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We predicted that Akt-mediated phosphorylation of SIN1 might be involved in regulating the activity of mTORC2 because its phosphorylation occurred on a timescale that would support such a function relative to Akt S473 phosphorylation, and PI3K inhibition impairs the activation of mTORC2 (Frias et al., 2006).
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Two types of mechanism can support such a U-shaped function.
Experimental evidence supports such a protective function for AT.
In support of such a function AN was reported to act outside the nucleus [ 28].
Although earlier studies on FGM model have used such linear fitness functions (for the sake of mathematical simplicity), recent experimental studies do not seem to support the use of such a function [17] [19].
Unfortunately, not all hospital directors, whose support is needed to create such a function, are convinced of this necessity.
More recent studies support such cytosolic NPR1 function as regulator of JA-dependent defense responses ([ 18- 20]).
Such a function is supported by recent studies that investigated plants impaired in TCA cycle enzymes.
However, at present, there is no experimental evidence to support such proposed functions.
Such a function is also supported by the observation that cob(I alamin is highly reactive and needs to be shielded from the environment [ 30].
On a node based level, this trend toward higher complexity is reflected by an considerable heightened connectivity of domains that support such functions in multicellular organisms [ 15].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com