Nova Publishers
My Account Nova Publishers Shopping Cart
HomeBooksSeriesJournalsReference CollectionseBooksInformationSalesImprintsFor Authors
  Top » Catalog » Books » Biology » Genetics » New Research on DNA Damage Chapters » My Account  |  Cart Contents  |  Checkout   
Quick Find
Use keywords to find the product you are looking for.
Advanced Search
What's New? more
Temporal Lobe Epilepsy: Pathologic Substrates and Causes
Shopping Cart more
0 items
Shipping & Returns
Privacy Notice
Conditions of Use
Contact Us
Notifications more
NotificationsNotify me of updates to HTLV-I Tax Promotes Genomic Instability by Interfering with Repair of DNA Breaks (pp. 125-144)
Tell A Friend
Tell someone you know about this product.
HTLV-I Tax Promotes Genomic Instability by Interfering with Repair of DNA Breaks (pp. 125-144) $100.00
Authors:  (Razvan I. Ducu, Susan J. Marriott, Department of Molecular Virology and Microbiology, Houston, USA)
An emerging mechanism of cellular transformation by oncogenic viruses is the
inhibition or suppression of cellular DNA repair. This review will focus on human T-cell
leukemia virus (HTLV-I), which is the causative agent of adult T-cell leukemia (ATL),
an aggressive clonal malignancy of CD4+ T lymphocytes. The oncogenic potential of
HTLV-I relies on expression of the viral transcriptional modulator, Tax. In addition to
activating viral transcription, Tax controls the expression of a large and diverse array of
cellular genes. By altering gene expression homeostasis, as well as by direct proteinprotein
interactions, Tax interferes with normal DNA replication and repair processes,
thereby contributing to an increased mutation frequency in HTLV-I infected cells. We
and others have shown that Tax can suppress DNA base and nucleotide excision repair
pathways by altering the expression of important factors involved in these pathways,
such as DNA polymerase beta and PCNA. Tax has also been shown to affect protein
interactions that regulate DNA repair pathways and to attenuate the ATM mediated
damage response, a major pathway for repair of DNA double strand breaks (DSBs). In
this chapter we will review the effect of Tax on DNA repair and genome stability and the
role of these processes in cellular transformation. We will discuss the inhibitory effect of
Tax on ATM kinase activity, which reveals novel insights into the normal function of
this signaling and repair pathway. Finally, we will discuss recent data suggesting a
critical role for the DNA double strand break repair pathway in retroviral replication and
tumor suppression. 

Available Options:
This Item Is Currently Unavailable.
Special Focus Titles
01.Peter Singerís Ethics: A Critical Appraisal
02.Sexism: Past, Present and Future Perspectives
03.Body and Politics: Elite Disability Sport in China
04.Childhood and Adolescence: Tribute to Emanuel Chigier, 1928-2017
05.Renal Replacement Therapy: Controversies and Future Trends
06.Food-Drug Interactions: Pharmacokinetics, Prevention and Potential Side Effects
07.Terrorism and Violence in Islamic History and Theological Responses to the Arguments of Terrorists
08.International Event Management: Bridging the Gap between Theory and Practice
09.The Sino-Indian Border War and the Foreign Policies of China and India (1950-1965)
10.Tsunamis: Detection, Risk Assessment and Crisis Management
11.Sediment Watch: Monitoring, Ecological Risk Assessment and Environmental Management
12.Self-Regulated Learners: Strategies, Performance, and Individual Differences

Nova Science Publishers
© Copyright 2004 - 2018

HTLV-I Tax Promotes Genomic Instability by Interfering with Repair of DNA Breaks (pp. 125-144)