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Internalization of beta-adrenergic receptors (betaARs) occurs by the sequential binding of beta-arrestin, the clathrin adaptor AP-2, and clathrin.
It is widely accepted that 3D-Cry toxins exert their toxic effect by the sequential binding to insect gut proteins named cadherins and glycosyl-phosphatidyl-inositol (GPI) anchored proteins such as aminopeptidase-N (APN) or alkaline phosphatase (ALP) resulting in toxin oligomerization and pore formation that finally cause cell lysis and disruption of the insect gut (Pardo-López et al. 2013).
HIV-1 entry into host cells is mediated by the sequential binding of the envelope glycoprotein gp120 to CD4 and a chemokine receptor.
This complex is formed at origins of replication by the sequential binding of ORC1-6, cdt1, cdt1 and MCM2-7, and is absolutely required for all subsequent processes of replication.
For example progression through G1 and into S phase is controlled by the CDK2 kinase activity and is stimulated by the sequential binding of cyclins D and E. Premature progression is prevented by the several CKIs such as p16, p27Kip1 and p21.
The pre-RCs are formed by the sequential binding of the origin recognition complex (ORC1 to ORC6), cell division cycle 6 (Cdt1), Cdt1 and minichromosome maintenance (MCM2 to MCM7) proteins to DNA [ 1].
Similar(52)
The titration data were analyzed by using the sequential binding model available in the Origin software provided by MicroCal, which yielded the following parameters associated with the bisANS/PDC-109 interaction: equilibrium association constant (Ka), enthalpy (ΔH), entropy (ΔS) and the stoichiometry of binding (n, which corresponds to the number of bisANS molecules bound per molecule of PDC-109).
The structure proposed by He et al. could represent the sequential binding of transcription factors and Pol II to the promoter to initiate the first round of transcription.
This assay may also evaluate the sequential binding of eIF4E to the cap followed by 4E-BP1 binding to cap-associated eIF4E and indicate in agreement with the far western data in Figure 1C that de novo binding is blocked by Thr46 phosphorylation.
In the present study, we provide further evidence in support of the sequential binding model.
Such evidence supports the sequential binding model of toxin pore formation.
More suggestions(16)
by the sequential recovery
by the sequential onset
by the sequential priority
by the sequential exposure
by the sequential improvement
by the sequential arrangement
by the sequential desaturation
by the sequential fusion
by the sequential induction
by the sequential removal
by the sequential Perception
by the sequential culture
by the sequential replacement
by the sequential balancing
by the sequential network
by the sequential expression
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