DNA Repair and Mutagenesis

Customer Reviews:

The Definitive Book.......2006-01-19

The first edition of this book was published in 1995 and it was noted then that this was a field that was rapidly progressing. Progress has not slowed, and for the past several years the authors, now expanded to five, have been reviewing, re-writing where necessary, and expanding the book to nearly double it's original size with nearly double the number of illustrations.

As a textbook, this volume is suitable for the advanced undergraduate and graduate students. As a reference book, this volume is the most complete survey of the field to date. It is excellent in its historical approach that illustrates how the present state of knowledge was reached. This provides a background understanding that sometimes opens the door to other types of research that might be conducted. There is further a series of comments on the directions that current research is going. Each chapter is heavily referenced, with 10,000 references to back up the content of the book.

This is the definite book on the subject.

Wow.......2005-12-27

This book is absolutely the most comprehensive and well written book in this field. The pictures are astounding, and the layout is superb. The whole book is great but, the chapters written by G. C. Walker are particularly enlightening. Anyone with even a mild intrest in DNA Repair and or Mutagenesis should purchase this book with utmost haste.

The best!.......2000-03-10

The most complete book in the subjet Cover all aspects of DNA repair Rich in experimental details If you're interessted in DNA repair this book is the bible

Chromosome Damage and Repair (Nato a S I Series Series a, Life Sciences)

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Chromosome Damage and Repair (Nato a S I Series Series a, Life Sciences)

Manufacturer: Springer
ProductGroup: Book
Binding: Hardcover

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DNA Repair and Mutagenesis in Eukaryotes (Basic Life Sciences)

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DNA Repair and Mutagenesis in Eukaryotes (Basic Life Sciences)

Manufacturer: Springer
ProductGroup: Book
Binding: Hardcover

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Oxidative Damage to Nucleic Acids (Molecular Biology Intelligence Unit)

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Oxidative Damage to Nucleic Acids (Molecular Biology Intelligence Unit)
Mark D. Evans
Manufacturer: Springer
ProductGroup: Book
Binding: Hardcover

Biochemistry | Biological Sciences | Science | Subjects | Books

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Product Description

This book provides an up-to-date coverage of selected topics in the area of nucleic acid oxidation. The topics have been selected to cover everything from basic chemical mechanisms, repair of damage and the biological and pathological meaning of DNA oxidation. The chapters are authored by leading, research active, international experts in the respective topics. In addition to some of the traditionally covered topics, we have included some areas that receive less attention in similar volumes, for example chapters focusing on damage to nucleic acids by halogenating and nitrating species, gene-specific damage, telomere shortening and damage to promoter regions. Through this approach, we recognize additionally the importance of nucleic acid damage beyond mutation and in pathological conditions other than carcinogenesis. The primary audience for the book would be research scientists and advanced postgraduate students, the book may also be of interest to clinicians with strong research interests. We would expect readers to come away from this book with a greater appreciation of the topic, particularly appraising the reader of areas that may not necessarily have been covered in such a volume before.

Recent Research Developments in DNA Repair and Mutagenesis

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Recent Research Developments in DNA Repair and Mutagenesis
Manuel Ruiz-Rubio and Encarna Alejandre-Dur?n
Manufacturer: Research Signpost
ProductGroup: Book
Binding: Paperback

Genetics | Evolution | Science | Subjects | Books
ASIN: 8177361058

A 1,4-dihydropyridine derivative reduces DNA damage and stimulates DNA repair in human cells in vitro [An article from: Mut.Res.-Genetic Toxicology and Environmental Mutagenesis]

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A 1,4-dihydropyridine derivative reduces DNA damage and stimulates DNA repair in human cells in vitro [An article from: Mut.Res.-Genetic Toxicology and Environmental Mutagenesis]
N.I. Ryabokon , R.I. Goncharova , G. Duburs , and Rzeszow
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital

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ASIN: B000RR826K

Book Description

Abnormal DNA repair in selenium-treated human cells [An article from: Mut.Res.-Genetic Toxicology and Environmental Mutagenesis]

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Abnormal DNA repair in selenium-treated human cells [An article from: Mut.Res.-Genetic Toxicology and Environmental Mutagenesis]
K.S. Abul-Hassan , B.E. Lehnert , L. Guant , and Walmsley
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital

