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829 results for “CRISPR screening”
Data for "An optimized genome-wide virus-free CRISPR screen for mammalian cells"
<p>This is the raw data from the article "An optimized genome-wide virus-free CRISPR screen for mammalian cells " and scripts for analyzing it.</p>
A scalable CRISPR-Cas9 gene editing system facilitates CRISPR screens in the malaria parasite Plasmodium berghei - sequencing data
<p>This holds raw sequencing data, and extracted sgRNA counts </p>
Data set: Genome scale CRISPR Cas9a knockout screen reveals genes that controls glioblastoma susceptibility to the alkylating agent temozolomide (TMZ).
<p>Glioblastoma is the deadliest of all primary brain tumor with a very poor survival outcome. Alkylating agent such as temozolomide is used as a mainstay drug used in treating of glioblastoma patients including radiation, tumor treating field and surgery. However, this drug offers little to no benefit for the glioblastoma patients. Hence, the objective of the generation of this data is to understand and unravel genes that controls glioblastoma susceptibility and resistance to temozolomide using an unbiased genome scale CRISPR Cas9a knockout screen</p>
RAD54L2 counters TOP2-DNA adducts to promote genome stability (Etoposide treated RPE1 CRISPR screens in TP53 and RAD53L2 knock outs)
<p>The catalytic cycle of topoisomerase 2 (TOP2) enzymes proceeds via a transient DNA double-strand break (DSB) intermediate termed the TOP2 cleavage complex (TOP2cc), in which the TOP2 protein is covalently bound to DNA. Anti-cancer agents such as etoposide operate by stabilising TOP2ccs, ultimately generating genotoxic TOP2-DNA protein crosslinks that require processing and repair. Here, we identify RAD54-like 2 (RAD54L2) as a factor promoting TOP2cc resolution. We demonstrate that RAD54L2 acts through a novel mechanism together with zinc finger protein associated with TDP2 and TOP2 (ZATT/ZNF451) and independent of tyrosyl-DNA phosphodiesterase 2 (TDP2). Our work suggests a model wherein RAD54L2 recognises sumoylated-TOP2 and, using its ATPase activity, promotes TOP2cc resolution and prevents DSB exposure. These findings suggest RAD54L2-mediated TOP2cc resolution as a potential mechanism for cancer-therapy resistance and highlight RAD54L2 as an attractive candidate for drug discovery.</p>
CRISPR-Cas9 screen upon Olaparib+CldU treatment
<p>DNA single-strand breaks (SSBs) disrupt DNA replication and induce chromosome breakage. However, whether SSBs induce chromosome breakage when present in nascent strands behind replication forks or template strands ahead of replication forks is unclear. To address this question, we exploited an exquisite sensitivity of SSB repair-defective human cells lacking PARP activity or XRCC1 to the thymidine analog 5-chloro-2'-deoxyuridine (CldU). We show that incubation with CldU in these cells results in chromosome breakage, sister chromatid exchange, and cytotoxicity by a mechanism that depends on the S phase activity of uracil DNA glycosylase (UNG). Importantly, we show that CldU incorporation in one cell cycle is cytotoxic only during the following cell cycle when it is present in template DNA. In agreement with this, while UNG induces SSBs both in nascent strands behind replication forks and in template strands ahead of replication forks, only the latter triggers fork collapse and chromosome breakage. Finally, we show that BRCA-defective cells are hypersensitive to CldU, either alone and/or in combination with PARP inhibitor, suggesting that CldU may have clinical utility.</p>
Reporter CRISPR screens decipher cis- and trans-regulatory principles at the Xist locus [Microscope images - Oct4 KDs]
<p>Microscope images related to Figure 2 in Schwämmle et al. 2025. </p> <p>The cells are undifferentiated or day 2 differentiated TX1072 XX SP427 mESCs with (or without) Oct4 knockdown in the indicated media.</p> <p>Exonic Xist is stained using Cy5 Stellaris probes. The nuclei are stained using DAPI.</p> <p>These files were used to manually count Xist clouds (see fish_sgOct4_manual.txt for counts). For code to visualize the results see https://github.com/EddaSchulz/TFiScreen_Paper. RA samples relate only to the biorXiv release of the manuscript (https://doi.org/10.1101/2024.10.08.617282).</p>
Reporter CRISPR screens decipher cis- and trans-regulatory principles at the Xist locus [FACS + BAMs + tables]
<div>FACS data related to Figures 1 and 4 in Schwämmle et al. 2025. </div> <div>Also include BAM files of published data and other files needed to replicate analyses included in https://github.com/EddaSchulz/TFiScreen_Paper. </div>
Reporter CRISPR screens decipher cis- and trans-regulatory principles at the Xist locus [Extra tables + files]
<p>This zenodo contains extra files and tables necessary to run code specified in https://github.com/EddaSchulz/TFiScreen_Paper/.</p> <p>These files are associated with analysis in Schwämmle et al., 2025.</p>
The raw data of the genome-wide CRISPR screens for VHL-WT and VHL-L188V Kelly cells
<p>The raw data including the conditions, reference, and PoolQ output files of the genome-wide CRISPR screens for VHL-WT and VHL-L188V Kelly cells were published in the paper "Total loss of VHL gene function impairs neuroendocrine cancer cell fitness due to excessive HIF2α activity".</p>
Data from: Genome-wide CRISPR synthetic lethality screen identifies a role for the ADP-ribosyltransferase PARP14 in replication fork stability controlled by ATR
