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According to Leber et al. [ 26], when ergosterol synthesis is inhibited, steryl esters are hydrolyzed and ergosterol levels remain sufficiently high to maintain membrane formation and growth for some time, and no genes involved in ergosterol synthesis are induced.
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During exponential growth of the yeast, these precursors are rather channeled to phospholipid synthesis than TAG formation for maintaining membrane formation, cell growth and viability.
AsuC15 thioesterase is also proposed to suppress excess ω-cyclohexyl fatty acid formation and help to maintain membrane homeostasis by releasing the CHC residue from FAS ACP, as the percentage of ω-cyclohexyl fatty acids was increased fivefold in the asuC15 mutant (Rui et al. 2010).
At low temperatures, several adaptive mechanisms are activated to maintain membrane fluidity, transport, transcription, translation, cell division, metabolism and enzyme activity and to avoid intracellular ice formation [ 8, 9].
The phenomenon suggested that SVH could effectively maintain membrane integrity.
It is required to build and maintain membrane, modulate membrane fluidity.
Cells modulate lipid metabolism in order to maintain membrane homeostasis.
They maintain membrane fluidity and permeability, and modulate activity of membrane-bound proteins and ion channels.
Treatments of AIB and BAIB effectively maintained membrane integrity and reduced MDA content (Fig. 2a, b).
Maintaining membrane proteins in a native-like environment is difficult.
Since the lipid composition of the stratum corneum (SC) membranes is critical for maintaining the epidermal water barrier, certain alterations in SC membrane formation or lipid composition appear to provoke a leaky barrier, which in turn 'drives' the ichthyosiform dermatosis [ 4].
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