ArticleThe EMBO journal1998
Induction of DNA synthesis and apoptosis by regulated inactivation of a temperature-sensitive retinoblastoma protein.
Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Immune response to RB1-regulated senescence limits radiation-induced osteosarcoma formation.The Journal of clinical investigation · 2013Article
- Loss of the retinoblastoma tumor suppressor protein in murine calvaria facilitates immortalization of osteoblast-adipocyte bipotent progenitor cells characterized by low expression of N-cadherin.Molecular and cellular biology · 2012Article
- Tumor suppression by p53: making cells senescent.Histology and histopathology · 2010Review
- Williams-Beuren syndrome-associated transcription factor TFII-I regulates osteogenic marker genes.The Journal of biological chemistry · 2009Article
- Impaired bone development and increased mesenchymal progenitor cells in calvaria of RB1-/- mice.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Cellular senescence requires CDK5 repression of Rac1 activity.Molecular and cellular biology · 2004Article
- Dual control of neurogenesis by PC3 through cell cycle inhibition and induction of Math1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Skip interacts with the retinoblastoma tumor suppressor and inhibits its transcriptional repression activity.Nucleic acids research · 2002Article
- Cyclin D3 activates Caspase 2, connecting cell proliferation with cell death.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Requirement for p27(KIP1) in retinoblastoma protein-mediated senescence.Molecular and cellular biology · 2001Article
- pRB and p107 have distinct effects when expressed in pRB-deficient tumor cells at physiologically relevant levels.Oncogene · 2000Article
- Pocket protein-independent repression of urokinase-type plasminogen activator and plasminogen activator inhibitor 1 gene expression by E2F1.Molecular and cellular biology · 2000Article
- Distinct glucocorticoid receptor transcriptional regulatory surfaces mediate the cytotoxic and cytostatic effects of glucocorticoids.Molecular and cellular biology · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retinoblastoma protein, pRb, controls entry into the S phase of the cell cycle and acts as a tumor suppressor in many tissues. Re-introduction of pRb into tumor cells lacking this protein results in growth arrest, due in part to transcriptional repression of genes required for S phase. Several studies suggest that pRb may also be involved in terminal cell cycle exit as a result of the instigation of senescence or differentiation programs. To understand better these multiple growth-inhibitory properties of pRb, a temperature-sensitive mutant of pRb has been produced. This tspRb induces G1 arrest and morphological changes efficiently at the permissive temperature of 32.5 degrees C, but is weakly functional at 37 degrees C. Consistent with this, tspRb is compromised in nuclear association and E2F regulation at the non-permissive temperature, but regains these properties at 32.5 degrees C. Serial activation and inactivation of tspRb in SAOS-2 cells does not allow proliferation, but rather leads to apoptotic cell death. Transient activation of pRb may kill tumor cells by establishing a conflict between persistent proliferation-inhibitory signals and renewed deregulation of pRb targets such as E2F, and may thus be a more potent means of eliminating these cells than through simple re-introduction of the tumor suppressor gene.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.