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
Advances in Health and Disease. Volume 8
$225.00
Shopping Cart more
0 items
Information
Shipping & Returns
Privacy Notice
Conditions of Use
Contact Us
Notifications more
NotificationsNotify me of updates to BRIT1, A Novel DNA Damage Responsive Protein Dysfunctioned in Primary Microcephaly and Cancer (pp. 99-112)
Tell A Friend
 
Tell someone you know about this product.
BRIT1, A Novel DNA Damage Responsive Protein Dysfunctioned in Primary Microcephaly and Cancer (pp. 99-112) $100.00
Authors:  (Guang Peng, Shiaw Yih Lin, Department of Systems Biology, The University of Texas, Anderson Cancer Center, USA)
Abstract:
BRIT1 (BRCT-Repeat Inhibitor of hTERT expression) was originally identified
from our laboratory as an inhibitor of human telomere reverse transcriptase (hTERT) by
a genome-wide genetic screen. The amino acid sequence of BRIT1 was later matched to
a putative disease gene called microcephalin (MCPH1). Aberrations of BRIT1 have been
identified in breast, ovarian and prostate cancer as well as autosomal recessive primary
microcephaly, a neuronal development disorder characterized by reduced brain size of
patients. Therefore, the functions of BRIT1 are of critical research interests that can
potentially contribute to two fundamental pathological processes, cancer and neurodevelopmental
disorder. In this chapter, we will present the most recent findings on
BRIT1ís functions in both DNA damage response and cell cycle control. Our studies
have revealed that BRIT1 functions as a novel regulator in the ATM/ATR pathway and a
proximal factor in DNA damage response controlling the recruitment of multiple sensors
and early mediators to the DNA damage sites. BRIT1 has also been shown to control G2-
M checkpoint and prevents premature entry into mitosis. These results support a role of
BRIT1 as a guardian of genomic integrity that prevents the pathogenesis of human
cancer and microcephaly. Finally, we will discuss our future research interests in
revealing the underlying mechanisms on how BRIT1 defect may contribute to the
development of cancer and primary microcephaly. 


Available Options:
Version:
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

BRIT1, A Novel DNA Damage Responsive Protein Dysfunctioned in Primary Microcephaly and Cancer (pp. 99-112)