ArticleDevelopmental cell2017
Large-Scale Analysis of CRISPR/Cas9 Cell-Cycle Knockouts Reveals the Diversity of p53-Dependent Responses to Cell-Cycle Defects.
Article in Developmental cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 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
134 citing papers in PubMed, 208 citations in OpenAlex.
- Article
- Laboratory Assessment and Clinical Outlook forAnnals of laboratory medicine · 2026Review
- Dysregulation of the Tau-Microtubule-End-Binding Protein Axis in Alzheimer's Disease and Related Tauopathies.International journal of molecular sciences · 2026Review
- Mechanistic design of cell-penetrating disruptors for phospho-dependent TACC3-CHC interaction.Structure (London, England : 1993) · 2026Article
- Conditional deletion of human STN1 leads to telomere dysfunction, genome instability and proliferation defects.Journal of cell science · 2026Article
- The nuclear structural protein NuMA is required for efficient DNA replication by ensuring association of core replication factors to replication forks.bioRxiv : the preprint server for biology · 2026Article
- Eg5 activity and density-driven bundling organize the human metaphase mitotic spindle independently of spindle bipolarity.bioRxiv : the preprint server for biology · 2026Article
- YBX1&YBX3 as novel targets to potentiate immune checkpoint blockade response in gliomas.Neuro-oncology · 2026Article
- MEIOC prevents continued mitotic cycling and promotes meiotic entry during mouse oogenesis.Development (Cambridge, England) · 2026Article
- MEIOC prevents continued mitotic cycling and promotes meiotic entry during mouse oogenesis.bioRxiv : the preprint server for biology · 2025Article
- 19S proteasome loss regulates mitotic spindle assembly through a ubiquitin-independent degradation mechanism.Cell reports · 2025Article
- NIS-Seq enables cell-type-agnostic optical perturbation screening.Nature biotechnology · 2025Article
- High-content image-based pooled screens reveal regulators of synaptogenesis.Cell reports · 2025Article
- Reversible and effective cell cycle synchronization method for studying stage-specific processes.Life science alliance · 2025Article
- An Aurora kinase A-BOD1L1-PP2A B56 axis promotes chromosome segregation fidelity.Cell reports · 2025Article
- Functional genetics reveals modulators of antimicrotubule drug sensitivity.The Journal of cell biology · 2025Article
- 19S proteasome loss causes monopolar spindles through ubiquitin-independent KIF11 degradation.bioRxiv : the preprint server for biology · 2025Article
- Systematic Identification of Microtubule Posttranslational Modification "Readers" by Quantitative Proteomics.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Chk2 sustains PLK1 activity in mitosis to ensure proper chromosome segregation.Nature communications · 2024Article
- Classification and functional characterization of regulators of intracellular STING trafficking identified by genome-wide optical pooled screening.Cell systems · 2024Article
74 more citing papers are in PubMed but not listed here.
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
Abstract
Defining the genes that are essential for cellular proliferation is critical for understanding organismal development and identifying high-value targets for disease therapies. However, the requirements for cell-cycle progression in human cells remain incompletely understood. To elucidate the consequences of acute and chronic elimination of cell-cycle proteins, we generated and characterized inducible CRISPR/Cas9 knockout human cell lines targeting 209 genes involved in diverse cell-cycle processes. We performed single-cell microscopic analyses to systematically establish the effects of the knockouts on subcellular architecture. To define variations in cell-cycle requirements between cultured cell lines, we generated knockouts across cell lines of diverse origins. We demonstrate that p53 modulates the phenotype of specific cell-cycle defects through distinct mechanisms, depending on the defect. This work provides a resource to broadly facilitate robust and long-term depletion of cell-cycle proteins and reveals insights into the requirements for cell-cycle progression.
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.