東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back

Switch To: Labeled | MARC Mode | ISBD

Cytoplasmic Mislocalization of CTCF ...

Wang, Jiance Atom.

Linked to FindBook

Google Book

Amazon

博客來

Cytoplasmic Mislocalization of CTCF by Leukemic Oncogene NPM1c in Acute Myeloid Leukemia.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Cytoplasmic Mislocalization of CTCF by Leukemic Oncogene NPM1c in Acute Myeloid Leukemia./
Author:	Wang, Jiance Atom.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2019,
Description:	144 p.
Notes:	Source: Dissertations Abstracts International, Volume: 81-05, Section: B.
Contained By:	Dissertations Abstracts International81-05B.
Subject:	Oncology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=22584727
ISBN:	9781392551059

Cytoplasmic Mislocalization of CTCF by Leukemic Oncogene NPM1c in Acute Myeloid Leukemia.
Wang, Jiance Atom.

Cytoplasmic Mislocalization of CTCF by Leukemic Oncogene NPM1c in Acute Myeloid Leukemia. - Ann Arbor : ProQuest Dissertations & Theses, 2019 - 144 p.

Source: Dissertations Abstracts International, Volume: 81-05, Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2019.

This item must not be sold to any third party vendors.

Acute myeloid leukemia (AML) cells with normal cytogenetics frequently harbor a TCTG insertion in exon 12 of Nucleophosmin 1 (NPM1), resulting in a frameshift creating a nuclear export signal and cytoplasmic localization of the mutant protein NPM1c. Although the mutation directs NPM1c to the cytoplasm, the underlying mechanism of how NPM1c causes AML remains incompletely understood. NPM1 participates in multiple protein-protein interactions; among those interacting proteins is the CCCTC binding factor (CTCF), the master weaver of the genome. CTCF is involved in several important nuclear functions including DNA looping, regulation of gene expression, and RNA splicing through binding to CTCF DNA binding sites. I hypothesized that NPM1c could mislocalize CTCF into the cytoplasm, thereby reducing the functional level of nuclear CTCF and so alter its regulatory roles regarding gene expression and epigenetic functions in the nucleus. Our studies verified the interaction of CTCF with NPM1. Furthermore I demonstrated that CTCF interacts with NPM1c, partially redistributing CTCF into the cytoplasm. The interaction of CTCF and NPM1c involves the amino terminus of CTCF and the last 50 amino acids on the C-terminus of NPM1. Moreover, cytoplasmic CTCF can be relocalized to the nucleus by interfering with the interaction of CTCF and NPM1c.

ISBN: 9781392551059Subjects--Topical Terms:

751006
Oncology.
Subjects--Index Terms:

Acute myeloid leukemia

Cytoplasmic Mislocalization of CTCF by Leukemic Oncogene NPM1c in Acute Myeloid Leukemia.
LDR:02564nmm a2200385 4500 001 2272686
005 20201105110156.5
008 220629s2019 ||||||||||||||||| ||eng d
020 $a 9781392551059
035 $a (MiAaPQ)AAI22584727
035 $a AAI22584727
040 $a MiAaPQ $c MiAaPQ
100 1 $a Wang, Jiance Atom. $3 3550114
245 1 0 $a Cytoplasmic Mislocalization of CTCF by Leukemic Oncogene NPM1c in Acute Myeloid Leukemia.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2019
300 $a 144 p.
500 $a Source: Dissertations Abstracts International, Volume: 81-05, Section: B.
500 $a Advisor: Minden, Mark David.
502 $a Thesis (Ph.D.)--University of Toronto (Canada), 2019.
506 $a This item must not be sold to any third party vendors.
520 $a Acute myeloid leukemia (AML) cells with normal cytogenetics frequently harbor a TCTG insertion in exon 12 of Nucleophosmin 1 (NPM1), resulting in a frameshift creating a nuclear export signal and cytoplasmic localization of the mutant protein NPM1c. Although the mutation directs NPM1c to the cytoplasm, the underlying mechanism of how NPM1c causes AML remains incompletely understood. NPM1 participates in multiple protein-protein interactions; among those interacting proteins is the CCCTC binding factor (CTCF), the master weaver of the genome. CTCF is involved in several important nuclear functions including DNA looping, regulation of gene expression, and RNA splicing through binding to CTCF DNA binding sites. I hypothesized that NPM1c could mislocalize CTCF into the cytoplasm, thereby reducing the functional level of nuclear CTCF and so alter its regulatory roles regarding gene expression and epigenetic functions in the nucleus. Our studies verified the interaction of CTCF with NPM1. Furthermore I demonstrated that CTCF interacts with NPM1c, partially redistributing CTCF into the cytoplasm. The interaction of CTCF and NPM1c involves the amino terminus of CTCF and the last 50 amino acids on the C-terminus of NPM1. Moreover, cytoplasmic CTCF can be relocalized to the nucleus by interfering with the interaction of CTCF and NPM1c.
590 $a School code: 0779.
650 4 $a Oncology. $3 751006
650 4 $a Molecular biology. $3 517296
650 4 $a Biostatistics. $3 1002712
653 $a Acute myeloid leukemia
653 $a Alternative splicing
653 $a CTCF
653 $a Cytoplasmic mislocalization
653 $a DNA methylation
653 $a NPM1c
690 $a 0992
690 $a 0307
690 $a 0308
710 2 $a University of Toronto (Canada). $b Medical Biophysics. $3 3181600
773 0 $t Dissertations Abstracts International $g 81-05B.
790 $a 0779
791 $a Ph.D.
792 $a 2019
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=22584727