ArticlePloS one2006
Separation of anti-proliferation and anti-apoptotic functions of retinoblastoma protein through targeted mutations of its A/B domain.
Article in PloS one, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Programmed Cell Death in Unicellular Versus Multicellular Organisms.Annual review of genetics · 2023Review
- Understanding Retinoblastoma Post-Translational Regulation for the Design of Targeted Cancer Therapies.Cancers · 2022Review
- Next-generation sequencing-based method shows increased mutation detection sensitivity in an Indian retinoblastoma cohort.Molecular vision · 2016Article
- RB1 dual role in proliferation and apoptosis: cell fate control and implications for cancer therapy.Oncotarget · 2015Review
- A retinoblastoma allele that is mutated at its common E2F interaction site inhibits cell proliferation in gene-targeted mice.Molecular and cellular biology · 2014Article
- Retinoblastoma protein regulates the crosstalk between autophagy and apoptosis, and favors glioblastoma resistance to etoposide.Cell death & disease · 2013Article
- DNA damage signals through differentially modified E2F1 molecules to induce apoptosis.Molecular and cellular biology · 2012Article
- Oncolytic specificity of Newcastle disease virus is mediated by selectivity for apoptosis-resistant cells.Journal of virology · 2011Article
- p38 phosphorylates Rb on Ser567 by a novel, cell cycle-independent mechanism that triggers Rb-Hdm2 interaction and apoptosis.Oncogene · 2011Article
- Tailoring to RB: tumour suppressor status and therapeutic response.Nature reviews. Cancer · 2008Review
- SerpinB2 protection of retinoblastoma protein from calpain enhances tumor cell survival.Cancer research · 2008Article
- pRB-E2F1 complexes are resistant to adenovirus E1A-mediated disruption.Journal of virology · 2008Article
- Human herpesvirus 6A (HHV-6A) and HHV-6B alter E2F1/Rb pathways and E2F1 localization and cause cell cycle arrest in infected T cells.Journal of virology · 2007Article
- Structure-function analysis of the retinoblastoma tumor suppressor protein - is the whole a sum of its parts?Cell division · 2007Article
- The molecular genetics of breast cancer and targeted therapy.Biologics : targets & therapy · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe human retinoblastoma susceptibility gene encodes a nuclear phosphoprotein RB, which is a negative regulator of cell proliferation. The growth suppression function of RB requires an evolutionarily conserved A/B domain that contains two distinct peptide-binding pockets. At the A/B interface is a binding site for the C-terminal trans-activation domain of E2F. Within the B-domain is a binding site for proteins containing the LxCxE peptide motif. METHODOLOGY/PRINCIPLE
findingsBased on the crystal structure of the A/B domain, we have constructed an RB-K530A/N757F (KN) mutant to disrupt the E2F- and LxCxE-binding pockets. The RB-K530A (K) mutant is sufficient to inactivate the E2F-binding pocket, whereas the RB-N757F (N) mutant is sufficient to inactivate the LxCxE-binding pocket. Each single mutant inhibits cell proliferation, but the RB-KN double mutant is defective in growth suppression. Nevertheless, the RB-KN mutant is capable of reducing etoposide-induced apoptosis. CONCLUSION/SIGNIFICANCE: Previous studies have established that RB-dependent G1-arrest can confer resistance to DNA damage-induced apoptosis. Results from this study demonstrate that RB can also inhibit apoptosis independent of growth suppression.
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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.