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ASIN: B000RR4MFK

Book Description

This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, published by Elsevier in 2004. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

Description:
Selenium (Se), a micronutrient and an environmental, a chemical and an industrial agent in many products, can have genotoxic effects as well as antimutagenic and/or anticarcinogenic properties, depending on its concentration and oxidation state. We investigated the cytotoxic response of human osteosarcoma (U2OS) cells to low doses of sodium selenite and assayed their resistivity to cisplatin treatment and their capacity to reactivate cisplatin-treated reporter system, whose repair occurs through the transcription coupled repair (TCR) pathway, using the Host Cell Reactivation (HCR) Assay. In addition, we examined the ability of Se-treated human primary lymphocytes for normal double-strand breaks rejoining (DSBR) using the Challenge assay. Although, U2OS cells did not demonstrate cytotoxicity to all Se doses used, as measured by the cell proliferation MTT assay, their resistivity to cisplatin was significantly reduced. Moreover, Se-treated cells exhibited a significant reduction in their capacity for TCR as compared with untreated control cells. Primary human blood lymphocytes demonstrated cytotoxicity to Se treatment at only a concentration of 10@mM. There were no significant increases in chromosome-type deletions or chromatid breaks or in mitotic indices in cells treated with Se alone or Se plus ionizing irradiation. However, dicentric chromosomes significantly increased upon treatment with 1@mM Se plus irradiation as compared with Se-untreated irradiated control. These findings demonstrate direct evidence on the inhibitory effect of inorganic Se on cellular DNA repair capacity.

Age at exposure and Apc status influence the levels of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-DNA adducts in mouse intestine and liver ... Toxicology and Environmental Mutagenesis]

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Age at exposure and Apc status influence the levels of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-DNA adducts in mouse intestine and liver ... Toxicology and Environmental Mutagenesis]
I.L. Steffensen , H.A.J. Schut , and J. Alexander
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital

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ASIN: B000RR823I

Book Description

This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

Description:
We have previously shown that C57BL/6J-Min/+ (multiple intestinal neoplasia) mice, heterozygous for the Min mutation in the adenomatous polyposis coli gene, were more susceptible to intestinal tumorigenesis and had higher intestinal PhIP-DNA adduct levels after exposure to the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) on day 12 than on day 36 after birth [I.-L. Steffensen, H.A.J. Schut, J.E. Paulsen, A. Andreassen, J. Alexander, Intestinal tumorigenesis in multiple intestinal neoplasia mice induced by the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine: perinatal susceptibility, regional variation, and correlation with DNA adducts, Cancer Res. 61 (200l) 8689-8696]. In the present study, we have evaluated further whether this difference in susceptibility is related to adduct formation/removal, cell proliferation, apoptosis or expression of the nucleotide excision repair protein Xeroderma pigmentosum group A (XPA) in the intestines. Min/+ and +/+ (wild-type) mice were given a subcutaneous injection of 50mg/kgbw PhIP on day 12 or 36, and the levels of PhIP-DNA adducts after 8, 12, 24h, 3 or 7 days were quantified by use of ^3^2P-postlabelling. In Min/+ mice, adduct levels were significantly higher after exposure on day 12 than on day 36 in the middle (1.5- to 8.5-fold) and distal (1.3- to 6.5-fold) small intestine from 8h to 3 days after administration of PhIP, but not in the colon and proximal small intestine. In the liver - a non-target organ for PhIP - adduct levels were 2.0- to 7.5-fold higher after exposure on day 12 than on day 36 from 8 to 24h after exposure. Adduct levels were generally higher in the middle (1.1- to 1.8-fold) and distal (1.1- to 2.0-fold) small intestines of Min/+ compared with +/+ mice after PhIP exposure on day 12, i.e. in the area of the intestines previously found also to have the highest number of tumors in Min/+ mice. PhIP increased cell proliferation and the number of apoptotic cells in the intestine and liver. However, the higher susceptibility to intestinal tumorigenesis in Min/+ mice exposed to PhIP at early age, or in Min/+ mice compared with +/+ mice, could not be explained by differences in cell proliferation, apoptosis or expression of the XPA repair protein.

