Apoptosis

Seymour Buts
SL1M
Dr. Frankenstein
12/8/08
Apoptosis Paper
In this paper, Idikò Szabò, Jürgen Bock, et al conducted research on the relationship of apoptosis, potassium channel Kv1.3, and Bax. The crush of Bax (a member of the Bcl-2 family of proteins) as a whole doesnt issue to be very well understood, however the authors of the paper hypothesized and demo through experimentation, that apoptosis induced by Bax are change by the mitochondrial ion channels. More specifically, in this paper the authors hypothesize that computer mouse and military personnel cells that are genetically deficient in every Kv1.3 or transfected with siRNA to suppress Kv1.3-expression resisted apoptosis induced by several(prenominal) stimuli, including Bax over-expression.
The first experiment conducted involved isolation of Kv1.3 to demonstrate the spot of Kv1.3 in apoptosis. To confirm the role of Kv1.3 in apoptosis, the experimenters transferred either human PBL or Jurkat cells with either siRNA, which almost completely suppressed some(prenominal) the expression and activity of Kv1.3 in the transfected population, or control siRNA, severally which was without effect on Kv1.3. To test the role of mitochondrial Kv1.3 precisely, they transfected Kv1.3-deficient CTLL-2 cells with an expression sender for an EYFP-Kv1.



3 construct that specifically targets the expression of Kv1.3 in mitochondria and found that transfection with Kv1.3 restored apoptosis.
The countenance experiment done, was to clarify the way that Kv1.3 mediates apoptosis. To do this the authors considered the interactions of Kv1.3 with proapopatic Bax. The first social function done in this experiment was to perform patch-clamp experiments on Bax proteins that lacked the C-terminal Tran tissue layer domain. It was found that the Bax proteins were unaffected. However, later coimmunoprecipitation experiments confirmed that Kv1.3 and Bax physically interacted in some(prenominal) mouse and human cellsonly upon induction of apoptosis. In the final percent of this series of...If you want to get a full essay, exhibition it on our website: Ordercustompaper.com



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