ArticleMolecular and cellular biology1993
Regions of the retinoblastoma gene product required for its interaction with the E2F transcription factor are necessary for E2 promoter repression and pRb-mediated growth suppression.
Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 131 citations in OpenAlex.
- Multiple molecular interactions redundantly contribute to RB-mediated cell cycle control.Cell division · 2017Article
- Pin1 inhibits PP2A-mediated Rb dephosphorylation in regulation of cell cycle and S-phase DNA damage.Cell death & disease · 2015Article
- PRMT4-mediated arginine methylation negatively regulates retinoblastoma tumor suppressor protein and promotes E2F-1 dissociation.Molecular and cellular biology · 2015Article
- In Vivo Exposures to Particulate Matter Collected from Saudi Arabia or Nickel Chloride Display Similar Dysregulation of Metabolic Syndrome Genes.Journal of toxicology and environmental health. Part A · 2015Article
- A retinoblastoma allele that is mutated at its common E2F interaction site inhibits cell proliferation in gene-targeted mice.Molecular and cellular biology · 2014Article
- Genetically engineered mouse models and human osteosarcoma.Clinical sarcoma research · 2012Article
- Conserved RB functions in development and tumor suppression.Protein & cell · 2011Review
- Regulation of survival, proliferation, invasion, angiogenesis, and metastasis of tumor cells through modulation of inflammatory pathways by nutraceuticals.Cancer metastasis reviews · 2010Review
- Phosphorylation-induced conformational changes in the retinoblastoma protein inhibit E2F transactivation domain binding.The Journal of biological chemistry · 2010Article
- Neurobeachin (NBEA) is a target of recurrent interstitial deletions at 13q13 in patients with MGUS and multiple myeloma.Experimental hematology · 2009Article
- Retinoblastoma protein phosphorylation at multiple sites is associated with neurofibrillary pathology in Alzheimer disease.International journal of clinical and experimental pathology · 2008Article
- Novel role for RbAp48 in tissue-specific, estrogen deficiency-dependent apoptosis in the exocrine glands.Molecular and cellular biology · 2006Article
- p55, the Drosophila ortholog of RbAp46/RbAp48, is required for the repression of dE2F2/RBF-regulated genes.Molecular and cellular biology · 2004Article
- Interactions between human cytomegalovirus IE1-72 and cellular p107: functional domains and mechanisms of up-regulation of cyclin E/cdk2 kinase activity.Journal of virology · 2003Article
- Article
- Destabilization of the retinoblastoma tumor suppressor by human papillomavirus type 16 E7 is not sufficient to overcome cell cycle arrest in human keratinocytes.Journal of virology · 2001Article
- The p107 tumor suppressor induces stable E2F DNA binding to repress target promoters.Oncogene · 2001Article
- RBP1 recruits the mSIN3-histone deacetylase complex to the pocket of retinoblastoma tumor suppressor family proteins found in limited discrete regions of the nucleus at growth arrest.Molecular and cellular biology · 2001Article
- Article
- Cells degrade a novel inhibitor of differentiation with E1A-like properties upon exiting the cell cycle.Molecular and cellular biology · 2000Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Studies of naturally occurring mutations of the RB1 tumor suppressor gene have indicated that the E1A/T antigen-binding domain is important for pRb function. Mutations engineered within the C-terminal 135 amino acids of pRb also abrogate its growth-suppressive function during the G1 interval of the cell cycle. Both the pRb E1A/T antigen-binding domain and the C-terminal domain are required for interaction with the E2F transcription factor. A series of mutated pRb proteins has been used to define the C-terminal sequences which determine E2F binding, adenovirus E2 promoter inhibition, and negative growth control. Deletion of the C terminus to residue 870 allowed full pRb function, while further deletion to residue 841 inactivated pRb in each assay. Amino acid sequences immediately C-terminal to the E1A/T antigen-binding domain were absolutely required for pRb activity. Mutations which prevented pRb from interacting with E2F also eliminated pRb-mediated E2 promoter repression and inactivated the ability of pRb to suppress cell growth.
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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.