ArticlePLoS genetics2021
Genome-scale CRISPR screening for modifiers of cellular LDL uptake.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 36 citations in OpenAlex.
- COPI Coatomer Regulates Several Steps of HDL Metabolism.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Article
- Article
- CRISPR and the Future of Cardiac Disease Therapy: A New Genetic Frontier.International journal of molecular sciences · 2026Review
- Functional interrogation of candidate cis-regulatory elements at the LDLR locus.PLoS genetics · 2026Article
- LDLR variant classification through activity-normalized prime editing screening.bioRxiv : the preprint server for biology · 2025Article
- ABCC4 impairs the clearance of plasma LDL cholesterol through suppressing LDLR expression in the liver.Communications biology · 2025Article
- Functional interrogation of cellular Lp(a) uptake by genome-scale CRISPR screening.Atherosclerosis · 2025Article
- Systematic interrogation of functional genes underlying cholesterol and lipid homeostasis.Genome biology · 2025Article
- Type I interferon signaling induces a delayed antiproliferative response in respiratory epithelial cells during SARS-CoV-2 infection.Journal of virology · 2023Article
- ARF6 is a host factor for SARS-CoV-2 infectionThe Journal of general virology · 2023Article
- Systematic elucidation of genetic mechanisms underlying cholesterol uptake.Cell genomics · 2023Article
- Massively Parallel Reporter Assays for High-Throughput In Vivo Analysis of Cis-Regulatory Elements.Journal of cardiovascular development and disease · 2023Review
- Gene editing for dyslipidemias: New tools to "cut" lipids.Atherosclerosis · 2023Review
- Type I interferon signaling induces a delayed antiproliferative response in Calu-3 cells during SARS-CoV-2 infection.bioRxiv : the preprint server for biology · 2023Article
- Systematic elucidation of genetic mechanisms underlying cholesterol uptake.bioRxiv : the preprint server for biology · 2023Article
- Development of a novel Guinea Pig model producing transgenerational endothelial transcriptional changes driven by maternal food restriction and a second metabolic insult of high fat diet.Frontiers in physiology · 2023Article
- CRISPR screening in cardiovascular research.Frontiers in cell and developmental biology · 2023Review
- Cold shock domain-containing protein E1 is a posttranscriptional regulator of the LDL receptor.Science translational medicine · 2022Article
- Identification of cell type specific ACE2 modifiers by CRISPR screening.PLoS pathogens · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Hypercholesterolemia is a causal and modifiable risk factor for atherosclerotic cardiovascular disease. A critical pathway regulating cholesterol homeostasis involves the receptor-mediated endocytosis of low-density lipoproteins into hepatocytes, mediated by the LDL receptor. We applied genome-scale CRISPR screening to query the genetic determinants of cellular LDL uptake in HuH7 cells cultured under either lipoprotein-rich or lipoprotein-starved conditions. Candidate LDL uptake regulators were validated through the synthesis and secondary screening of a customized library of gRNA at greater depth of coverage. This secondary screen yielded significantly improved performance relative to the primary genome-wide screen, with better discrimination of internal positive controls, no identification of negative controls, and improved concordance between screen hits at both the gene and gRNA level. We then applied our customized gRNA library to orthogonal screens that tested for the specificity of each candidate regulator for LDL versus transferrin endocytosis, the presence or absence of genetic epistasis with LDLR deletion, the impact of each perturbation on LDLR expression and trafficking, and the generalizability of LDL uptake modifiers across multiple cell types. These findings identified several previously unrecognized genes with putative roles in LDL uptake and suggest mechanisms for their functional interaction with LDLR.
Indexed as
Identifiers
What Socratic 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 Socratic graph.