AlkB dioxygenase in preventing MMS-induced mutagenesis in Escherichia coli: Effect of Pol V and AlkA proteins [An article from: DNA Repair]

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AlkB dioxygenase in preventing MMS-induced mutagenesis in Escherichia coli: Effect of Pol V and AlkA proteins [An article from: DNA Repair]
J. Nieminuszczy , A. Sikora , M. Wrzesinski , and Janion
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital

Elsevier | By Publisher | e-Docs | Formats | Books
ASIN: B000RR6KW8

Book Description

This digital document is a journal article from DNA Repair, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

Description:
The deleterious effect of defective alkB allele encoding 1meA/3meC dioxygenase on reactivation of MMS-treated phage DNA has been frequently studied. Here, it is shown that: (i) AlkB protects the cells not only against the genotoxic but also against the potent mutagenic activity of MMS; (ii) mutations arising in alkB-defected strains are umuDC-dependent, and deletion of umuDC dramatically reduce MMS-induced mutations resulting from the presence of 1meA/3meC in DNA; (iii) specificity of MMS-induced argE3->Arg^+ reversions in AB1157 alkB-defective cells are predominantly AT->TA transversions and GC->AT transitions; (iv) overproduction of AlkA and the resultant decrease in 3meA residues in DNA dramatically reduce MMS-induced mutations. This reduction is most probably a secondary effect of AlkA due to a decrease in 3meA residues in DNA and, in consequence, suppression of SOS induction and Pol V expression. Overproduction of UmuD'C proteins reverses this effect.

The Arg280His polymorphism in X-ray repair cross-complementing gene 1 impairs DNA repair ability [An article from: Mut.Res.-Genetic Toxicology and Environmental Mutagenesis]

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The Arg280His polymorphism in X-ray repair cross-complementing gene 1 impairs DNA repair ability [An article from: Mut.Res.-Genetic Toxicology and Environmental Mutagenesis]
T. Takanami , J. Nakamura , Y. Kubota , and S. Horiuchi
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital

Elsevier | By Publisher | e-Docs | Formats | Books
ASIN: B000RR4M5U

Book Description

This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, published by Elsevier in 2005. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

Description:
The contribution of three single nucleotide polymorphisms (SNPs) that substitute amino acids in the X-ray repair cross-complementing gene 1 (XRCC1) protein, Arg194Trp (R194W), Arg280His (R280H), and Arg399Gln (R399Q), to the risk of various types of cancers has been extensively investigated by epidemiological researches. To investigate whether two of these polymorphisms directly influence their repair ability, we established Chinese hamster ovary (CHO) EM9 cell lines transfected with XRCC1^W^T, XRCC1^R^1^9^4^W, or XRCC1^R^2^8^0^H genes and analyzed the DNA repair ability of these cells. The EM9 cells that lack functional XRCC1 proteins exhibit severe sensitivity to methyl methanesulfonate (MMS). Introduction of the human XRCC1^W^T and XRCC1^R^1^9^4^W gene to EM9 cells restored the MMS sensitivity to the same level as the AA8 cells, a parental cell line. However, introduction of the XRCC1^R^2^8^0^H gene partially restored the MMS sensitivity, resulting in a 1.7- to 1.9-fold higher sensitivity to MMS compared with XRCC1^W^T and XRCC1^R^1^9^4^W cells at the LD"5"0 value. The alkaline comet assay determined diminished base excision repair/single strand break repair (BER/SSBR) efficiency in XRCC1^R^2^8^0^H cells as observed in EM9 cells. In addition, the amount of intracellular NAD(P)H decreased in XRCC1^R^2^8^0^H cells after MMS treatment. Indirect immunofluorescence staining of the XRCC1 protein showed an intense increase in the signals and clear foci of XRCC1 in the nuclei of the XRCC1^W^T cells, but a faint increase in the XRCC1^R^2^8^0^H cells, after MMS exposure. These results suggest that the XRCC1^R^2^8^0^H variant protein is defective in its efficient localization to a damaged site in the chromosome, thereby reducing the cellular BER/SSBR efficiency.

