In an independent study using human mammary epithelial cells, we demonstrated that inhibition of RARα function with various genetic strategies triggers the concerted repression of both RARβ2 and another target downstream of RARβ2, CRBP1, encoding the cellular retinol binding protein 1, which is pivotal for breast epithelial cell acinar morphogenesis [7].
Indeed, DF-1 cells retain various genetic alterations of down-regulated p53 function, an up-regulated pRB (retinoblastoma protein) and E2F1 pathway, and elongated telomere length, which are commonly found in immortalized cells [ 19].
Like other cancers, thyroid carcinogenesis involves gradual accumulation of various genetic and epigenetic alterations, leading to gain-of-function in oncogenes and loss-of-function in tumor suppressor genes [ 5, 6].
Indeed, elevated BP and altered vascular function were observed in various genetic and diet-induced models of metabolic syndrome [ 86].
Although various genetic and pharmacologic interventions can improve markers of cardiac function in heart failure, prolongation of survival is the gold standard outcome.
This has necessitated the creation of various genetic tools for conditional loss- or gain-of-function genetic studies.
XIAP loss of function has been studied extensively using various genetic tools including germ line deletion [ 9], somatic cell deletion [ 10], and both transient and stable mRNA knockdown.
Understanding these various genetic and biochemical equilibria in the context of cellular function led to a hypothesis that was experimentally validated.
Antibody genes are easily cloned and manipulated, and various genetic engineering approaches have been used to improve affinity, pharmacokinetics, and effector functions.
The loss of E-cadherin function during tumor progression can be caused by various genetic or epigenetic mechanisms.
