<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-09-22T14:49:01Z</responseDate><request verb="GetRecord" identifier="oai:wakespace.lib.wfu.edu:10339/92370" metadataPrefix="dim">https://wakespace.lib.wfu.edu/server/oai/request</request><GetRecord><record><header><identifier>oai:null:10339/92370</identifier><datestamp>2026-09-18T12:20:22Z</datestamp><setSpec>com_10339_14934</setSpec><setSpec>col_10339_38132</setSpec></header><metadata><dim:dim xmlns:dim="http://www.dspace.org/xmlns/dspace/dim" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.dspace.org/xmlns/dspace/dim http://www.dspace.org/schema/dim.xsd">
   <dim:field mdschema="dc" element="contributor" qualifier="author" lang="en_US">Davis, Ryan Richard</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="accessioned">2018-08-23T08:35:25Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="available">2019-08-22T08:30:14Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="issued" lang="en_US">2018</dim:field>
   <dim:field mdschema="dc" element="identifier" qualifier="uri">https://wakespace.lib.wfu.edu/handle/10339/92370</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="abstract" lang="en_US">TREX1 is a 3′ to 5′ exonuclease found in metazoan cells. TREX1 acts on both ssDNA and dsDNA and functions to prevent adverse immune activation by degrading cytosolic nucleic acids that would otherwise activate DNA sensors resulting in interferon production. Mutations in TREX1 cause multifactoral, systemic autoimmune diseases. Lack of TREX1 activity is not the only means of causing disease. Patients with fully active TREX1 who have mutations or frameshifts in the C-terminal region develop autoimmune disease presumably by disrupting protein-protein interactions or proper localization vital for normal cell biology. Understanding this multifaceted role of TREX1 in cell biology requires a thorough investigation of the regulation and involvement of TREX1 in nucleotide metabolism.</dim:field>
   <dim:field mdschema="dc" element="language" qualifier="iso" lang="en_US">en</dim:field>
   <dim:field mdschema="dc" element="publisher" lang="en_US">Wake Forest University</dim:field>
   <dim:field mdschema="dc" element="subject" lang="en_US">DNA</dim:field>
   <dim:field mdschema="dc" element="subject" lang="en_US">exonuclease</dim:field>
   <dim:field mdschema="dc" element="subject" lang="en_US">macrophage</dim:field>
   <dim:field mdschema="dc" element="subject" lang="en_US">nucleic acid</dim:field>
   <dim:field mdschema="dc" element="subject" lang="en_US">phosphorylation</dim:field>
   <dim:field mdschema="dc" element="subject" lang="en_US">TREX1</dim:field>
   <dim:field mdschema="dc" element="title" lang="en_US">TREX1 DNASE ACTIVITY IS REGULATED BY PHOSPHORYLATION AND MACROPHAGES LACKING TREX1 HAVE IMPAIRED EFFEREOCYTOSIS</dim:field>
   <dim:field mdschema="dc" element="type" lang="en_US">Dissertation</dim:field>
   <dim:field mdschema="thesis" element="contributor" qualifier="committeeChair" lang="en_US">Hollis, Thomas</dim:field>
   <dim:field mdschema="thesis" element="contributor" qualifier="committeeMember" lang="en_US">Perrino, Fred W</dim:field>
   <dim:field mdschema="thesis" element="contributor" qualifier="committeeMember" lang="en_US">Daniel, Larry W</dim:field>
   <dim:field mdschema="thesis" element="contributor" qualifier="committeeMember" lang="en_US">Poole, Leslie B</dim:field>
   <dim:field mdschema="thesis" element="degree" qualifier="discipline" lang="en_US">Biochemistry and Molecular Biology</dim:field>
   <dim:field mdschema="thesis" element="embargo" qualifier="terms" lang="en_US">2019-08-22</dim:field>
   <dim:field mdschema="others" element="access-status">open.access</dim:field>
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