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Initially the eQTL was regarded as a master regulator considering its ability to regulate the expression of multiple biochemically related genes.
It participates in the regulation of cell cycle progression through its effects on cyclin D1 expression [ 24] and most importantly it has been implicated in the regulation of cell death through its ability to regulate the expression of cellular factors that affect the apoptotic threshold [ 25].
Owing to their ability to regulate the expression of genes involved in cell-cycle regulation (cyclin D1, c- myc, and p21) and cellular survival (Bcl-XL), STAT5a and STAT5b have emerged as possible targets for cancer therapeutics [ 10].
We speculate that MIF regulation of tumour vascularisation occurs through its ability to regulate the expression of pro-angiogenic chemokines and the modulation of the recruitment and/or the activity of pro-inflammatory cells.
Taken together, the RNA interference study showed that SREBP1 has the ability to regulate the expression of ACCα.
In that case, NR have the ability to regulate the expression of specific genes and associated with various diseases, which make it essential drug targets.
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The ability to regulate the expression level of a therapeutic gene is vital for the advancement of gene therapy into the clinic.
Of particular interest is htt's ability to regulate the expression and transport of neurotrophin BDNF, which plays an important role in neuronal survival and differentiation (7– 10).
This subsequently interfered with the ability of YB-1 to regulate the expression of EGFR.
Thus the ability of these stimuli to regulate the expression of phosphorylated mTOR both individually and together in human myotubes was assessed.
We investigated the ability of HA to block the cytotoxic effects of the chemotherapy drug carboplatin, and to regulate the expression of ABC transporters in ovarian cancer cells.
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