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Therefore, these results altogether confirm functionally that p110α/p85β and p110α/p55γ are the largely predominant PI3-K isoform complexes in HIEC cells, in addition to indicating that both complexes contribute in the activation of Akt-1 and a consequent promotion/maintenance of survival in these cells.
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Although future studies are needed to clarify the role of hMena and its isoforms in breast cancer progression, our observation raised the possibility that hMena overexpression may contribute in mediating the activation of various ErbB receptors.
To this effect, the two predominant PI3-K complexes in HIEC cells (p110α/p85β and p110α/p55γ) not only contribute distinctively in the activation of Akt-1 and the maintenance of HIEC cell survival, but are furthermore engaged selectively by β1 integrin/Fak/Src signaling in the suppression of anoikis (Fig. 8).
In fact, significant CREB activity was remaining in AKHR mutant flies (Figure 5A), suggesting that other signaling pathways might contribute to the activation of CREB activity in the fat body.
In response to stretch, ROS, in particular H2O2, contribute to the activation of arteriolar myogenic response, contraction, and reorientation, through p38 MAPK signaling activation in VSMCs [ 90– 92].
Thus, the frequently observed haploinsufficiency of NKX3.1 in prostate cancer may significantly contribute to the activation of ERG protooncogene in the TMPRSS2-ERG fusion genomic context.
The UPS components that, in our experimental system, appear to be specifically activated in the Pet during ethylene-induced abscission, could contribute to the activation of defense mechanisms in the tissues that remain attached to the plant as previously suggested [ 18].
Although it has been recently shown that IKKα can activate the canonical pathway as a compensatory mechanism in the absence of IKKβ [17], our data demonstrates that in sarcomas both catalytic subunits mutually contribute to the activation of NF-κB in response to doxorubicin.
Mitochondria are versatile and dynamic organelles that play a key role in the regulation of metabolism, cellular signaling and apoptosis, during which they release cytochrome c and other cofactors that once in the cytosol contribute to the activation of the effector caspases required to demolish the dying cell [52].
We did not detect NME1 expression at the protein level in PBMC, vaginal, or colorectal tissue, suggesting NME1 is unlikely to contribute to the activation of TFV in the cells and tissues investigated.
However, in LCSC6, EGFR was highly expressed and phosphorylated in the absence of increased gene copies, suggesting that other mechanisms may contribute to the activation of EGFR in this context.
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