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Further, the precise role of the majority of SCF-based E3 ligases in neoplasia have not been established, although repression of FBXL2 in human lung adenocarcinoma raises the possibility that it might regulate molecular programs involved in mitosis and cell division.
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Equally important is knowing how an organism's experiences, social interactions and environment regulate molecular biology and gene function.
Post-translational modifications as phosphorylation and mono-ubiquitination might regulate Eps15 functioning, but molecular details of these processes are still unknown.
In summary, the EO771-derived isogenic model of spontaneous breast cancer metastasis described here and the 4T1 model described primarily in previous publications (Eckhardt et al., 2005; Lelekakis et al., 1999) have enabled the identification of genes and molecular pathways that might regulate metastasis in two different strains of mice.
The molecular mechanisms how Cytip might regulate cytokine production and T-cell activation remain to be elucidated.
It is clear from the time course of fast mechanical hyperalgesia (hours) that local action of NGF might regulate the steps outlined above, but the molecular details are still completely unclear.
In order to investigate the molecular mechanisms by which MSX2 might regulate apoptosis and cell invasion, the expression of several proteins involved in respective signalling pathways was examined.
Since S-nitrosation has been reported to facilitate protein-protein interactions [9], we speculated that NO-mediated specific molecular modification of Pias3 (or Trim32) might regulate its interaction with Trim32 (or Pias3).
However, little is known about the molecular mechanism of how mechanical boundary conditions might regulate BMP signalling.
Except for 30 known LIPUS-regulated genes, our study demonstrated for the first time that over 100 genes were related to the underlying molecular mechanism of LIPUS and suggested that LIPUS might regulate a transient expression of numerous critical genes in osteoblastic cells.
Overall, our data suggest the existence of molecular mechanisms in 6-OHDA-lesioned rats that might regulate D2R-A2AR interactions.
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