By Daniel Durocher (auth.), Kum Kum Khanna, Yosef Shiloh (eds.)

ISBN-10: 904812560X

ISBN-13: 9789048125609

ISBN-10: 9048125618

ISBN-13: 9789048125616

The e-book The DNA harm reaction: Implications on melanoma Formation and Treatment brings jointly an exceptional number of overview articles. The articles were written through a bunch of specialists who've a deep wisdom of the new advances within the fields of DNA harm signalling and service and their implications in carcinogenesis.

The e-book is split into chapters that care for the flowery surveillance procedure and service mechanisms utilized by cells to suppress mutagenic lesions to prevent melanoma. It offers snapshots of:
* present knowing of DNA harm signalling,
* cellphone cycle checkpoints,
* the various significant DNA fix pathways,
* useful hyperlinks among DNA harm,
* genomic instability and melanoma,
* implications of DNA harm for the improvement of recent therapy modalities for cancer.

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Extra info for The DNA Damage Response: Implications on Cancer Formation and Treatment

Example text

150. Olive PL (2004) Detection of DNA damage in individual cells by analysis of histone H2AX phosphorylation. Methods Cell Biol 75: 355–373. 151. Teicher BA (2008) Next generation topoisomerase I inhibitors: Rationale and biomarker strategies. Biochem Pharmacol 75: 1262–1271. 152. Ichijima Y, Sakasai R, Okita N, Asahina K, Mizutani S, and Teraoka H (2005) Phosphorylation of histone H2AX at M phase in human cells without DNA damage response. Biochem Biophys Res Commun 336: 807–812. 153. McManus KJ, and Hendzel MJ (2005) ATM-dependent DNA damage-independent mitotic phosphorylation of H2AX in normally growing mammalian cells.

This requires the ATP-dependent binding of a six-subunit origin recognition complex (ORC) to origins. ORC recruits the initiation factors Cdc6 and Cdt1, which together function to load the mini-chromosome maintenance (MCM) helicase complex onto chromatin and form the pre-RC [80]. Once the MCM complex is loaded onto chromatin, the origin is ‘licensed’ for replication [9, 59]. Many additional factors are required for the conversion of the pre-RC to a functional replication fork. In S phase, activation of pre-RCs or ‘firing of origins’ requires the activity of cyclin-dependent kinase (CDK) and Cdc7/Dbf4-dependent kinase (DDK) that promote the recruitment of additional replication proteins, including CDC45, GINS, and polymerases to origins.

Claspin is phosphorylated in response to replication stress and this phosphorylation is required for the binding of Claspin to CHK1 [47]. Sustained CHK1 phosphorylation requires ATR phosphorylation of RAD17. Phosphorylated RAD17 interacts with Claspin, which may be a mechanism to maintain Claspin at stalled replication forks [107]. The requirement for an adaptor protein that regulates the phosphorylation of the effector kinase specifically in response to stalled replication forks is conserved in yeast.

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The DNA Damage Response: Implications on Cancer Formation and Treatment by Daniel Durocher (auth.), Kum Kum Khanna, Yosef Shiloh (eds.)

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