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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
BRIT1’s 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. 


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