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DNA replication starts at initiation sites termed replication origins. Metazoan cells contain many more potential origins than are activated (fired) during each S phase. Origin activation is controlled by the ATR checkpoint kinase and its downstream effector kinase Chk1, which suppresses origin firing in response to replication blocks and during normal S phase by inhibiting the cyclin-dependent kinase Cdk2. In addition to increased origin activation, cells deficient in Chk1 activity display reduced rates of replication fork progression. Here we investigate the causal relationship between increased origin firing and reduced replication fork progression. We use the Cdk inhibitor roscovitine or RNAi depletion of Cdc7 to inhibit origin firing in Chk1-inhibited or RNAi-depleted cells. We report that Cdk inhibition and depletion of Cdc7 can alleviate the slow replication fork speeds in Chk1-deficient cells. Our data suggest that increased replication initiation leads to slow replication fork progression and that Chk1 promotes replication fork progression during normal S phase by controlling replication origin activity.

Titel:	Chk1 promotes replication fork progression by controlling replication initiation.
Autor/in / Beteiligte Person:	Petermann, E ; Woodcock, M ; Helleday, T
Link:	Full Text Finder (Volltext)
Zeitschrift:	Proceedings of the National Academy of Sciences of the United States of America, Jg. 107 (2010-09-14), Heft 37, S. 16090-5
Veröffentlichung:	Washington, DC : National Academy of Sciences, 2010
Medientyp:	academicJournal
ISSN:	1091-6490 (electronic)
DOI:	10.1073/pnas.1005031107
Schlagwort:	Cell Cycle Proteins genetics Cell Cycle Proteins metabolism Cell Line, Tumor Checkpoint Kinase 1 Humans Protein Kinases genetics Protein Serine-Threonine Kinases genetics Protein Serine-Threonine Kinases metabolism RNA Interference S Phase DNA genetics DNA Replication Protein Kinases metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, Non-U.S. Gov't Language: English [Proc Natl Acad Sci U S A] 2010 Sep 14; Vol. 107 (37), pp. 16090-5. <i>Date of Electronic Publication: </i>2010 Aug 30. MeSH Terms: DNA Replication* ; DNA / genetics ; Protein Kinases / metabolism ; Cell Cycle Proteins / genetics ; Cell Cycle Proteins / metabolism ; Cell Line, Tumor ; Checkpoint Kinase 1 ; Humans ; Protein Kinases / genetics ; Protein Serine-Threonine Kinases / genetics ; Protein Serine-Threonine Kinases / metabolism ; RNA Interference ; S Phase References: Proc Natl Acad Sci U S A. 2008 Jul 1;105(26):8956-61. (PMID: 18579778) ; Nat Chem Biol. 2008 Jun;4(6):357-65. (PMID: 18469809) ; Curr Opin Cell Biol. 2006 Jun;18(3):231-9. (PMID: 16650748) ; Cell Cycle. 2003 Jul-Aug;2(4):316-24. (PMID: 12851482) ; Cell Cycle. 2004 Jul;3(7):941-5. (PMID: 15190204) ; Mol Cell Biol. 2004 Aug;24(16):7140-50. (PMID: 15282313) ; Cell. 2003 Aug 8;114(3):385-94. (PMID: 12914702) ; J Biol Chem. 2007 Mar 30;282(13):9458-9468. (PMID: 17276990) ; Nature. 2001 Apr 12;410(6830):842-7. (PMID: 11298456) ; J Cell Biol. 1998 Mar 23;140(6):1285-95. (PMID: 9508763) ; Oncogene. 2008 May 29;27(24):3475-82. (PMID: 18084324) ; Mol Cell. 2010 Feb 26;37(4):492-502. (PMID: 20188668) ; Cancer Res. 2004 Oct 1;64(19):7110-6. (PMID: 15466207) ; Mol Biol Cell. 2008 Jun;19(6):2373-8. (PMID: 18353973) ; Cancer Res. 2005 Feb 1;65(3):780-6. (PMID: 15705874) ; Mol Cell Biol. 2002 Dec;22(24):8552-61. (PMID: 12446774) ; J Biol Chem. 2005 Sep 2;280(35):31208-19. (PMID: 15975926) ; J Biol Chem. 2007 Jan 5;282(1):208-15. (PMID: 17062569) ; Science. 2003 Jun 6;300(5625):1542-8. (PMID: 12791985) ; Nat Cell Biol. 2004 Jul;6(7):648-55. (PMID: 15220931) ; Genes Dev. 2000 Jun 15;14(12):1448-59. (PMID: 10859164) ; Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20752-7. (PMID: 19091954) ; EMBO J. 2008 Mar 19;27(6):876-85. (PMID: 18309293) ; Eur J Biochem. 1997 Jan 15;243(1-2):527-36. (PMID: 9030781) ; EMBO J. 2003 Feb 3;22(3):713-23. (PMID: 12554671) ; Science. 2007 Dec 21;318(5858):1928-31. (PMID: 18096807) ; Chromosoma. 2007 Aug;116(4):341-7. (PMID: 17404750) ; Mol Cell. 2003 Apr;11(4):1109-17. (PMID: 12718895) ; Nature. 2008 Sep 25;455(7212):557-60. (PMID: 18716622) ; Genes Dev. 2007 Dec 15;21(24):3331-41. (PMID: 18079179) ; Mol Cell Biol. 2006 Apr;26(8):3319-26. (PMID: 16581803) ; J Cell Biol. 2001 Sep 3;154(5):913-23. (PMID: 11535615) ; Mol Cell Biol. 2001 Jul;21(13):4129-39. (PMID: 11390642) ; Genes Dev. 2000 Nov 1;14(21):2745-56. (PMID: 11069891) ; Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):14795-800. (PMID: 12399544) ; J Biol Chem. 2003 Feb 7;278(6):4295-304. (PMID: 12424256) ; Eur J Cancer. 2010 Jan;46(1):33-40. (PMID: 19815406) ; Proc Natl Acad Sci U S A. 1997 Dec 23;94(26):14320-5. (PMID: 9405610) ; EMBO J. 2007 Jun 6;26(11):2719-31. (PMID: 17491592) ; Mol Cell Biol. 2005 May;25(9):3553-62. (PMID: 15831461) Grant Information: G0700730 United Kingdom MRC_ Medical Research Council; United Kingdom CRUK_ Cancer Research UK Substance Nomenclature: 0 (Cell Cycle Proteins) ; 9007-49-2 (DNA) ; EC 2.7.- (Protein Kinases) ; EC 2.7.1.- (CDC7 protein, human) ; EC 2.7.11.1 (CHEK1 protein, human) ; EC 2.7.11.1 (Checkpoint Kinase 1) ; EC 2.7.11.1 (Protein Serine-Threonine Kinases) Entry Date(s): Date Created: 20100901 Date Completed: 20101028 Latest Revision: 20211203 Update Code: 20231215 PubMed Central ID: PMC2941317

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Chk1 promotes replication fork progression by controlling replication initiation.