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In vivo studies and mice model studies have suggested that BRCA1/2 is involved in translation regulation and the Insulin-Like Growth factor signaling axis [30], [31], but whether these pathways are directly related to premature aging is not clear.
The former enrichment was expected, since ECM pathways are directly associated with the myofibroblast phenotype.
Several of these pathways are directly related with the parasite infection and inflammatory responses.
However, there is very little molecular evidence to show that these two pathways are directly linked.
Thus, receptor mediated death pathways are directly connected to mitochondrial death pathways.
Interestingly, three of these pathways are directly connected to MAP kinase pathway in the KEGG database.
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The impact of mutations in the GA, ABA, and BR biosynthetic pathways was directly tested to assess their interactive network.
That is to say, activation of signaling pathways is directly related to integrin binding and focal adhesion formation, which are regulated by the availability of binding domains in FN upon adsorption on different chemistries (Figures 1, 2, 3).
Whatever the explanation is, a positive feedback mechanism between BRCA1-IRIS and AKT pathways is directly correlated with the BRCA1-IRIS chemotherapy resistance-inducing role in TNBC survival.
This idea is supported by our observation that transcription of many components of these silencing pathways is directly activated by Pou5f1, Sox2, and Nanog.
Further considering the role of ER stress in C-6-induced cell death, it is interesting to note that multiple signaling arms of the unfolded protein response (UPR) can be activated during periods of ER stress and interplay between these signaling pathways is directly responsible for the activation of either pro-survival or pro-death pathways (reviewed in [ 39]).
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