The relatively high levels of circulating estrogens (E2) across gestation preclude E2 concentration as a viable direct modulator of the myometrial transition between quiescence and contractility at term. We hypothesize that changes in alternatively spliced Estrogen Receptor alpha (ERα) isoforms across gestation permit uterine specific temporal contractile responses to increasing E2 levels as term approaches. In this study we examined the role of alternately spliced myometrial ERα variants by identifying and knocking down the relevant splice factors utilizing siRNA and lentiviral shRNAs and consequently examining the expression profile of ERα isoform ratios and their downstream targets, the contractile associated proteins (CAPs).
Biochemistry, molecular Biology, genetics and physiology are desirable prerequisites.
Starting now . 6 semesters.
Would be require to do molecular techniques. All required methodology would be taught by senior lab personnel. Techniques include qPCR, western blotting, tissue culture and histology (immunohistochemistry.)
April 5, 2016