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A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
TLDR
It is shown that several human cells express a beta-galactosidase, histochemically detectable at pH 6, upon senescence in culture, which provides in situ evidence that senescent cells may exist and accumulate with age in vivo. Expand
Regulation of a Senescence Checkpoint Response by the E2F1 Transcription Factor and p14ARF Tumor Suppressor
TLDR
It is shown that E2F1, a multifunctional transcription factor that binds the retinoblastoma (pRb) tumor suppressor and that can either promote or suppress tumorigenesis, induces a senescent phenotype when overexpressed in normal human fibroblasts and identifies p14ARF as a potentially important mediator of the senescence phenotype. Expand
Methods to detect biomarkers of cellular senescence: the senescence-associated beta-galactosidase assay.
TLDR
The method to detect SA-beta-gal is a convenient, single cell-based assay, which can identify senescent cells even in heterogeneous cell populations and aging tissues, such as skin biopsies from older individuals. Expand
Bmi-1 is a novel molecular marker of nasopharyngeal carcinoma progression and immortalizes primary human nasopharyngeal epithelial cells.
TLDR
This study provides the first cellular proto-oncogene immortalized nasopharyngeal epithelial cell line, which may serve as a cell model system for studying the mechanisms involved in the tumorigenesis of nasopharygeal carcinoma. Expand
Control of the Replicative Life Span of Human Fibroblasts by p16 and the Polycomb Protein Bmi-1
TLDR
It is reported that Bmi-1 is downregulated when WI-38 human fibroblasts undergo replicative senescence, but not quiescence, and extends replicative life span when overexpressed, and suggested that some human Fibroblast strains are more sensitive to stress-inducedsenescence and have both p16-dependent and p53/telomere-dependent pathways of senescENCE. Expand
The Bmi-1 oncogene induces telomerase activity and immortalizes human mammary epithelial cells.
TLDR
It is reported that Bmi-1, originally identified as a c-Myc cooperating oncoprotein, can bypass senescence, extend the replicative life span, and immortalize MECs and plays a role in the development of human breast cancer. Expand
Elevated Bmi-1 expression is associated with dysplastic cell transformation during oral carcinogenesis and is required for cancer cell replication and survival
TLDR
The data suggest that Bmi-1 may act through p16INK4A-independent pathways to regulate cellular proliferation during oral cancer progression, and is likely to occur at a very early stage in oral carcinogenesis. Expand
Mel-18, a polycomb group protein, regulates cell proliferation and senescence via transcriptional repression of Bmi-1 and c-Myc oncoproteins.
TLDR
It is reported that Mel-18, a PcG ring finger protein (PCGF) transcriptionally down-regulates Bmi-1, and suggested that c-Myc and polycomb function in cell proliferation and senescence via down-regulation of c- myc. Expand
Regulation of cellular senescence by p53.
TLDR
P53 is essential for the senescence response to short telomeres, DNA damage, oncogenes and supraphysiological mitogenic signals, and overexpression of certain tumor suppressor genes. Expand
Human Papillomavirus Oncoprotein E6 Inactivates the Transcriptional Coactivator Human ADA3
TLDR
Findings reveal a novel strategy of HPV E6-induced loss of p53 function that is independent of direct p53 degradation, and inactivation of its function may allow E6 to perturb numerous cellular pathways during HPV oncogenesis. Expand
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