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[58] [56] Knockdown of myostatin has been shown to reduce formation of osteoclasts (multinucleated cells responsible for the breakdown of bone tissue) in mice modeling rheumatoid arthritis. [58] Rheumatoid arthritis is an autoimmune disorder that, among other effects, leads to the degradation of the bone tissue in affected joints.
Gene knockdown is an experimental technique by which the expression of one or more of an organism's genes is reduced. The reduction can occur either through genetic modification or by treatment with a reagent such as a short DNA or RNA oligonucleotide that has a sequence complementary to either gene or an mRNA transcript.
Additionally, gene knockouts are not always a good model for human disease as the mouse genome is not identical to the human genome, and mouse physiology is different from human physiology. The KO technique is essentially the opposite of a gene knock-in. Knocking out two genes simultaneously in an organism is known as a double knockout (DKO).
A dual role of EFS in mature T cells function has been proposed because both overexpression and siRNA knockdown of this protein in cell models resulted in decreased transcriptional activation of IL-2 dependent promoters following TCR stimulation. [46] Altered EFS function has been associated with various human immunopathological conditions.
Examples of research in which knockout mice have been useful include studying and modeling different kinds of cancer, obesity, heart disease, diabetes, arthritis, substance abuse, anxiety, aging and Parkinson's disease. Knockout mice also offer a biological and scientific context in which drugs and other therapies can be developed and tested.
This story was reviewed by Mike Bohl, MD. In the ‘80s, researchers set out to test a medication called sildenafil citrate for treating high blood pressure and angina (chest pain) from heart disease.