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Activation of a G protein-coupled receptor (GPCR) triggers downstream signalling pathways whose identity is determined not only by the genetic background of the cell, but also by the interacting ligand.
The observed activities of the various secosteroids and steroidal 5 7dienes we tested were influenced by the genetic background of the cell lines used, suggesting the existence of cell-type specific factors that can modulate activities.
Firstly, whole-genome sequencing is used to determine the genetic background of the cell line.
The genetic background of the cell lines might play a role in the observed variation.
This could be either specific to the genetic background of the cell lines used or due to different experimental approaches.
The differential effects of SIRT1 could therefore be specific to the genetic background of the cell or tumor in question and may not fit into the classical definitions of an oncogene or tumor suppessor.
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Due to the shared genetic background of the cells, our rationale was that the differential expression of miRNAs would correlate well with their differential aggressive phenotype.
Differentially regulated genes in 3Amut LCLs and 3BKO LCLs were identified using an ANOVA model including the donor ID (for genetic background of the cells).
We hypothesized that due to the isogenic background of the cells, the differentially expressed miRNA groups would be enriched for miRNAs with a direct effect on aggressive melanoma features.
Inhibitory effects of CIP2A downregulation on proliferation of melanoma cells were not related to the genetic background of the cells.
Autophagy may precede apoptosis or be induced simultaneously depending on the genetic context and cellular background of the cells.
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