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The anti-apoptotic members like BCL-2 itself regulate this process, preventing at multiple points the activation of the proapoptotic multidomains [48].
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When the level of drosomycin expression was normalized for the number of bacteria present in infected flies at each particular time point, the activation of the drosomycin expression was higher for the atl mutant than for the wild type S. aureus strain at 12 h post-infection.
At this point, the activation of genes involved in floral organ identity takes place and we observed that genes such as APETALA3, PISTILLATA and AGAMOUS, all well-known regulators of flower development, showed an increase their transcript abundance from zero to their maximum levels at M10 (Fig. 2b).
c) When casing deformation points appear near point A, the activation of the weak plane in the beddings during fracturing causes the casing deformation.
We propose that the selective involvement of left temporal areas points to the activation of conceptual representations, whereas more posterior temporal, parietal, and occipital areas probably reflect perceptual aspects of higher-order visual object processing.
Two distinct starting points for the activation of caspases have been characterized [ 10] as follows.
HepG2 cells were treated with doxorubine, TRAIL or the combination thereof for various time points, and the activation of JNK was monitored by the detection of phospho-JNK.
αSMA staining points to the activation of stellate cells, which is known to play a crucial role for pancreatic regeneration, fibrosis, and the production of extracellular matrix.
These key points include the activation of pro-apoptotic proteins preceding damage to the mitochondria (0.5 to 1 hour STS incubation), cytochrome c release from the mitochondria (2 hour STS incubation), and activation of caspase-3 before significant damage to the HeLa nuclei (2.75 hour STS incubation).
Since the induction of CytC is a reflection of oxidative stress and the upregulation of Casp9 may point to the activation of mitochondrial apoptosis, we assume that p53 in BMR downregulates apoptosis to avoid excessive cell loss under hypoxic conditions.
The specific intracellular signaling mechanism linking TrkA activation to nociception and TRPV1 sensitization still remains to be fully clarified, despite being the subject of intense study, and initial evidence pointing to the activation of PLC−γ1 via TrkA [54] was followed by studies implicating the PI3K and MAPK pathways [55].
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