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Characterization of hydroxyurea resistance in C. elegans

Publikation: KonferencebidragPosterForskning

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Characterization of hydroxyurea resistance in C. elegans. / Brejning, Jeanette.

2009. Poster session præsenteret ved 17th International C. elegans Meeting, Los Angeles, USA.

Publikation: KonferencebidragPosterForskning

Harvard

Brejning, J 2009, 'Characterization of hydroxyurea resistance in C. elegans', 17th International C. elegans Meeting, Los Angeles, USA, 24/06/2009 - 28/06/2009.

APA

Brejning, J. (2009). Characterization of hydroxyurea resistance in C. elegans. Poster session præsenteret ved 17th International C. elegans Meeting, Los Angeles, USA.

CBE

Brejning J. 2009. Characterization of hydroxyurea resistance in C. elegans. Poster session præsenteret ved 17th International C. elegans Meeting, Los Angeles, USA.

MLA

Brejning, Jeanette Characterization of hydroxyurea resistance in C. elegans. 17th International <em>C. elegans</em> Meeting, 24 jun. 2009, Los Angeles, USA, Poster, 2009.

Vancouver

Brejning J. Characterization of hydroxyurea resistance in C. elegans. 2009. Poster session præsenteret ved 17th International C. elegans Meeting, Los Angeles, USA.

Author

Brejning, Jeanette. / Characterization of hydroxyurea resistance in C. elegans. Poster session præsenteret ved 17th International C. elegans Meeting, Los Angeles, USA.

Bibtex

@conference{a8e76810fe9a11de9c17000ea68e967b,
title = "Characterization of hydroxyurea resistance in C. elegans",
abstract = "The soil nematode Caenorhabditis elegans has become a prominent model organism for studying aging and many age-related diseases. We use C. elegans to study the relationship between cancer and aging. To prevent cancer, cells are equipped with surveillance systems that detect damage and stop cells from dividing. These surveillance systems are collectively called cellular checkpoints. We have found that inactivation of certain checkpoint proteins, including p53, also cause resistance to the chemotherapeutic drug hydroxyurea (HU) that stalls replication. We have found that in C. elegans, HU inhibits ribonucleotide reductase (RNR). RNR is involved in synthesis of deoxyribonucleotide (dNTP) precursors for DNA replication and repair. Previously we have shown that inactivation of some checkpoint proteins can increase stress resistance and lifespan of C. elegans1. Interestingly, several genes that influence HU resistance also influence lifespan and stress resistance. At least one of these genes seems to function in the S-M checkpoint pathway.  1.    A. Olsen, M. C. Vantipalli, G. J. Lithgow, Science 312, 1381 (2006).  ",
keywords = "Checkpoint proteiner, Hydroxyurea resistens, checkpoint proteins, hydroxyurea resistance",
author = "Jeanette Brejning",
year = "2009",
language = "English",
note = "null ; Conference date: 24-06-2009 Through 28-06-2009",

}

RIS

TY - CONF

T1 - Characterization of hydroxyurea resistance in C. elegans

AU - Brejning, Jeanette

PY - 2009

Y1 - 2009

N2 - The soil nematode Caenorhabditis elegans has become a prominent model organism for studying aging and many age-related diseases. We use C. elegans to study the relationship between cancer and aging. To prevent cancer, cells are equipped with surveillance systems that detect damage and stop cells from dividing. These surveillance systems are collectively called cellular checkpoints. We have found that inactivation of certain checkpoint proteins, including p53, also cause resistance to the chemotherapeutic drug hydroxyurea (HU) that stalls replication. We have found that in C. elegans, HU inhibits ribonucleotide reductase (RNR). RNR is involved in synthesis of deoxyribonucleotide (dNTP) precursors for DNA replication and repair. Previously we have shown that inactivation of some checkpoint proteins can increase stress resistance and lifespan of C. elegans1. Interestingly, several genes that influence HU resistance also influence lifespan and stress resistance. At least one of these genes seems to function in the S-M checkpoint pathway.  1.    A. Olsen, M. C. Vantipalli, G. J. Lithgow, Science 312, 1381 (2006).  

AB - The soil nematode Caenorhabditis elegans has become a prominent model organism for studying aging and many age-related diseases. We use C. elegans to study the relationship between cancer and aging. To prevent cancer, cells are equipped with surveillance systems that detect damage and stop cells from dividing. These surveillance systems are collectively called cellular checkpoints. We have found that inactivation of certain checkpoint proteins, including p53, also cause resistance to the chemotherapeutic drug hydroxyurea (HU) that stalls replication. We have found that in C. elegans, HU inhibits ribonucleotide reductase (RNR). RNR is involved in synthesis of deoxyribonucleotide (dNTP) precursors for DNA replication and repair. Previously we have shown that inactivation of some checkpoint proteins can increase stress resistance and lifespan of C. elegans1. Interestingly, several genes that influence HU resistance also influence lifespan and stress resistance. At least one of these genes seems to function in the S-M checkpoint pathway.  1.    A. Olsen, M. C. Vantipalli, G. J. Lithgow, Science 312, 1381 (2006).  

KW - Checkpoint proteiner

KW - Hydroxyurea resistens

KW - checkpoint proteins

KW - hydroxyurea resistance

M3 - Poster

ER -