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
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
Cysteine oxidation triggers amyloid fibril formation of the tumor suppressor p16INK4A.
Göbl C et al.
Redox Biology, 2020
Nucleotide variations of TP53 exon 4 found in intracranial meningioma and in silico prediction of their significance.
Bukovac A et al.
Molecular and Clinical Oncology, 2019
Targeted Next-Generation Sequencing of Plasma DNA from Cancer Patients: Factors Influencing Consistency with Tumour DNA and Prospective Investigation of Its Utility for Diagnosis.
Kaisaki PJ et al.
Plos One, 2016
Gliomatosis cerebri: molecular pathology and clinical course.
Herrlinger U et al.
Annals of Neurology, 2002
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