ArticleThe EMBO journal2003
Degradation of origin recognition complex large subunit by the anaphase-promoting complex in Drosophila.
Article in The EMBO journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 55 citations in OpenAlex.
- The E3 ligase RFWD3 stabilizes ORC in a p53-dependent manner.Cell cycle (Georgetown, Tex.) · 2020Article
- Mechanisms for the temporal regulation of substrate ubiquitination by the anaphase-promoting complex/cyclosome.Cell division · 2019Review
- Nonreplicative functions of the origin recognition complex.Nucleus (Austin, Tex.) · 2018Review
- Regulation of Mammalian DNA Replication via the Ubiquitin-Proteasome System.Advances in experimental medicine and biology · 2017Review
- APC/C and retinoblastoma interaction: cross-talk of retinoblastoma protein with the ubiquitin proteasome pathway.Bioscience reports · 2016Review
- Diverged composition and regulation of the Trypanosoma brucei origin recognition complex that mediates DNA replication initiation.Nucleic acids research · 2016Article
- Targeting Cdc20 as a novel cancer therapeutic strategy.Pharmacology & therapeutics · 2015Review
- The Non-Canonical Role of Aurora-A in DNA Replication.Frontiers in oncology · 2015Review
- Co-activator independent differences in how the metaphase and anaphase APC/C recognise the same substrate.Biology open · 2014Article
- Functional characterization of Anaphase Promoting Complex/Cyclosome (APC/C) E3 ubiquitin ligases in tumorigenesis.Biochimica et biophysica acta · 2014Review
- Orc2 protects ORCA from ubiquitin-mediated degradation.Cell cycle (Georgetown, Tex.) · 2012Article
- The origin recognition complex: a biochemical and structural view.Sub-cellular biochemistry · 2012Review
- The APC/C Ubiquitin Ligase: From Cell Biology to Tumorigenesis.Frontiers in oncology · 2011Article
- Study of DNA replication in Drosophila using cell free in vitro system.Cell cycle (Georgetown, Tex.) · 2010Article
- The emerging role of APC/CCdh1 in controlling differentiation, genomic stability and tumor suppression.Oncogene · 2010Review
- Endoreplication: polyploidy with purpose.Genes & development · 2009Review
- Developmentally programmed endoreduplication in animals.Cell cycle (Georgetown, Tex.) · 2009Article
- Differential targeting of Tetrahymena ORC to ribosomal DNA and non-rDNA replication origins.The EMBO journal · 2009Article
- Binding of Drosophila ORC proteins to anaphase chromosomes requires cessation of mitotic cyclin-dependent kinase activity.Molecular and cellular biology · 2009Article
- Mechanisms of ubiquitin transfer by the anaphase-promoting complex.Journal of biology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The initiation of DNA synthesis is thought to occur at sites bound by a heteromeric origin recognition complex (ORC). Previously, we have shown that in Drosophila, the level of the large subunit, ORC1, is modulated during cell cycle progression and that changes in ORC1 concentration alter origin utilization during development. Here, we investigate the mechanisms underlying cell cycle-dependent degradation of ORC1. We show that signals in the non-conserved N-terminal domain of ORC1 mediate its degradation upon exit from mitosis and in G1 phase by the anaphase-promoting complex (APC) in vivo. Degradation appears to be the result of direct action of the APC, as the N-terminal domain is ubiquitylated by purified APC in vitro. This regulated proteolysis is potent, sufficient to generate a normal temporal distribution of protein even when transcription of ORC1 is driven by strong constitutive promoters. These observations suggest that in Drosophila, ORC1 regulates origin utilization much as does Cdc6 in budding yeast.
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.