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It has been found that somatic cell knockdown of both KRAS G12V and oncogenic PIK3CA mutations in human breast epithelial cells results in cooperative activation of the PI3K and mitogen-activated protein (MAP) kinase pathways in vitro and in vivo.
Besides, a possible catalytic mechanism involving cooperative activation of epoxide and ring-opening by one-component and bifunctional catalyst was proposed.
These results indicate that the ternary complex, including HOXA9, plays an important role in inducing leukemia, Cooperative activation of MEIS1 and HOXA9 perturbs myeloid differentiation and eventually leads myeloid progenitors to leukemia.
We identify that the interaction between the crystalline second phase and the local shear bands is dominated by the cooperative activation of lattice dislocations on the glass crystal interfaces and discrete shearing events in the neighboring glass matrix.
This is determined by the clustering and cooperative activation of voltage-gated sodium channels [20], for which Ankyrin3 is required [6].
Cooperative activation of striated muscle by calcium is based on the movement of tropomyosin described by the steric blocking theory of muscle contraction.
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A potential basis for cooperative activation is the association of myosin with thin filaments [1], [2].
Based on the experimental results and the model analysis, we discuss the mechanism of cooperative activation by the ADP-bound cross-bridges in sarcomeres.
We discuss below the possible mechanisms of cooperative activation in sarcomeres based on the interfilament spacing and its modulation by the strongly bound cross-bridges.
To overcome these difficulties and reveal the mechanism of cooperative activation in sarcomeres mediated exclusively by the cross-bridges, we examined the force-SL relationship in skeletal myofibrils (with a thickness of only a few micrometers) in the absence of Ca2+ at various levels of activation induced by exogenous MgADP in the presence of MgATP.
The physiological significance of the activating and inhibitory effects of cMyBP-C are not completely understood, but a role for activating effects to prime the thin filament, to contribute to cooperative activation, and/or to counteract deactivation of the thin filament during muscle shortening are all possibilities.
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