• Consistent with their repression of TGF-β-induced gene expression, introduction of E2F sites into the promoter of cyclin-dependent kinase inhibitor p15 INK4B gene effectively inhibited its induction by TGF-β. (pnas.org)
  • Experiments utilizing Gal4-RB and Gal4-p107 chimeric constructs demonstrated that either RB or p107 could directly repress TGF-β induction of p15 INK4B gene when tethered to p15 INK4B promoter through Gal4 DNA binding sites. (pnas.org)
  • 19 p15 is highly homologous to and colocalized with p16 within a ∼25-kb region on the short arm of human chromosome 9. (bloodjournal.org)
  • Ataxia-telangiectasia-mutated (ATM)-dependent DNA-damage response, non-homologous end joining, and homologous recombination pathways coordinately contribute to repairing DSBs in higher eukaryotes. (frontiersin.org)
  • Thus, these authors suggested that inability to up-regulate p15 and p16 would promote cellular proliferation and atherosclerosis. (onlinejacc.org)
  • In this study we tested the expression of CDKIs p15, p16, p21 and p27 by immunohistochemistry to determine the role of CDKIs in the initiation of primordial follicle growth. (biomedcentral.com)
  • p15, p16, p21 and p27 in mouse ovaries by immunohistochemistry to assess whether the initiation of primordial follicle growth was associated with the expression of CDKIs. (biomedcentral.com)
  • p15 expression was serially examined in bone marrow biopsies by immunohistochemistry. (bloodjournal.org)
  • 1 5-7 Several TSGs altered by hypermethylation encode genes involved in cell cycle regulation (eg, Rb, p16 , p15 , VHL). (bloodjournal.org)
  • Using these primers, the expression of p16, p15 and p14 mRNAs could be individually evaluated by reverse transcriptase polymerase chain reaction. (ceek.jp)
  • We examined p15 and p16 methylation status in bone marrow mononuclear cells from patients with high-risk MDS during treatment with decitabine, using a methylation-sensitive primer extension assay (Ms-SNuPE) to quantitate methylation, and denaturing gradient gel electrophoresis (DGGE) and bisulfite-DNA sequencing to distinguish individually methylated alleles. (bloodjournal.org)
  • Immunohistochemical staining for p15 protein in bone marrow biopsies from 8 patients with p15 hypermethylation revealed low or absent expression in 4 patients, which was induced to normal levels during decitabine treatment. (bloodjournal.org)
  • The emergence of partially demethylated epigenotypes and re-establishment of normal p15 protein expression following the initial decitabine courses implicate pharmacologic demethylation as a possible mechanism resulting in hematologic response in MDS. (bloodjournal.org)
  • Both NAD-dependent and Pttg1-dependent pathways were responsible for mediating different subsets of these alterations, also incorporating changes in VCP/p97 localization and Ube1 expression. (biomedcentral.com)
  • Among 12 patients with hypermethylation sequentially analyzed after at least one course of decitabine treatment, a decrease in p15 methylation occurred in 9 and was associated with clinical response. (bloodjournal.org)
  • Based on the sequence data, primers specific for p16, p15 and p14 were designed. (ceek.jp)
  • In conclusion, frequent, selective p15 hypermethylation was reversed in responding MDS patients following treatment with a methylation inhibitor. (bloodjournal.org)