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The PI(3 K/Akt/mTOR pathway seems to operate in mice expressing a dominant negative IGF-1 receptor in muscle (Spangenburg et al., 2008), suggesting that overload hypertrophy is at least not solely dependent on activation of the IGF-1 receptor, and that the pathway can be activated also by other signals.
Its noteworthy to mention here that ERK1/2 belong to the family of mitogen-activated protein (MAP) kinases, that regulate cell survival, motility, and proliferation and were activated also by "external stimuli" at cell membrane [ 21, 22, 24], we speculated that NPs can induced cell proliferation, partly, through ERK1/2 modulation.
In addition, Lactobacillus casei l-LDH requires some divalent metal ions (e.g., Mn2+) (Arai et al. [2011]), and the Thermus caldophilus enzyme is activated also by citrate under slightly acidic conditions (Taguchi et al. [1984]).
Moreover, HIF-1α expression seems to depend on mTOR signaling control [6] and mTOR seems to be activated also by BMP in murine CNS precursor cells cultured at high density [7].
It has been demonstrated that CREB can be activated also by other signal transduction pathways and results from the CRE-SEAP reporter gene assay can differ when compared with other second messenger assays [32], [37].
Furthermore, mTOR signaling pathway seems to be activated also by BMP in murine CNS precursor cells cultured at high density [7]; one of the possible effects mediated by mTOR activation is serine phosphorylation of Stat3, which finally leads to generation of glia [8].
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Moreover, it is activated, although weakly, also by the SV40 enhancer.
It is intensely released in asthmatic airways by pro-inflammatory cells, including activated macrophages, but also by structural cells [101].
AKT is also activated by phosphorylation at Thr308 by PDK1.
They also revealed that EGFR was also activated by HGF stimulation in human epidermal keratinocytes.
Anthocyanin accumulation is also activated by phosphate or sulphate nutrient deficiencies, which are also dependent on C availability [40] [42].
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