AustralieFrV1, PascalFrancis, Corpus, bibRecord, 002250

Alternative Cyclin D1 Splice Forms Dififerentially Regulate the DNA Damage Response

Identifieur interne : 002250 ( PascalFrancis/Corpus ); précédent : 002249; suivant : 002251

Alternative Cyclin D1 Splice Forms Dififerentially Regulate the DNA Damage Response

Auteurs : ZHIPING LI ; XUANMAO JIAO ; CHENGUANG WANG ; L. Andrew Shirley ; Hany Elsaleh ; Olav Dahl ; MIN WANG ; Evi Soutoglou ; Erik S. Knudsen ; Richard G. Pestell

Source :

Cancer research : (Baltimore) [ 0008-5472 ] ; 2010.

RBID : Pascal:10-0515705

Descripteurs français

Pascal (Inist)
- Cycline D1, Protooncogène, Gène onc cellulaire, Epissage, Epissure, Réponse à une lésion d'ADN.

English descriptors

KwdEn :
- C-Onc gene, Cyclin D1, DNA damage response, Protooncogene, Splice, Splicing.

Abstract

The DNA damage response (DDR) activates downstream pathways including cell cycle checkpoints. The cyclin D1 gene is overexpressed or amplified in many human cancers and is required for gastrointestinal, breast, and skin tumors in murine models. A common polymorphism in the human cyclin D1 gene is alternatively spliced, resulting in cyclin D1a and D1b proteins that differ in their carboxyl terminus. Cyclin D1 overexpression enhances DNA damage-induced apoptosis. The role of cyclin D1 and the alternative splice form in regulating the DDR is not well understood. Herein cyclin D1a overexpression enhanced the DDR as characterized by induction of γH2AX phosphorylation, the assembly of DNA repair foci, specific recruitment of DNA repair factors to chromatin, and G₂-M arrest. Cyclin D1 deletion in fibroblasts or small interfering RNA-mediated reduction of endogenous cyclin D1 in colon cancer cells reduced the 5-fluorouracil-mediated DDR. Mechanistic studies showed that cyclin D1a, like DNA repair factors, elicited the DDR when stably associated with chromatin.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0008-5472`
A02	`01`			`@0 CNREA8`
A03		`1`		`@0 Cancer res. : (Baltimore)`
A05				`@2 70`
A06				`@2 21`
A08	`01`	`1`	`ENG`	`@1 Alternative Cyclin D1 Splice Forms Dififerentially Regulate the DNA Damage Response`
A11	`01`	`1`		`@1 ZHIPING LI`
A11	`02`	`1`		`@1 XUANMAO JIAO`
A11	`03`	`1`		`@1 CHENGUANG WANG`
A11	`04`	`1`		`@1 SHIRLEY (L. Andrew)`
A11	`05`	`1`		`@1 ELSALEH (Hany)`
A11	`06`	`1`		`@1 DAHL (Olav)`
A11	`07`	`1`		`@1 MIN WANG`
A11	`08`	`1`		`@1 SOUTOGLOU (Evi)`
A11	`09`	`1`		`@1 KNUDSEN (Erik S.)`
A11	`10`	`1`		`@1 PESTELL (Richard G.)`
A14	`01`			`@1 Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University @2 Philadelphia, Pennsylvania @3 USA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 7 aut. @Z 9 aut. @Z 10 aut.`
A14	`02`			`@1 The Australian National University, ANU College of Medicine and Health Sciences, Radiation Oncology, The Canberra Hospital, Woden, Australian Capital Territory @3 AUS @Z 5 aut.`
A14	`03`			`@1 Department of Oncology, Haukeland University Hospital @2 Bergen @3 NOR @Z 6 aut.`
A14	`04`			`@1 Cancer Department, IGBMC @2 Illkirch @3 FRA @Z 8 aut.`
A20				`@1 8802-8811`
A21				`@1 2010`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 5088 @5 354000193936780570`
A44				`@0 0000 @1 © 2010 INIST-CNRS. All rights reserved.`
A45				`@0 49 ref.`
A47	`01`	`1`		`@0 10-0515705`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Cancer research : (Baltimore)`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 The DNA damage response (DDR) activates downstream pathways including cell cycle checkpoints. The cyclin D1 gene is overexpressed or amplified in many human cancers and is required for gastrointestinal, breast, and skin tumors in murine models. A common polymorphism in the human cyclin D1 gene is alternatively spliced, resulting in cyclin D1a and D1b proteins that differ in their carboxyl terminus. Cyclin D1 overexpression