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Transcriptome and proteome analyses ...
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The Johns Hopkins University.
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Transcriptome and proteome analyses of heart failure.
Record Type:
Language materials, printed : Monograph/item
Title/Author:
Transcriptome and proteome analyses of heart failure./
Author:
Yung, Christina K.
Description:
181 p.
Notes:
Adviser: Raimond L. Winslow.
Contained By:
Dissertation Abstracts International68-04B.
Subject:
Biology, Bioinformatics. -
Online resource:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3262529
Transcriptome and proteome analyses of heart failure.
Yung, Christina K.
Transcriptome and proteome analyses of heart failure.
- 181 p.
Adviser: Raimond L. Winslow.
Thesis (Ph.D.)--The Johns Hopkins University, 2007.
The disease mechanisms of heart failure, the leading cause of cardiovascular mortality and morbidity, are complex and remain largely unknown. The studies presented in this dissertation take a broad-based approach to analyze and contrast the transcriptome and proteome of healthy and diseased hearts.Subjects--Topical Terms:
1018415
Biology, Bioinformatics.
Transcriptome and proteome analyses of heart failure.
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Transcriptome and proteome analyses of heart failure.
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181 p.
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Adviser: Raimond L. Winslow.
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Source: Dissertation Abstracts International, Volume: 68-04, Section: B, page: 2491.
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Thesis (Ph.D.)--The Johns Hopkins University, 2007.
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The disease mechanisms of heart failure, the leading cause of cardiovascular mortality and morbidity, are complex and remain largely unknown. The studies presented in this dissertation take a broad-based approach to analyze and contrast the transcriptome and proteome of healthy and diseased hearts.
520
$a
Using microarray technology, we are able to measure the expression over 20,000 human genes simultaneously and find that 165 genes are regulated in dilated cardiomyopathy when compared to controls. The biological functions of these genes can be classified into the following major categories: apoptosis and oxidant stress, cell growth and maintenance, cytoskeleton, extracellular matrix, ion transport, metabolism, signal transduction, translational regulation and protein modification, DNA replication and repair, and transcription factors. This finding provides some new candidates for studying the mechanisms underlying the increased cell death, cytoskeleton disruptions and ECM remodeling in heart failure.
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In addition to gene transcription, functions are altered through the regulation of protein expression and their post-translational modifications (PTMs). Hence, we complement a transcriptome analysis of a canine model of tachycardia pacing-induced heart failure with a proteome analysis of mitochondrial proteins by two-dimensional gel electrophoresis (2DE). Because 2DE allows only partial observation of any proteome, we increase proteome coverage by focusing our efforts on the mitochondria because of its important role in energy metabolism and apoptosis during heart failure. The majority of changes at the mRNA level are decreased expression contrasting the dominantly increased expression of the mitochondrial proteins. This extensive discordance between mRNA and proteins observed across all mitochondrial functions suggests that the regulation of the mitochondria in failing hearts is at the translational rather than transcriptional level. Another possible mode of regulation is through PTMs as we find that 50% of the mitochondrial proteome (based on 2DE analysis) have potential PTMs, one being phosphorylation which we validate through dephosphorylation treatment and difference gel electrophoresis.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3262529
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