<p>The DNA damage response is essential to maintain genomic stability, suppress replication stress, and protect against carcinogenesis. The ATR-CHK1 pathway is an essential component of this response, which regulates cell cycle progression in the face of replication stress. PARP14 is an ADP-ribosyltransferase with multiple roles in transcription, signaling, and DNA repair. To understand the biological functions of PARP14, we catalogued the genetic components that impact cellular viability upon loss of PARP14 by performing an unbiased, comprehensive, genome-wide CRISPR knockout genetic screen in PARP14-deficient cells. We uncovered the ATR-CHK1 pathway as essential for viability of PARP14-deficient cells, and identified regulation of DNA replication dynamics as an important mechanistic contributor to the synthetic lethality observed. Our work shows that PARP14 is an important modulator of the response to ATR-CHK1 pathway inhibitors.</p>
10k 1:1 Mixture of Jurkat and MM1S Cells, 5' v2.0, CRISPR Screening, Chromium X - BESCA
<p>This dataset is a BESCA processed version of the example resources found at https://www.10xgenomics.com/resources/datasets/10k-1-1-mixture-of-jurkat-and-mm1s-cells-5-v2-0-chromium-x-2-standard</p>
Data from: Pooled genome-wide CRISPR activation screening for rapamycin resistance genes in Drosophila cells
<p>Loss-of-function and gain-of-function genetic perturbations provide valuable insights into gene function. In <em>Drosophila</em> cells, while genome-wide loss-of-function screens have been extensively used to reveal mechanisms of a variety of biological processes, approaches for performing genome-wide gain-of-function screens are still lacking. Here, we describe a pooled CRISPR activation (CRISPRa) screening platform in <em>Drosophila</em> cells and apply this method to both focused and genome-wide screens to identify rapamycin resistance genes. The screens identified three genes as novel rapamycin resistance genes: a member of SLC16 family of monocarboxylate transporters (<em>CG8468)</em>, a member of the lipocalin protein family (<em>CG5399</em>), and a zinc finger C2H2 transcription factor (<em>CG9932</em>). Mechanistically, we demonstrate that <em>CG5399</em> overexpression activates the RTK-Akt-mTOR signaling pathway and that activation of insulin receptor (InR) by <em>CG5399</em> requires cholesterol and clathrin-coated pits at the cell membrane. This study establishes a novel platform for functional genetic studies in <em>Drosophila</em> cells.</p>
Data from: CRISPR screening by AAV episome-sequencing (CrAAVe-seq): A scalable cell type-specific in vivo platform uncovers neuronal essential genes
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Data from: Pooled genome-wide CRISPR activation screening for rapamycin resistance genes in Drosophila cells
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CRISPR-Cas9 screen upon Olaparib+CldU treatment
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RAD54L2 counters TOP2-DNA adducts to promote genome stability (Etoposide treated RPE1 CRISPR screens in TP53 and RAD53L2 knock outs)
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A novel CRISPR screen identifies mediators of cfDNA release
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Data from: Genome-wide CRISPR synthetic lethality screen identifies a role for the ADP-ribosyltransferase PARP14 in replication fork stability controlled by ATR
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Parallel CRISPR-Cas9 screens clarify impacts of p53 on screen performance
<p>CRISPR-Cas9 genome engineering has revolutionised high-throughput functional genomic screens. However, recent work has raised concerns regarding the performance of CRISPR-Cas9 screens using <i>TP53</i> wild-type human cells due to a p53-mediated DNA damage response (DDR) limiting the efficiency of generating viable edited cells. To directly assess the impact of cellular p53 status on CRISPR-Cas9 screen performance, we carried out parallel CRISPR-Cas9 screens in wild-type and <i>TP53</i> knockout human retinal pigment epithelial cells using a focused dual guide RNA library targeting 852 DDR-associated genes. Our work demonstrates that although functional p53 status negatively affects identification of significantly depleted genes, optimal screen design can nevertheless enable robust screen performance. Through analysis of our own and published screen data, we highlight key factors for successful screens in both wild-type and p53-deficient cells.</p>
Mitochondrial and ER membrane protein trafficking CRISPR screens
<p><span>The trafficking of specific protein cohorts to the correct subcellular location at the correct time is essential for every signaling and regulatory process in biology. Gene perturbation screens could provide a powerful approach to probe the molecular mechanisms of protein trafficking, but only if protein localization or mislocalization can be tied to a simple and robust phenotype for cell selection, such as cell proliferation or FACS. To broadly empower the study of protein trafficking processes with gene perturbation, we developed a genetically-encoded molecular tool named HiLITR. HiLITR converts protein colocalization into proteolytic release of a membrane-anchored transcription factor, which drives the expression of a chosen reporter gene. Using HiLITR in combination with FACS-based CRISPRi screening in human cell lines, we identify genes that influence the trafficking of mitochondrial and ER tail-anchored proteins. </span>We show that loss of the SUMO E1 component SAE1 results in the mislocalization and destabilization of mitochondrial tail-anchored proteins. We also demonstrate a distinct regulatory role for EMC10 in the ER membrane complex, opposing the transmembrane-domain insertion activity of the complex. Through transcriptional integration of complex cellular functions, HiLITR expands the scope of biological processes that can be studied by genetic perturbation screening technologies.</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.