AustralieFrV1, Main, Exploration, bibRecordById, Pascal:10-0515705

Alternative Cyclin D1 Splice Forms Dififerentially Regulate the DNA Damage Response

Identifieur interne : 007A53 ( Main/Exploration ); précédent : 007A52; suivant : 007A54

Alternative Cyclin D1 Splice Forms Dififerentially Regulate the DNA Damage Response

Auteurs : ZHIPING LI [États-Unis] ; XUANMAO JIAO [États-Unis] ; CHENGUANG WANG [États-Unis] ; L. Andrew Shirley [États-Unis] ; Hany Elsaleh [Australie] ; Olav Dahl [Norvège] ; MIN WANG [États-Unis] ; Evi Soutoglou [France] ; Erik S. Knudsen [États-Unis] ; Richard G. Pestell [États-Unis]

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.

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>C-Onc gene</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Cycline D1</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>
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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

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

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