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RNA Polymerase I Elongation Kinetics...
~
Scull, Catherine Elizabeth.
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RNA Polymerase I Elongation Kinetics: A Biochemical and Global Study of a Cancer Therapeutic Target.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
RNA Polymerase I Elongation Kinetics: A Biochemical and Global Study of a Cancer Therapeutic Target./
作者:
Scull, Catherine Elizabeth.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2020,
面頁冊數:
245 p.
附註:
Source: Dissertations Abstracts International, Volume: 81-12.
Contained By:
Dissertations Abstracts International81-12.
標題:
Biochemistry. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=27742166
ISBN:
9798645466190
RNA Polymerase I Elongation Kinetics: A Biochemical and Global Study of a Cancer Therapeutic Target.
Scull, Catherine Elizabeth.
RNA Polymerase I Elongation Kinetics: A Biochemical and Global Study of a Cancer Therapeutic Target.
- Ann Arbor : ProQuest Dissertations & Theses, 2020 - 245 p.
Source: Dissertations Abstracts International, Volume: 81-12.
Thesis (Ph.D.)--The University of Alabama at Birmingham, 2020.
This item must not be sold to any third party vendors.
My graduate research has focused on understanding the elongation kinetics of RNA polymerase I (Pol I), the enzyme responsible for synthesizing ribosomal RNA (rRNA), and defining how inhibition of ribosome biogenesis may be used as a cancer therapeutic strategy. Here, I have defined key biophysical features of Pol I and I have expanded the field's understanding of Pol I elongation by: 1) characterizing the enzymatic properties of Pol I by mutational analysis of the polymerase itself, and by 2) elucidating the role of DNA sequence on Pol I arrest and nucleolytic cleavage activity. In recent years, Pol I has become an attractive target for cancer therapeutics, as enhanced ribosome biogenesis is necessary for the rapid growth and proliferation of cancer cells. I have demonstrated that ribosome biogenesis inhibition by a novel inhibitor, RBI2 (ribosome biogenesis inhibitor 2) specifically decreases cancer cell growth and proliferation, likely by increasing premature rRNA turnover. Collectively, my studies on Pol I's enzymatic properties have resulted in a better understanding of the relationship between cancer cell growth and ribosome biogenesis. As a whole, my thesis research has resulted in a more detailed understanding of RNA polymerase I (Pol I) elongation kinetics and it has further validated inhibition of ribosome biogenesis as a promising cancer chemotherapeutic target.
ISBN: 9798645466190Subjects--Topical Terms:
518028
Biochemistry.
Subjects--Index Terms:
Cancer
RNA Polymerase I Elongation Kinetics: A Biochemical and Global Study of a Cancer Therapeutic Target.
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My graduate research has focused on understanding the elongation kinetics of RNA polymerase I (Pol I), the enzyme responsible for synthesizing ribosomal RNA (rRNA), and defining how inhibition of ribosome biogenesis may be used as a cancer therapeutic strategy. Here, I have defined key biophysical features of Pol I and I have expanded the field's understanding of Pol I elongation by: 1) characterizing the enzymatic properties of Pol I by mutational analysis of the polymerase itself, and by 2) elucidating the role of DNA sequence on Pol I arrest and nucleolytic cleavage activity. In recent years, Pol I has become an attractive target for cancer therapeutics, as enhanced ribosome biogenesis is necessary for the rapid growth and proliferation of cancer cells. I have demonstrated that ribosome biogenesis inhibition by a novel inhibitor, RBI2 (ribosome biogenesis inhibitor 2) specifically decreases cancer cell growth and proliferation, likely by increasing premature rRNA turnover. Collectively, my studies on Pol I's enzymatic properties have resulted in a better understanding of the relationship between cancer cell growth and ribosome biogenesis. As a whole, my thesis research has resulted in a more detailed understanding of RNA polymerase I (Pol I) elongation kinetics and it has further validated inhibition of ribosome biogenesis as a promising cancer chemotherapeutic target.
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