Biology Reference
In-Depth Information
139. Busso CS, Wedgeworth CM, Izumi T. Ubiquitination of human AP-endonuclease 1 (APE1)
enhanced by T233E substitution and by CDK5.
Nucleic Acids Res
2011;
:8017-28.
140. Fischer JA, Muller-Weeks S, Caradonna S. Proteolytic degradation of the nuclear isoform of
uracil-DNA glycosylase occurs during the S phase of the cell cycle.
DNA Repair (Amst)
2004;
39
:505-13.
141. Chen J, Bozza W, Zhuang Z. Ubiquitination of PCNA and its essential role in eukaryotic
translesion synthesis.
Cell Biochem Biophys
2011;
3
:47-60.
142. Lehmann AR. Ubiquitin-family modifications in the replication of DNA damage.
FEBS Lett
2011;
60
:2772-9.
143. Katyal S, McKinnon PJ. DNA strand breaks, neurodegeneration and aging in the brain.
Mech
Ageing Dev
2008;
585
:483-91.
144. Al-Tassan N, Chmiel NH, Maynard J, Fleming N, Livingston AL, Williams GT, et al. Inherited
variants of MYH associated with somatic G:C
129
!
T:A mutations in colorectal tumors.
Nat Genet
:227-32.
145. Goodenberger M, Lindor NM. Lynch syndrome and MYH-associated polyposis: review and
testing strategy.
J Clin Gastroenterol
2011;
2002;
30
:488-500.
146. Boiteux S, Radicella JP. The human OGG1 gene: structure, functions, and its implication in
the process of carcinogenesis.
Arch Biochem Biophys
2000;
45
:1-8.
147. Shinmura K, Yokota J. The OGG1 gene encodes a repair enzyme for oxidatively damaged
DNA and is involved in human carcinogenesis.
Antioxid Redox Signal
2001;
377
:597-609.
148. Dherin C, Radicella JP, Dizdaroglu M, Boiteux S. Excision of oxidatively damaged DNA bases
by the human alpha-hOgg1 protein and the polymorphic alpha-hOgg1(Ser326Cys) protein
which is frequently found in human populations.
Nucleic Acids Res
1999;
3
:4001-7.
149. Hill JW, Evans MK. Dimerization and opposite base-dependent catalytic impairment of
polymorphic S326C OGG1 glycosylase.
Nucleic Acids Res
2006;
27
:1620-32.
150. Weiss JM, Goode EL, Ladiges WC, Ulrich CM. Polymorphic variation in hOGG1 and risk of
cancer: a review of the functional and epidemiologic literature.
Mol Carcinog
2005;
34
42
:
127-41.
151. Klungland A, Rosewell I, Hollenbach S, Larsen E, Daly G, Epe B, et al. Accumulation of
premutagenic DNA lesions in mice defective in removal of oxidative base damage.
Proc Natl
Acad Sci USA
1999;
:13300-5.
152. Osterod M, Hollenbach S, Hengstler JG, Barnes DE, Lindahl T, Epe B. Age-related and
tissue-specific accumulation of oxidative DNA base damage in 7,8-dihydro-8-oxoguanine-
DNA glycosylase (Ogg1) deficient mice.
Carcinogenesis
2001;
96
:1459-63.
153. Xie Y, Yang H, Cunanan C, Okamoto K, Shibata D, Pan J, et al. Deficiencies in mouse Myh
and Ogg1 result in tumor predisposition and G to T mutations in codon 12 of the K-ras
oncogene in lung tumors.
Cancer Res
2004;
22
:3096-102.
154. Parsons JL, Elder RH. DNA N-glycosylase deficient mice: a tale of redundancy.
Mutat Res
2003;
64
:165-75.
155. Wilson 3rd DM, Bohr VA. The mechanics of base excision repair, and its relationship to aging
and disease.
DNA Repair (Amst)
2007;
531
:544-59.
156. Friedberg EC, Walker GC, Siede W, Wood RD, Schultz RA, Ellenberger T.
DNA repair and
mutagenesis
. 2nd ed. Washington: ASM Press; 2006.
157. Wilson 3rd DM, Thompson LH. Life without DNA repair.
Proc Natl Acad Sci USA
1997;
6
:12754-7.
158. Zheng L, Dai H, Hegde ML, Zhou M, Guo Z, Wu X, et al. Fen1 mutations that specifically
disrupt its interaction with PCNA cause aneuploidy-associated cancer.
Cell Res
2011;
94
:
21
1052-67.
159. Zheng L, Dai H, Zhou M, Li M, Singh P, Qiu J, et al. Fen1 mutations result in autoimmunity,
chronic inflammation and cancers.
Nat Med
2007;
:812-9.
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