p57Kip2 knock-in mouse reveals CDK-independent contribution in the development of Beckwith–Wiedemann syndrome

Journal of Pathology

Volumn 239, Issue 3, 2016, Pages 250-261

  Duquesnes, Nicolas ^a,b,c   Callot, Caroline ^a,b,c   Jeannot, Pauline ^a,b,c   Daburon, Virginie ^b,d   Nakayama, Keiichi I ^e   Manenti, Stephane ^a,b,c   Davy, Alice ^b,f   Besson, Arnaud ^a,b,c  

^a CANCER RESEARCH CENTER OF TOULOUSE   (France)

^b UNIVERSITÉ DE TOULOUSE   (France)

^c CNRS ERL5294   (France)

^d Laboratoire de Biologie Cellulaire et Moleculaire du Controle de la Proliferation   (France)

^e KYUSHU UNIVERSITY   (Japan)

^f CNRS UMR5547   (France)

Author keywords

animal model; Beckwith Wiedemann syndrome; CDK; CDKN1C; cell cycle; p57Kip2

Indexed keywords

CYCLIN DEPENDENT KINASE; CYCLIN DEPENDENT KINASE INHIBITOR 1C;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BECKWITH WIEDEMANN SYNDROME; CONTROLLED STUDY; HUMAN; HUMAN CELL; MOUSE; NONHUMAN; PHENOTYPE; POINT MUTATION; PRIORITY JOURNAL; PROTEIN FUNCTION; PROTEIN INTERACTION; PROTEIN PROTEIN INTERACTION; PROTEOMICS;

EID: 85027937928     PISSN: 00223417     EISSN: 10969896     Source Type: Journal    
DOI: 10.1002/path.4721     Document Type: Article

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