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The intra- or extra-cellular environment of a cell or organism may switch gene transcription on or off.
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Many TFs directly switch gene expression on or off, whereas others factors may serve as constraints (e.g., by controlling the access of TFs to DNA).
Jane (daughter and sister ) invoked the language of current molecular genetics: 'environment and genetics … a particular gene may switch [schizophrenia] on, because of some sort of environmental factors'.
This indicates that silencing mechanisms of many genes may switch during the progression of melanoma.
In particular, it refines the notion of targets and anti-targets [ 35] examined in detail by several recent studies: On/off genes may switch from being targets and anti-targets depending on their UTR.
Although during this process, a gene lineage may switch into a pseudogene lineage, a pseudogene lineage is not allowed to switch back to a gene lineage.
Securin gene knockdown may switch radiation-induced apoptosis to growth arrest and senescence, and thus only minimal apoptosis is observed in irradiated MDA-MB-231-2A MDA-MB-231-2A MDA-MB-231-2A MDA-MB-231-2A
Although the fine mechanisms of regulation of the "epigenetic" machinery are still poorly understood, the DNA methylation may switch on or off several genes and, in particular, those regulating important biological phenomena, such as cell growth and differentiation [ 25].
The new science of epigenetics shows that chemicals can switch genes on and off, and this may explain the "reversibility" of cancer.
Trying to switch genes on and off is even more difficult, and such switches tend to weaken over time.
Cellular genes thus can be placed under the control of heterologous promoter or enhancer elements and may switch off cellular growth regulation.
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