enhances DNA damage-induced apoptosis. The role of cyclin D1 and the alternative splice form in regulating the DDR is not well understood. Herein cyclin D1a overexpression enhanced the DDR as characterized by induction of γH2AX phosphorylation, the assembly of DNA repair foci, specific recruitment of DNA repair factors to chromatin, and G₂-M arrest. Cyclin D1 deletion in fibroblasts or small interfering RNA-mediated reduction of endogenous cyclin D1 in colon cancer cells reduced the 5-fluorouracil-mediated DDR. Mechanistic studies showed that cyclin D1a, like DNA repair factors, elicited the DDR when stably associated with chromatin.
C02	`01`	`X`		`@0 002B02R`
C02	`02`	`X`		`@0 002B04`
C03	`01`	`X`	`FRE`	`@0 Cycline D1 @5 01`
C03	`01`	`X`	`ENG`	`@0 Cyclin D1 @5 01`
C03	`01`	`X`	`SPA`	`@0 Ciclina D1 @5 01`
C03	`02`	`X`	`FRE`	`@0 Protooncogène @5 02`
C03	`02`	`X`	`ENG`	`@0 Protooncogene @5 02`
C03	`02`	`X`	`SPA`	`@0 Protooncogen @5 02`
C03	`03`	`X`	`FRE`	`@0 Gène onc cellulaire @5 03`
C03	`03`	`X`	`ENG`	`@0 C-Onc gene @5 03`
C03	`03`	`X`	`SPA`	`@0 Gen onc celular @5 03`
C03	`04`	`X`	`FRE`	`@0 Epissage @5 04`
C03	`04`	`X`	`ENG`	`@0 Splicing @5 04`
C03	`04`	`X`	`SPA`	`@0 Empalme @5 04`
C03	`05`	`X`	`FRE`	`@0 Epissure @5 05`
C03	`05`	`X`	`ENG`	`@0 Splice @5 05`
C03	`05`	`X`	`SPA`	`@0 Punto empalme @5 05`
C03	`06`	`X`	`FRE`	`@0 Réponse à une lésion d'ADN @4 CD @5 96`
C03	`06`	`X`	`ENG`	`@0 DNA damage response @4 CD @5 96`
N21				`@1 347`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 10-0515705 INIST
ET :	Alternative Cyclin D1 Splice Forms Dififerentially Regulate the DNA Damage Response
AU :	ZHIPING LI; XUANMAO JIAO; CHENGUANG WANG; SHIRLEY (L. Andrew); ELSALEH (Hany); DAHL (Olav); MIN WANG; SOUTOGLOU (Evi); KNUDSEN (Erik S.); PESTELL (Richard G.)
AF :	Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University/Philadelphia, Pennsylvania/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 7 aut., 9 aut., 10 aut.); The Australian National University, ANU College of Medicine and Health Sciences, Radiation Oncology, The Canberra Hospital, Woden, Australian Capital Territory/Australie (5 aut.); Department of Oncology, Haukeland University Hospital/Bergen/Norvège (6 aut.); Cancer Department, IGBMC/Illkirch/France (8 aut.)
DT :	Publication en série; Niveau analytique
SO :	Cancer research : (Baltimore); ISSN 0008-5472; Coden CNREA8; Etats-Unis; Da. 2010; Vol. 70; No. 21; Pp. 8802-8811; Bibl. 49 ref.
LA :	Anglais
EA :	The DNA damage response (DDR) activates downstream pathways including cell cycle checkpoints. The cyclin D1 gene is overexpressed or amplified in many human cancers and is required for gastrointestinal, breast, and skin tumors in murine models. A common polymorphism in the human cyclin D1 gene is alternatively spliced, resulting in cyclin D1a and D1b proteins that differ in their carboxyl terminus. Cyclin D1 overexpression enhances DNA damage-induced apoptosis. The role of cyclin D1 and the alternative splice form in regulating the DDR is not well understood. Herein cyclin D1a overexpression enhanced the DDR as characterized by induction of γH2AX phosphorylation, the assembly of DNA repair foci, specific recruitment of DNA repair factors to chromatin, and G₂-M arrest. Cyclin D1 deletion in fibroblasts or small interfering RNA-mediated reduction of endogenous cyclin D1 in colon cancer cells reduced the 5-fluorouracil-mediated DDR. Mechanistic studies showed that cyclin D1a, like DNA repair factors, elicited the DDR when stably associated with chromatin.
CC :	002B02R; 002B04
FD :	Cycline D1; Protooncogène; Gène onc cellulaire; Epissage; Epissure; Réponse à une lésion d'ADN
ED :	Cyclin D1; Protooncogene; C-Onc gene; Splicing; Splice; DNA damage response
SD :	Ciclina D1; Protooncogen; Gen onc celular; Empalme; Punto empalme
LO :	INIST-5088.354000193936780570
ID :	10-0515705

