Associated Papers
Functional characterization of all CDKN2A missense variants and comparison to in silico models of pathogenicity.
Kimura H et al.
Elife, 2025
40238651 (PubMed )
Supplement: elife-95347-supp9.xlsx › Appendix_1-table_9
Functional characterization of all CDKN2A missense variants and comparison to in silico models of pathogenicity.
Kimura H et al.
Biorxiv : the Preprint Server for Biology, 2025
38234851 (PubMed )
Supplement: media-2.pdf
Amyloid formation and depolymerization of tumor suppressor p16INK4a are regulated by a thiol-dependent redox mechanism.
Heath SG et al.
Nature Communications, 2024
Sequence and Structure-Based Analyses of Human Ankyrin Repeats.
Chakrabarty B et al.
Molecules (basel, Switzerland), 2022
35056738 (PubMed )
Supplement: molecules-27-00423-s001.zip › SupplementaryFileS4.xlsx › Sheet1
Classifying variants of CDKN2A using computational and laboratory studies.
Miller PJ et al.
Human Mutation, 2011
The structural impact of cancer-associated missense mutations in oncogenes and tumor suppressors.
Stehr H et al.
Molecular Cancer, 2011
21575214 (PubMed )
Supplement: 1476-4598-10-54-S3.XLS › mutations.txt
Recurrent patterns of dual RB and p53 pathway inactivation in melanoma.
Yang G et al.
The Journal of Investigative Dermatology, 2005
Characterization of the cyclin-dependent kinase inhibitory domain of the INK4 family as a model for a synthetic tumour suppressor molecule.
Fåhraeus R et al.
Oncogene, 1998
The CDKN2A (p16) gene and human cancer.
Foulkes WD et al.
Molecular Medicine (cambridge, Mass.), 1997
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