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-fig2-figsupp3-data1.xlsx › Figure_2-figure_supplement_3A
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-11.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
The LOVD3 platform: efficient genome-wide sharing of genetic variants.
Fokkema IFAC et al.
European Journal of Human Genetics : Ejhg, 2021
34521998 (PubMed )
Supplement: 41431_2021_959_MOESM4_ESM.pdf
Classifying variants of CDKN2A using computational and laboratory studies.
Miller PJ et al.
Human Mutation, 2011
Genome-wide analysis to predict protein sequence variations that change phosphorylation sites or their corresponding kinases.
Ryu GM et al.
Nucleic Acids Research, 2009
19139070 (PubMed )
Supplement: gkn1008_nar-01723-s-2008-File009.xls › TypeI_
The CDKN2A (p16) gene and human cancer.
Foulkes WD et al.
Molecular Medicine (cambridge, Mass.), 1997
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