The phrase "activate entry" is correct and usable in written English.
It can be used in contexts where you want to initiate or enable access to a specific entry point, such as in software, databases, or systems.
Example: "To proceed with the installation, please activate entry by clicking the 'Start' button."
Alternatives: "enable access" or "initiate entry".
The women booked their places at the Games safely but, needing a top-eight finish in qualifying to activate automatic entry for the full team at London 2012, the men crumbled to place 10th.
If the compounds bind to the E proteins as predicted, they may interfere with the interactions between the E protein and the host surface receptor, particularly with the E protein conformational change that is necessary to activate viral entry.
The main question concerns the origin of the signal [43], [50]: how does depletion of the internal Ca2+ store activate Ca2+ entry through the SOC in the plasma membrane.
This specific phosphorylation triggers the dissociation of STIM1 from EB1, which in turn facilitates STIM1 clustering and the binding to SOCs to activate Ca2+ entry.
The combined action of CCh and CPA (bottom panel) was used in these experiments to maximally deplete the store and activate Ca entry via SOC (Fig. 11B).
IP3 binds to the IP3R, which initiates Ca2+ release from the ER stores, thereby facilitating stromal interacting molecule-1 (StoM1) to rearrange and activate Ca2+ entry via the store-operated channels.
It is not clear at the moment whether ATP hydrolysis is required for actual transport of the peptide across the plasma membrane or for upstream processes that activate the entry pathway.
In this process, antigen-stimulated hydrolysis of PIP2 by phospholipase Cγ (PLCγ) results in production of inositol 1,4,5-trisphosphate (IP3) to cause release of Ca2+ from the endoplasmic reticulum (ER), which initiates direct coupling of the ER membrane protein STIM1 with the plasma membrane channel protein Orai1 to activate Ca2+ entry (Vig and Kinet, 2009).
Recent work indicates that hypertrophic agonists linked to Gαq-protein coupled receptors such as Ang II activate calcium entry through transient receptor potential canonical (TRPC) channels [ 34] and that these channels, especially TRPC1, C3 and C6, can trigger pathologic, hypertrophic calcium signalling in the heart [ 34, 41].
With the discovery of key proteins involved, e.g. Orai1/CRACM1 (calcium release-activated calcium modulator 1) [ 14, 15] and Stim1 (stromal interaction molecule 1) [ 16], it became clear that Stim1, by sensing decreasing luminal Ca2+ concentration upon store depletion, would activate Ca2+ entry involving Orai1/CRACM1 as channels, or as part of a larger channel complex.