Book Description

This digital document is an article from Congressional Research Service (CRS) Reports and Issue Briefs, published by Thomson Gale on May 1, 2006. The length of the article is 9362 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

Citation Details
Title: Central Asia: regional developments and implications for U.S. interests.
Author: Jim Nichol
Publication: Congressional Research Service (CRS) Reports and Issue Briefs (Report)
Date: May 1, 2006
Publisher: Thomson Gale
Page: NA

Distributed by Thomson Gale

Our northern frontier: Being observations on the recent advances of Russia towards Hindoostan, and the prospects of trade with central Asia,

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Our northern frontier: Being observations on the recent advances of Russia towards Hindoostan, and the prospects of trade with central Asia,
Alfred Frederick Pollock Harcourt
Manufacturer: J. Madden
ProductGroup: Book
Binding: Unknown Binding

Red road through Asia: A journey by the Arctic ocean to Siberia, Central Asia and Armenia; with an account of the peoples living in those countries under the hammer and sickle (Devereux books)

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Red road through Asia: A journey by the Arctic ocean to Siberia, Central Asia and Armenia; with an account of the peoples living in those countries under the hammer and sickle (Devereux books)
Bosworth Goldman
Manufacturer: Methuen and Co
ProductGroup: Book
Binding: Unknown Binding

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Red road through Asia;: A journey by the Arctic ocean to Siberia, Central Asia and Armenia; with an account of the peoples now living in those countries under the hammer and sickle,

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Red road through Asia;: A journey by the Arctic ocean to Siberia, Central Asia and Armenia; with an account of the peoples now living in those countries under the hammer and sickle,
Bosworth Goldman
Manufacturer: Methuen and Co., Ltd
ProductGroup: Book
Binding: Unknown Binding

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Book Description

A summer in Aruba, on the beach, in the sun–what else could a girl want? A summer romance, of course!

Imagine spending your entire summer vacation on the beautiful Islands of Aruba. Who could ask for anything more? Well, for Morgan Callahan, spending her entire summer in Aruba with the father, she hardly knows, is barely anything to look forward to. In fact, she is dreading the next few months.

Nonetheless, she is in for the time of her life! From secret operatives to finding romance.Morgan is in for some international intrigue!

Customer Reviews:

Cute.......2007-02-23

I found this book to be very cute. Its a very quick read, which surprised me. I did not find it that all exciting though. I thought there could have been more to this book. But Overall, like I said its a cute novel. If youre looking for a quick romantic read this would be it.

~After three years of not seeing him, Morgan is going to visit her dad in Aruba. Expecting to be alone and bored out of her mind she finds herself having the time of her life and even falling in love. The relationship between she and her father is getting better but she cant help but think that he's dealing in something illegal. She fears that now finally their relationship is how it should be as father and daughter that he may once again be ruining it.

Amazing Book !.......2007-01-28

I loveeeed it !!! It was awesome. The story is about a soon-to-be high school senior that has to spend her summer in Aruba. That sounds like a dream come true, but not to Morgan. She believes that with her mother getting remarried and on a honeymoon with her new husband and living in Aruba with her father (that she hasn't seen for years) will be the worst summer of her life. Adding to the fact, she broke her leg just after her ex-boyfriend broke up with her. What she didn't expect was to get to know a very attractive college student, Cy(Cyrus)Reed who works for her dad. Cy helps Morgan get closer to her father and to himself as well.
This book is a must read if you like romance novels. You will not regret reading it.

Amazing book!.......2006-07-19

This book was absolutley amazing. I read a lot of young adult romance type books, and this one definitely stood out. It didn't just follow your basic "girl meets boy, girl falls in love with boy, boy falls in love with girl, the end" story line. Morgan is a character a lot of teenage girls can relate themselves to and Cy is a character that any girl would love. I definitely think this book is worth while to read.

If you go on to read this book and like it, "Caribbean Cruising" and "Maine Squeeze" were really good too.

Tropical Read.......2006-05-21

I read this book in three days. It had a lot of suspense and it held my attention. I would recommend this book to anyone over the age of 12 because some parts are very sexual....and they are written in detail. It is the perfect beach read.

good ole fun in the sun.......2006-01-02

Tropical kiss was a great book. Morgan goes to live with her father, to whom she has barely spoken with in two years, and she ends up finding love with a guy named Cy. This book was a great novel I just couldn't put down! Morgan and her father's relationship was also a good focal point of the novel. I thought the whole thing with the mob that was going on to be a little to 'godfather' for my taste but it didn't ruin the novel.

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Tropical Kiss
Jan Coffey
Manufacturer: Avon
ProductGroup: Book
Binding: Paperback
ASIN: B000OF1VA4

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