David Santamarı́a

Centro de Investigación del Cáncer

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Chiara Ambrogio

University of Turin

Mariano Barbacid

Spanish National Cancer Research Centre

Ernest Nadal

Institut Català d'Oncologia

Alberto Villanueva

Institut d'Investigació Biomédica de Bellvitge

Marie‐Julie Nokin

University of Liège

Alessia Mira

University of Turin

Enrico Patrucco

University of Turin

Pasi A. Jänne

Dana-Farber Cancer Institute

Raymond M. Paranal

Johns Hopkins University

Jens Köhler

Nuremberg Hospital

Cooperative Institutions

Spanish National Cancer Research Centre

Inserm

Harvard University

Centro de Investigación del Cáncer

Centre National de la Recherche Scientifique

Revolution Medicines (United States)

Dana-Farber Cancer Institute

Université de Bordeaux

University of Turin

Instituto de Salud Carlos III

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Cloning, sequencing and expression in MEL cells of a cDNA encoding the mouse ribosomal protein S51The nucleotide sequence reported in this paper has been submitted to the GenBank/EMBL Data Bank under the accession number U78085.1

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (1997)

Natasha Vanegas V Castañeda David Santamarı́a Pablo Hernández Jorge B. Schvartzman

Homology

Ribosomal protein

Cloning (programming)

10.1016/s0167-4889(97)00054-2

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Citations (3)

Author response for "Oncogenic mutant <scp>KRAS</scp> inhibition through oxidation at cysteine 118"

Maximilian Kramer‐Drauberg E. Petrini Alessia Mira Enrico Patrucco Rossella Scardaci

10.1002/1878-0261.13798/v2/response1

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Review for "Rational combination of <scp>SHP2</scp> and <scp>mTOR</scp> inhibition for the treatment of hepatocellular carcinoma"

David Santamarı́a

10.1002/1878-0261.13377/v1/review3

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Cell Cycle and Cancer: Genetic Analysis of the Role of Cyclin-dependent Kinases

Cold Spring Harbor Symposia on Quantitative Biology (2005)

Mariano Barbacid Sagrario Ortega Rocı́o Sotillo Junko Odajima Alberto Martín

Most human tumors harbor mutations that misregulate the early phases of the cell cycle. Here, we summarize genetic evidence, mostly obtained in our laboratory using strains of gene-targeted mice, that provides direct experimental support for a role of Cdk4 in tumor development. Moreover, these genetic studies challenge some well-established concepts regarding the role of Cdks during the early phases of the cell cycle. For instance, they have illustrated that Cdk4 and Cdk6 are not essential for cell division during embryonic development except in the hematopoietic system. More surprisingly, mice lacking Cdk2 survive for over 2 years without detectable abnormalities except in their germ cells, indicating that Cdk2 is essential for meiosis but dispensable for the normal mitotic cell cycle. Cdk2 is also dispensable for cell cycle inhibition and tumor suppression by the Cip/Kip inhibitors, p21(Cip1) and p27(Kip1). These observations have important implications not only to understand cell cycle regulation, but also to validate Cdks as potential targets for the development of therapeutic strategies to block proliferation of tumor cells.

Cyclin-dependent kinase 6

Restriction point

10.1101/sqb.2005.70.005

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Citations (35)

Genetic inactivation of Cdk7 leads to cell cycle arrest and induces premature aging due to adult stem cell exhaustion

The EMBO Journal (2012)

Miguel Ganuza Cristina Sáiz-Ladera Marta Cañamero Gonzalo Gómez‐López Ralph P. Schneider

Premature aging

10.1038/emboj.2012.94

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Citations (105)

Scientific Programme

European Journal of Cancer (2012)

Julio Celis C Wedge Serena Nik‐Zainal Mike Stratton Cynthia Ambrogio

10.1016/s0959-8049(12)70704-9

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Cdk1 is sufficient to drive the mammalian cell cycle

Nature (2007)

David Santamarı́a Cédric Barrière Antonio Cerqueira Sarah L. Hunt Claudine Tardy

Interphase

Cyclin-dependent kinase 6

Polo-like kinase

Cyclin B

Cyclin A

10.1038/nature06046

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Citations (996)

Myc stimulates cell cycle progression through the activation of Cdk1 and phosphorylation of p27

bioRxiv (Cold Spring Harbor Laboratory) (2018)

Javier León Lucía García-Gutiérrez Gabriel Bretones Ester Molina Iñaki Arechaga

Cell cycle stimulation is a major transforming mechanism of Myc oncoprotein. This is achieved through at least three concomitant mechanisms: upregulation of cyclins and Cdks, downregulation of Cdk inhibitors p15 and p21 and the degradation of p27. The Myc-p27 antagonism has been shown to be relevant in human cancer. To be degraded, p27 must be phosphorylated at Thr-187 to be recognized by Skp2, a component of the ubiquitination complex. We previously described that Myc induces Skp2 expression. Here we show that not only Cdk2 but Cdk1 phosphorylates p27 at the Thr187, which was previously unreported. Moreover, Myc induced p27 degradation in murine fibroblasts through Cdk1 activation, which was achieved by Myc-dependent cyclin A and B induction. In the absence of Cdk2, p27 phosphorylation at Thr-187 was mainly carried out by cyclin A2-Cdk1 and cyclin B1-Cdk1. We also show that Cdk1 inhibition was sufficient for the synthetic lethal interaction with Myc. This result is relevant because Cdk1 is the only Cdk strictly required for cell cycle and the reported synthetic lethal interaction between Cdk1 and Myc.

CDK inhibitor

Cyclin A

Cyclin B

Cyclin A2

Cyclin B1

SKP2

10.1101/492694

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Citations (3)

Cdk7: Open questions beyond the prevailing model

Cell Cycle (2012)

Miguel Ganuza David Santamarı́a