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Functional Genomics of Human Ion Channels

Edited by Zhiguo Wang

ISBN 10: 8178954346 / ISBN 13: 9788178954349
Editorial: Transworld Research Network, 2010
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Título: Functional Genomics of Human Ion Channels

Editorial: Transworld Research Network

Año de publicación: 2010

Encuadernación: Hardcover

Condición del libro: Acceptable

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With the completion of the human genome project, we have entered the post-genome era. During the past decade, the complete genomes of more than 150 different organisms have been sequenced and made available in databases. These databases provide extremely useful collections of organized, validated data that are indispensable for genomics and proteomics research and the drug discovery process. Transcription factors, making up 6% of the human genome and ranking second because of their abundance, play a critical role in the transcription regulation of gene expression, and have recently been considered a new class of candidate targets for drug discovery. MicroRNAs (miRNAs), endogenous noncoding regulatory mRNAs of around 22-nucleotides long, have rapidly emerged as one of the key governors of the gene expression regulatory program in cells of varying species. Accumulating evidence suggests that miRNAs constitutes a novel, universal mechanism for fine regulation of gene expression in all organisms, tuning the cellular phenotype during delicate processes. Owing to their ever-increasing number in the mammalian cells and their ever-increasing implication in the control of the fundamental biological processes (such as development, cell growth and differentiation, cell death, etc), miRNAs have now become a research subject capturing major interest of scientists worldwide. Moreover, with recent studies revealing the macro roles of miRNAs in the pathogenesis of adult humans, we have now entered a new era of miRNA research. The exciting findings in this field have inspired us with a premise and a promise that miRNAs will ultimately be taken to the heart for therapy of human disease. Yet these mysterious tiny molecules still remain mystifying in their cellular function and pathological role. Homeostatic regulation of ion channel expression determines the functional status of the proteins encoded by these genes thereby the cardiac electrical activities. Homeostatic regulation occurs at every step along the biosynthesis of ion channel proteins. Transcription regulation by the interactions between transcription factors and cis-acting elements within the promoter region of ion channels genes, and post-transcription regulation by the interaction between microRNAs and the seed binding sites within the 3 UTR of ion channel genes, are the two most important regulatory mechanisms. In the past two years, we have witnessed a rapid evolving in the field of functional genomics of human ion channels. And this motivates me to write this book entitled Functional Genomics of Human Ion Channels. This book is written for fundamentalists (starting from graduate students to principal investigtors) in the field of studies involving functional genomics and miRNAs, in universities and research institutions. The aim of this book is to collect the published studies on functional genomics of human cardiac ion channel genes providing the new findings on transcription regulation conferred by 5 -flanking regions and post-transcription regulation conferred by 3 UTRs. It is my expectation that from this book readers would be able to acquire the basic knowledge of transcription factors and miRNAs, and their roles in homeostatic regulation of human cardiac ion channels. Functional Genomics of Human Ion Channels contains includes 9 chapters. It begins with Chapter 1 with an introduction of basic knowledge of cardiac ion channels and their role in determining cardiac electrical activities. Particular emphasis is placed on the concepts of homeostatic regulation and functional genomics of ion channel genes. Chapter 2 introduces another new concept Channelopathies , the diseases directly caused by, and indirectly related to, dysfunction of ion-channel subunits as consequences of deregulation of expression, genetic mutation, epigenetic single nucleotide polymorphysm

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