| Aberrant DNA Methylation of Two Tumor Suppressor Genes, p14(ARF) and p15(INK4b), after Chronic Occupational Exposure to Low Level of Benzene | None |
| These results confirm that CDKN2A is a tumor suppressor gene driving human cancer development by inducing cell aneuploidy and cell cycle up-regulation | None |
| Results suggest that hampering proliferation of aneuploid cells could be an additional role of the p14(ARF) tumor suppressor. | None |
| Regulation of Tumor Suppressor Gene CDKN2A and Encoded p16-INK4a Protein by Covalent Modifications | None |
| the Cdkn2a alternate reading frame (Arf) serves as a gatekeeper tumor suppressor in mice that prevents PN progression by inducing senescence-mediated growth arrest in aberrantly proliferating Nf1-/- SC. | None |
| Cysteine oxidation triggers amyloid fibril formation of the tumor suppressor p16(INK4A). | None |
| NPM1 exhibits structural and dynamic heterogeneity upon phase separation with the p14ARF tumor suppressor | None |
| Deficiency of PTEN and CDKN2A Tumor?-Suppressor Genes in Conventional and Chondroid Chordomas: Molecular Characteristics and Clinical Relevance | None |
| Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest. | None |
| Tumor suppressor p16INK4A: structural characterization of wild-type and mutant proteins by NMR and circular dichroism. | None |
| Sequence variation and chromosomal mapping of the murine Cdkn2a tumor suppressor gene. | None |
| Expression of the p16INK4a tumor suppressor versus other INK4 family members during mouse development and aging. | None |
| An AC-repeat adjacent to mouse Cdkn2B allows the detection of specific allelic losses in the p15INK4b and p16INK4a tumor suppressor genes. | None |
| E2f3 loss is sufficient to derepress Arf, triggering activation of p53 and expression of p21(Cip1); oncogenic activation of Arf is associated with recruitment of the endogenous activating E2Fs, E2F1, and E2F3a, to the Arf promoter | None |
| Data indicate that Arf-deficient cells transformed by oncogenic Ras were dependent on increased Drosha expression as Drosha knockdown was sufficient to inhibit Ras-dependent cellular transformation. | None |