Links to Exploration step

Pascal:10-0515705

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Alternative Cyclin D1 Splice Forms Dififerentially Regulate the DNA Damage Response</title>
<author><name sortKey="Zhiping Li" sort="Zhiping Li" uniqKey="Zhiping Li" last="Zhiping Li">ZHIPING LI</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University</s1>
<s2>Philadelphia, Pennsylvania</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
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<author><name sortKey="Xuanmao Jiao" sort="Xuanmao Jiao" uniqKey="Xuanmao Jiao" last="Xuanmao Jiao">XUANMAO JIAO</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University</s1>
<s2>Philadelphia, Pennsylvania</s2>
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<author><name sortKey="Chenguang Wang" sort="Chenguang Wang" uniqKey="Chenguang Wang" last="Chenguang Wang">CHENGUANG WANG</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University</s1>
<s2>Philadelphia, Pennsylvania</s2>
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<s3>AUS</s3>
<sZ>5 aut.</sZ>
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<author><name sortKey="Dahl, Olav" sort="Dahl, Olav" uniqKey="Dahl O" first="Olav" last="Dahl">Olav Dahl</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Oncology, Haukeland University Hospital</s1>
<s2>Bergen</s2>
<s3>NOR</s3>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Min Wang" sort="Min Wang" uniqKey="Min Wang" last="Min Wang">MIN WANG</name>
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<author><name sortKey="Soutoglou, Evi" sort="Soutoglou, Evi" uniqKey="Soutoglou E" first="Evi" last="Soutoglou">Evi Soutoglou</name>
<affiliation><inist:fA14 i1="04"><s1>Cancer Department, IGBMC</s1>
<s2>Illkirch</s2>
<s3>FRA</s3>
<sZ>8 aut.</sZ>
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</author>
<author><name sortKey="Knudsen, Erik S" sort="Knudsen, Erik S" uniqKey="Knudsen E" first="Erik S." last="Knudsen">Erik S. Knudsen</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University</s1>
<s2>Philadelphia, Pennsylvania</s2>
<s3>USA</s3>
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<author><name sortKey="Pestell, Richard G" sort="Pestell, Richard G" uniqKey="Pestell R" first="Richard G." last="Pestell">Richard G. Pestell</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University</s1>
<s2>Philadelphia, Pennsylvania</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
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<series><title level="j" type="main">Cancer research : (Baltimore)</title>
<title level="j" type="abbreviated">Cancer res. : (Baltimore)</title>
<idno type="ISSN">0008-5472</idno>
<imprint><date when="2010">2010</date>
</imprint>
</series>
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<seriesStmt><title level="j" type="main">Cancer research : (Baltimore)</title>
<title level="j" type="abbreviated">Cancer res. : (Baltimore)</title>
<idno type="ISSN">0008-5472</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>C-Onc gene</term>
<term>Cyclin D1</term>
<term>DNA damage response</term>
<term>Protooncogene</term>
<term>Splice</term>
<term>Splicing</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Cycline D1</term>
<term>Protooncogène</term>
<term>Gène onc cellulaire</term>
<term>Epissage</term>
<term>Epissure</term>
<term>Réponse à une lésion d'ADN</term>
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<front><div type="abstract" xml:lang="en">The DNA damage response (DDR) activates downstream pathways including cell cycle checkpoints. The cyclin D1 gene is overexpressed or amplified in many human cancers and is required for gastrointestinal, breast, and skin tumors in murine models. A common polymorphism in the human cyclin D1 gene is alternatively spliced, resulting in cyclin D1a and D1b proteins that differ in their carboxyl terminus. Cyclin D1 overexpression enhances DNA damage-induced apoptosis. The role of cyclin D1 and the alternative splice form in regulating the DDR is not well understood. Herein cyclin D1a overexpression enhanced the DDR as characterized by induction of γH2AX phosphorylation, the assembly of DNA repair foci, specific recruitment of DNA repair factors to chromatin, and G<sub>2</sub>
