Klotho
July 30, 2019
HSP90
January 6, 2020
- Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis
- Human SIR2 deacetylates p53 and antagonizes PML/p53‐induced cellular senescence
- Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas
- Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
- PML regulates p53 acetylation and premature senescence induced by oncogenic Ras
- Regulation of cellular senescence by p53
- Reversal of human cellular senescence: roles of the p53 and p16 pathways
- Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor
- A role for both RB and p53 in the regulation of human cellular senescence
- Senescence and aging: the critical roles of p53
- A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy
- Paradoxical suppression of cellular senescence by p53
- Skp2 targeting suppresses tumorigenesis by Arf-p53-independent cellular senescence
- Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling
- Oncogenic ras and p53 cooperate to induce cellular senescence
- Escape from senescence in human diploid fibroblasts induced directly by mutant p53.
- Wild-type p53 triggers a rapid senescence program in human tumor cells lacking functional p53
- Telomere shortening triggers senescence of human cells through a pathway involving ATM, p53, and p21CIP1, but not p16INK4a
- Tumor suppression in the absence of p53-mediated cell-cycle arrest, apoptosis, and senescence
- JunD protects cells from p53-dependent senescence and apoptosis
- Mutant p53 drives metastasis and overcomes growth arrest/senescence in pancreatic cancer
- p53, ROS and senescence in the control of aging
- Adriamycin-induced senescence in breast tumor cells involves functional p53 and telomere dysfunction
- Pathways connecting telomeres and p53 in senescence, apoptosis, and cancer
- Reversal of senescence in mouse fibroblasts through lentiviral suppression of p53
- p53-independent upregulation of miR-34a during oncogene