cotranscriptional chromatin remodeling by small rna species an htlv-1 perspective由小型rna cotranscriptional染色质重塑物种htlv 1的角度.pdfVIP
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cotranscriptional chromatin remodeling by small rna species an htlv-1 perspective由小型rna cotranscriptional染色质重塑物种htlv 1的角度
Hindawi Publishing Corporation
Leukemia Research and Treatment
Volume 2012, Article ID 984754, 15 pages
doi:10.1155/2012/984754
Review Article
Cotranscriptional Chromatin Remodeling by Small RNA Species:
An HTLV-1 Perspective
Nishat Aliya, Saifur Rahman, Zafar K. Khan, and Pooja Jain
Department of Microbiology and Immunology, Drexel Institute for Biotechnology and Virology Research,
Drexel University College of Medicine, 3805 Old Easton Road, Doylestown, PA 18902, USA
Correspondence should be addressed to Pooja Jain, pjain@
Received 23 August 2011; Revised 28 October 2011; Accepted 3 November 2011
Academic Editor: Mineki Saito
Copyright © 2012 Nishat Aliya et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Cell type specificity of human T cell leukemia virus 1 has been proposed as a possible reason for differential viral outcome in pri-
mary target cells versus secondary. Through chromatin remodeling, the HTLV-1 transactivator protein Tax interacts with cellular
factors at the chromosomally integrated viral promoter to activate downstream genes and control viral transcription. RNA inter-
ference is the host innate defense mechanism mediated by short RNA species (siRNA or miRNA) that regulate gene expression.
There exists a close collaborative functioning of cellular transcription factors with miRNA in order to regulate the expression of a
number of eukaryotic genes including those involved in suppression of cell growth, induction of apoptosis, as well as repressing
viral replication and propagation. In addition, it has been suggested that retroviral latency is influenced by chromatin alterations
brought ab
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