ArticleMolecular and cellular biology1994
A gene involved in control of human cellular senescence on human chromosome 1q.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 95 citations in OpenAlex.
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- Enhanced tumorigenicity by mitochondrial DNA mild mutations.Oncotarget · 2015Article
- The anti-tumor effect of shikonin on osteosarcoma by inducing RIP1 and RIP3 dependent necroptosis.BMC cancer · 2013Article
- CREG1 enhances p16(INK4a) -induced cellular senescence.Cell cycle (Georgetown, Tex.) · 2011Article
- Establishment and characterization of a new highly metastatic human osteosarcoma cell line.Clinical & experimental metastasis · 2009Article
- An orthotopic model of human osteosarcoma growth and spontaneous pulmonary metastasis.Clinical & experimental metastasis · 2005Article
- Role of IFI 16 in cellular senescence of human fibroblasts.Oncogene · 2004Article
- Role of IFI 16, a member of the interferon-inducible p200-protein family, in prostate epithelial cellular senescence.Oncogene · 2003Article
- Article
- Identification of a </= 600-kb region on human chromosome 1q42.3 inducing cellular senescence.Oncogene · 2003Article
- Functional cloning of a tumor suppressor gene, TSLC1, in human non-small cell lung cancer.Oncogene · 2002Review
- Functional evidence for a squamous cell carcinoma mortality gene(s) on human chromosome 4.Oncogene · 2002Article
- Review
- Article
- Identification of a gene at 16q24.3 that restores cellular senescence in immortal mammary tumor cells.Oncogene · 1999Article
- Identification of a gene that reverses the immortal phenotype of a subset of cells and is a member of a novel family of transcription factor-like genes.Molecular and cellular biology · 1999Article
- Wild-type p53 triggers a rapid senescence program in human tumor cells lacking functional p53.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Normal cells in culture exhibit limited division potential and have been used as a model for cellular senescence. In contrast, tumor-derived or carcinogen- or virus-transformed cells are capable of indefinite division. Fusion of normal human diploid fibroblasts with immortal human cells yielded hybrids having limited life spans, indicating that cellular senescence was dominant. Fusions of various immortal human cell lines with each other led to the identification of four complementation groups for indefinite division. The purpose of this study was to determine whether human chromosome 1 could complement the recessive immortal defect of human cell lines assigned to one of the four complementation groups. Using microcell fusion, we introduced a single normal human chromosome 1 into immortal human cell lines representing the complementation groups and determined that it caused loss of proliferative potential of an osteosarcoma-derived cell line (TE85), a cytomegalovirus-transformed lung fibroblast cell line (CMV-Mj-HEL-1), and a Ki-ras(+)-transformed derivative of TE85 (143B TK-), all of which were assigned to complementation group C. This chromosome 1 caused no change in proliferative potential of cell lines representing the other complementation groups. A derivative of human chromosome 1 that had lost most of the q arm by spontaneous deletion was unable to induce senescence in any of the immortal cell lines. This finding indicates that the q arm of human chromosome 1 carries a gene or set of genes which is altered in the cell lines assigned to complementation group C and is involved in the control of cellular senescence.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.