The phrase "alternatively activation of the" is not correct as it stands and is incomplete in written English.
It can be used when discussing different methods or options for activating something, but it needs to be part of a complete sentence.
Example: "Alternatively, activation of the system can be achieved through manual input."
Alternatives: "On the other hand, activation of the" or "As another option, activation of the."
Alternatively, activation of regulatory T cells that suppress the specific immunity may be too efficient.
Alternatively, activation of α7 NNRs on glutamate afferents within the nucleus accumbens can, through spillover of glutamate, activate metabotropic glutamate receptors on dopamine terminals and depress dopamine release.
Alternatively, activation of transposons could have occurred at an earlier stage of the habituation process (e.g., in the presence of TA) to be silenced later on due to epigenetic modifications [ 79].
Our finding that Daple binds preferentially to some FZDRs, and not others, could influence the decision of canonical vs non-canonical Wnt signaling, or alternatively, activation of Gαi and inhibition of cellular cAMP by Daple could directly antagonize a previously described role of the adenylate cyclase/cAMP/PKA pathway in phosphorylating and stabilizing β-catenin (Hino et al., 2005).
Alternatively, activation of factors in noncanonical TGF-β signaling, such as MAP kinases, small GTPases, PI3K/AKT, and NF-κB, also couples TGF-β to regulation of EMT expression programs.
Therefore, appropriate inhibition of profibrotic angiotensins such as angiotensin II or angiotensin IV, production pathways, or, alternatively, activation of an antiprofibrotic angiotensin pathway such as ACE2 or angiotensin- 1-7) could be angiotensin- 1-7e for antifibroticouldrapy.
Alternatively, activation of other signaling pathways may augment AHR function (Seidel et al. 2001) or result in a synergistic increase in AHR-dependent gene expression (Chen and Tukey 1996; Long et al. 1998).
Alternatively, activation of weak cr3′ss+81 in U2AF35-depleted cells could be promoted by an upstream G-repeat that is likely to act as an intronic splicing enhancer (Fig. 2a).
Alternatively, marked activation of the Hh pathway could lead to a decrease in SMOH and GLI mRNA levels by a negative feedback.
He discussed the potential use of PI3K inhibitors, and showed that alternatively an activation of the antagonistic phosphatase SHIP (SH2-containing inositol-5-phosphatase) might provide a target of hematopoietic and immune disorders in which the PI3K pathway is dysregulated.
