p57Kip2knock-in mouse reveals CDK-independent contribution in the development of Beckwith-Wiedemann syndrome-Reference-Cited by-同舟云学术

p57Kip2knock-in mouse reveals CDK-independent contribution in the development of Beckwith-Wiedemann syndrome

Published:2016-05-04 Issue:3 Volume:239 Page:250-261
ISSN:0022-3417
Container-title:The Journal of Pathology
language:en
Short-container-title:J. Pathol.

Author:

Duquesnes Nicolas¹²³,Callot Caroline¹²³,Jeannot Pauline¹²³,Daburon Virginie²⁴,Nakayama Keiichi I⁵,Manenti Stephane¹²³,Davy Alice²⁶,Besson Arnaud¹²³^ORCID

Affiliation:

1. INSERM UMR1037, Cancer Research Centre of Toulouse; France

2. Université de Toulouse; France

3. CNRS ERL5294; Toulouse France

4. CNRS UMR5088 LBCMCP; Toulouse France

5. Division of Cell Biology, Medical Institute of Bioregulation; Kyushu University; Fukuoka Japan

6. CNRS UMR5547, Centre de Biologie du Développement; Toulouse France

Funder

Fondation ARC pour la Recherche sur le Cancer

Ligue Nationale Contre le Cancer, France

Publisher

Wiley

Subject

Pathology and Forensic Medicine

Reference46 articles.

1. CDK Inhibitors: cell cycle regulators and beyond;Besson;Dev Cell,2008

2. p57KIP2: 'Kip'ing the cell under control;Pateras;Mol Cancer Res,2009

3. Ablation of the CDK inhibitor p57Kip2 results in increased apoptosis and delayed differentiation during mouse development;Yan;Genes Dev,1997

4. Altered cell differentiation and proliferation in mice lacking p57KIP2 indicates a role in Beckwith-Wiedemann syndrome;Zhang;Nature,1997

5. Common and specific roles of the related CDK inhibitors p27 and p57 revealed by a knock-in mouse model;Susaki;Proc Natl Acad Sci USA,2009

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