A cancer‐associated CDKN1B mutation induces p27 phosphorylation on a novel residue: a new mechanism for tumor suppressor loss‐of‐function-Reference-Cited by-同舟云学术

A cancer‐associated CDKN1B mutation induces p27 phosphorylation on a novel residue: a new mechanism for tumor suppressor loss‐of‐function

Published:2021-02-06 Issue:4 Volume:15 Page:915-941
ISSN:1574-7891
Container-title:Molecular Oncology
language:en
Short-container-title:Mol Oncol

Author:

Bencivenga Debora¹^ORCID,Stampone Emanuela¹^ORCID,Aulitto Arianna¹,Tramontano Annunziata¹,Barone Clementina¹,Negri Aide²,Roberti Domenico³,Perrotta Silverio³,Della Ragione Fulvio¹^ORCID,Borriello Adriana¹^ORCID

Affiliation:

1. Department of Precision Medicine University of Campania “Luigi Vanvitelli” Naples Italy

2. Department of Medicine and Surgery University of Parma Italy

3. Department of Woman, Child and General and Specialized Surgery University of Campania “Luigi Vanvitelli” Naples Italy

Funder

Associazione Italiana per la Ricerca sul Cancro

Publisher

Wiley

Subject

Cancer Research,Genetics,Molecular Medicine,General Medicine,Oncology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/1878-0261.12881

Reference65 articles.

1. New functional activities for the p21 family of CDK inhibitors.

2. p27Kip1, a cyclin-Cdk inhibitor, links transforming growth factor-beta and contact inhibition to cell cycle arrest.

3. Cloning of p27Kip1, a cyclin-dependent kinase inhibitor and a potential mediator of extracellular antimitogenic signals

4. A novel inhibitor of cyclin-Cdk activity detected in transforming growth factor beta-arrested epithelial cells.

5. p27, a novel inhibitor of G1 cyclin-Cdk protein kinase activity, is related to p21

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