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(Project Overview)
(Project Overview)
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===Project Overview===
===Project Overview===
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We are planning to use Site-Directed Mutagenesis to increase the binding affinity of CCR5 zinc finger nucleases.  This mutation aims to increase the level CCR5 receptor disruption in genetically haploid cells in an effort to facilitate HIV therapy.
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We are planning to use site-directed mutagenesis to increase the binding affinity of CCR5 zinc finger nucleases.  This mutation aims to increase the level CCR5 receptor disruption in genetically haploid cells in an effort to facilitate HIV therapy.
===Background Information===
===Background Information===

Revision as of 07:15, 8 May 2013

Contents

Project Overview

We are planning to use site-directed mutagenesis to increase the binding affinity of CCR5 zinc finger nucleases. This mutation aims to increase the level CCR5 receptor disruption in genetically haploid cells in an effort to facilitate HIV therapy.

Background Information

CCR5 is a receptor on the outside of T cells that HIV uses to dalfdlsakjflas;kfjdlas;kfjs CCR5 delta 32 is an isoform of CCR5 found in certain Northern European individuals that confers resistance, or immunity, to HIV. Zinc Finger nucleases are tools that can be used to modify the human genome in a very target specific manner. Homology repair is a mechanism that cells use to repair damaged DNA. It is a mechanism that can be used to introduce new modified DNA sequences into the genome at very specific target locations.

Purpose and Goals

Project Details

Predicted Outcomes

Needed Resources

Zinc Finger nucleases specific to CCR5. CCR5 delta 32 sequence and a construct with the CCR5delta32 sequence within arms of CCR5 sequences. KBM7 cells that are haploid for every chromosome except for chromosome 8. It will be easier to see the effects of a change in haploid cells because there won't be an ambiguous heterozygous phenotype.

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