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dc.identifier.urihttp://hdl.handle.net/1951/55602
dc.identifier.urihttp://hdl.handle.net/11401/72651
dc.description.sponsorshipThis work is sponsored by the Stony Brook University Graduate School in compliance with the requirements for completion of degree.en_US
dc.formatMonograph
dc.format.mediumElectronic Resourceen_US
dc.language.isoen_US
dc.publisherThe Graduate School, Stony Brook University: Stony Brook, NY.
dc.typeDissertation
dcterms.abstractProduction and breakdown of certain phosphoinositides plays key roles in a variety of cellular processes. Among these, phosphatidylinositol-4, 5-phosphate (PIP <sub>2</sub>) is well known for its critical functions in membrane trafficking, cytoskeletal organization, and signal transduction. Type I phosphatidylinositol-4-phosphate 5-kinase (PIPKI) is the main enzyme responsible for the synthesis of PIP<sub>2</sub>. Although PIPKI activity is regulated by small G proteins and phosphatidic acid (PA), the contribution of these upstream regulators in actin cytoskeletal reorganization remains unclear. The binding region of some other PA-regulated proteins has been identified. From these, it appears that binding may either be direct or electrostatic in nature. I have identified basic residues in the proposed membrane-binding region of PIPKI&#915; that are required for membrane translocation, actin reorganization, and stimulation by PA. I also demonstrate here that the direct binding of PIPKI to PA through these residues is required for these important functions.
dcterms.available2012-05-15T18:06:22Z
dcterms.available2015-04-24T14:53:02Z
dcterms.contributorJoav Privesen_US
dcterms.contributorDu, Guangweien_US
dcterms.contributorDeborah A. Brownen_US
dcterms.contributorMichael A. Frohman.en_US
dcterms.creatorRoach, Akua Ntiamoah
dcterms.dateAccepted2012-05-15T18:06:22Z
dcterms.dateAccepted2015-04-24T14:53:02Z
dcterms.dateSubmitted2012-05-15T18:06:22Z
dcterms.dateSubmitted2015-04-24T14:53:02Z
dcterms.descriptionDepartment of Molecular and Cellular Pharmacologyen_US
dcterms.formatMonograph
dcterms.formatApplication/PDFen_US
dcterms.identifierhttp://hdl.handle.net/1951/55602
dcterms.identifierRoach_grad.sunysb_0771E_10274.pdfen_US
dcterms.identifierhttp://hdl.handle.net/11401/72651
dcterms.issued2010-08-01
dcterms.languageen_US
dcterms.provenanceMade available in DSpace on 2012-05-15T18:06:22Z (GMT). No. of bitstreams: 1 Roach_grad.sunysb_0771E_10274.pdf: 6322827 bytes, checksum: 8df74ca74fa83c130db32226b82439cc (MD5) Previous issue date: 1en
dcterms.provenanceMade available in DSpace on 2015-04-24T14:53:02Z (GMT). No. of bitstreams: 3 Roach_grad.sunysb_0771E_10274.pdf.jpg: 1894 bytes, checksum: a6009c46e6ec8251b348085684cba80d (MD5) Roach_grad.sunysb_0771E_10274.pdf.txt: 91916 bytes, checksum: 6b63c026f0747645621df71a26925466 (MD5) Roach_grad.sunysb_0771E_10274.pdf: 6322827 bytes, checksum: 8df74ca74fa83c130db32226b82439cc (MD5) Previous issue date: 1en
dcterms.publisherThe Graduate School, Stony Brook University: Stony Brook, NY.
dcterms.subjectactin reorganization, Lipid Signaling, phosphatidic acid, PIPKI
dcterms.subjectHealth Sciences, Pharmacology
dcterms.titleThe Role of Phosphatidic Acid in PIPKI-regulated Actin Reorganization
dcterms.typeDissertation


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