CHARACTERIZATION AND TARGETING OF THE MULTIPLE DNA SECONDARY STRUCTURES IN THE KRAS PROXIMAL PROMOTER TO MODULATE GENE EXPRESSION

Persistent Link:
http://hdl.handle.net/10150/559576
Title:
CHARACTERIZATION AND TARGETING OF THE MULTIPLE DNA SECONDARY STRUCTURES IN THE KRAS PROXIMAL PROMOTER TO MODULATE GENE EXPRESSION
Author:
Kaiser, Christine Elizabeth
Issue Date:
2015
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Embargo:
Dissertation not available (per author's request)
Abstract:
KRAS is a well-validated drug target for anti-cancer therapy, yet no clinically useful drugs that directly inhibit its function currently exist. We aim to target KRAS at the transcriptional level, through DNA secondary structures.
Type:
text; Electronic Dissertation
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Graduate College; Pharmaceutical Sciences
Degree Grantor:
University of Arizona
Advisor:
Hurley, Laurence H.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen
dc.titleCHARACTERIZATION AND TARGETING OF THE MULTIPLE DNA SECONDARY STRUCTURES IN THE KRAS PROXIMAL PROMOTER TO MODULATE GENE EXPRESSIONen_US
dc.creatorKaiser, Christine Elizabethen
dc.contributor.authorKaiser, Christine Elizabethen
dc.date.issued2015en
dc.publisherThe University of Arizona.en
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en
dc.description.releaseDissertation not available (per author's request)en
dc.description.abstractKRAS is a well-validated drug target for anti-cancer therapy, yet no clinically useful drugs that directly inhibit its function currently exist. We aim to target KRAS at the transcriptional level, through DNA secondary structures.en
dc.typetexten
dc.typeElectronic Dissertationen
thesis.degree.namePh.D.en
thesis.degree.leveldoctoralen
thesis.degree.disciplineGraduate Collegeen
thesis.degree.disciplinePharmaceutical Sciencesen
thesis.degree.grantorUniversity of Arizonaen
dc.contributor.advisorHurley, Laurence H.en
dc.contributor.committeememberHurley, Laurence H.en
dc.contributor.committeememberYang, Danzhouen
dc.contributor.committeememberWondrak, Georgen
dc.contributor.committeememberSun, Daekyuen
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