ArticleG3 (Bethesda, Md.)2016
Synthetic Physical Interactions Map Kinetochore-Checkpoint Activation Regions.
Article in G3 (Bethesda, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Proteome-wide forced interactions reveal a functional map of cell-cycle phospho-regulation inNucleus (Austin, Tex.) · 2024Article
- Yeast goes viral: probing SARS-CoV-2 biology usingMicrobial cell (Graz, Austria) · 2022Article
- ScreenGarden: a shinyR application for fast and easy analysis of plate-based high-throughput screens.BMC bioinformatics · 2022Article
- Forced association of SARS-CoV-2 proteins with the yeast proteome perturb vesicle trafficking.Microbial cell (Graz, Austria) · 2021Article
- A platform for post-translational spatiotemporal control of cellular proteins.Synthetic biology (Oxford, England) · 2021Article
- Polo kinase recruitment via the constitutive centromere-associated network at the kinetochore elevates centromeric RNA.PLoS genetics · 2020Article
- Synthetic Physical Interactions with the Yeast Centrosome.G3 (Bethesda, Md.) · 2019Article
- Cell cycle-dependent association of polo kinase Cdc5 with CENP-A contributes to faithful chromosome segregation in budding yeast.Molecular biology of the cell · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The spindle assembly checkpoint (SAC) is a key mechanism to regulate the timing of mitosis and ensure that chromosomes are correctly segregated to daughter cells. The recruitment of the Mad1 and Mad2 proteins to the kinetochore is normally necessary for SAC activation. This recruitment is coordinated by the SAC kinase Mps1, which phosphorylates residues at the kinetochore to facilitate binding of Bub1, Bub3, Mad1, and Mad2. There is evidence that the essential function of Mps1 is to direct recruitment of Mad1/2. To test this model, we have systematically recruited Mad1, Mad2, and Mps1 to most proteins in the yeast kinetochore, and find that, while Mps1 is sufficient for checkpoint activation, recruitment of either Mad1 or Mad2 is not. These data indicate an important role for Mps1 phosphorylation in SAC activation, beyond the direct recruitment of Mad1 and Mad2.
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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.