This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on ISI (1)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Topic Collections  • Neurogenetics  • Genetic Disorders  • Genetics, Other  • Alert me on articles by topic

Savitha Kalidas, PhD; Dean P. Smith, MD, PhD

Arch Neurol. 2003;60:1197-1200.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

A remarkable revolution is occurring in biomedical science that is likely to have profound implications for the way we treat human diseases in the future. In the past 2 years, we have learned that introduction of short double-stranded RNA (dsRNA) molecules into vertebrate cells can silence any gene homologous to the dsRNA. This process is called RNA interference (RNAi) and is based on the ability of the cell to recognize and degrade messenger RNAs (mRNAs) that base-pair with the antisense component of the dsRNA. RNA interference probably arose as a defense against viruses and transposable elements that replicate by means of dsRNA intermediates. This form of genetic immunity is ancient; organisms from paramecium to humans use similar mechanisms. In addition, it is now evident that RNAi normally regulates some cellular genes, and a whole host of noncoding antisense mRNAs are produced in . . . [Full Text of this Article]

THE MECHANISTIC BASIS OF RNAi

A LINK BETWEEN RNAi AND FRAGILE X SYNDROME

RNAi AND FUNCTIONAL GENOMICS

RNAi AND TREATMENT OF HUMAN NEUROLOGICAL DISEASE

From the Department of Pharmacology and Center for Basic Neuroscience, The University of Texas Southwestern Medical Center at Dallas.