-M arrest. Cyclin D1 deletion in fibroblasts or small interfering RNA-mediated reduction of endogenous cyclin D1 in colon cancer cells reduced the 5-fluorouracil-mediated DDR. Mechanistic studies showed that cyclin D1a, like DNA repair factors, elicited the DDR when stably associated with chromatin.</div>
</front>
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<fA11 i1="01" i2="1"><s1>ZHIPING LI</s1>
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<fA11 i1="02" i2="1"><s1>XUANMAO JIAO</s1>
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<fA11 i1="03" i2="1"><s1>CHENGUANG WANG</s1>
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<fA11 i1="04" i2="1"><s1>SHIRLEY (L. Andrew)</s1>
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<fA11 i1="05" i2="1"><s1>ELSALEH (Hany)</s1>
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<fA11 i1="07" i2="1"><s1>MIN WANG</s1>
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<fC01 i1="01" l="ENG"><s0>The DNA damage response (DDR) activates downstream pathways including cell cycle checkpoints. The cyclin D1 gene is overexpressed or amplified in many human cancers and is required for gastrointestinal, breast, and skin tumors in murine models. A common polymorphism in the human cyclin D1 gene is alternatively spliced, resulting in cyclin D1a and D1b proteins that differ in their carboxyl terminus. Cyclin D1 overexpression enhances DNA damage-induced apoptosis. The role of cyclin D1 and the alternative splice form in regulating the DDR is not well understood. Herein cyclin D1a overexpression enhanced the DDR as characterized by induction of γH2AX phosphorylation, the assembly of DNA repair foci, specific recruitment of DNA repair factors to chromatin, and G<sub>2</sub>
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<server><NO>PASCAL 10-0515705 INIST</NO>
<ET>Alternative Cyclin D1 Splice Forms Dififerentially Regulate the DNA Damage Response</ET>
<AU>ZHIPING LI; XUANMAO JIAO; CHENGUANG WANG; SHIRLEY (L. Andrew); ELSALEH (Hany); DAHL (Olav); MIN WANG; SOUTOGLOU (Evi); KNUDSEN (Erik S.); PESTELL (Richard G.)</AU>
<AF>Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University/Philadelphia, Pennsylvania/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 7 aut., 9 aut., 10 aut.); The Australian National University, ANU College of Medicine and Health Sciences, Radiation Oncology, The Canberra Hospital, Woden, Australian Capital Territory/Australie (5 aut.); Department of Oncology, Haukeland University Hospital/Bergen/Norvège (6 aut.); Cancer Department, IGBMC/Illkirch/France (8 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Cancer research : (Baltimore); ISSN 0008-5472; Coden CNREA8; Etats-Unis; Da. 2010; Vol. 70; No. 21; Pp. 8802-8811; Bibl. 49 ref.</SO>
<LA>Anglais</LA>
<EA>The DNA damage response (DDR) activates downstream pathways including cell cycle checkpoints. The cyclin D1 gene is overexpressed or amplified in many human cancers and is required for gastrointestinal, breast, and skin tumors in murine models. A common polymorphism in the human cyclin D1 gene is alternatively spliced, resulting in cyclin D1a and D1b proteins that differ in their carboxyl terminus. Cyclin D1 overexpression enhances DNA damage-induced apoptosis. The role of cyclin D1 and the alternative splice form in regulating the DDR is not well understood. Herein cyclin D1a overexpression enhanced the DDR as characterized by induction of γH2AX phosphorylation, the assembly of DNA repair foci, specific recruitment of DNA repair factors to chromatin, and G<sub>2</sub>
-M arrest. Cyclin D1 deletion in fibroblasts or small interfering RNA-mediated reduction of endogenous cyclin D1 in colon cancer cells reduced the 5-fluorouracil-mediated DDR. Mechanistic studies showed that cyclin D1a, like DNA repair factors, elicited the DDR when stably associated with chromatin.</EA>
<CC>002B02R; 002B04</CC>
<FD>Cycline D1; Protooncogène; Gène onc cellulaire; Epissage; Epissure; Réponse à une lésion d'ADN</FD>
<ED>Cyclin D1; Protooncogene; C-Onc gene; Splicing; Splice; DNA damage response</ED>
<SD>Ciclina D1; Protooncogen; Gen onc celular; Empalme; Punto empalme</SD>
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Alternative Cyclin D1 Splice Forms Dififerentially Regulate the DNA Damage Response

Alternative Cyclin D1 Splice Forms Dififerentially Regulate the DNA Damage Response

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