity is lost, both in cell cultures and in vivo, in the absence of Nrf2 [26] [28], [28].
Hence, when TSC1 or TSC2 activity is lost through mutation, Rheb becomes activated which in turn activates mTOR.
DIF dechlorinase is active when expressed in bacteria, and activity is lost from Dictyostelium cells when its gene, drcA, is knocked out.
Said activity is lost to the ether.
Some activity is lost from the first to second runs, but thereafter stabilizes.
The transhydrogenation activity is also lost when the main dehydrogenation activity is lost.
T. reesei xylanase II (XYNII) is stable at 40 45°C, whereas temperatures above 50°C cause conformational changes and the enzyme activity is lost quite quickly.
Upon mutation, its intrinsic GTPase activity is lost and GAPs are unable to bind RAS resulting in RAS primarily bound to GTP and therefore constitutively activated [16].
In pathological conditions the balance between the free radical generation and the antioxidant activity is lost, resulting in oxidative damage to the cells and tissues.
Node 10 is not directly deactivated but the activity is lost further up the network so it is set to negated, this is a subset of a larger deactivation context.
