Evidence map›Paper›PMID 29449584›Full record

ArticleCell death & disease2018

CRISPR whole-genome screening identifies new necroptosis regulators and RIPK1 alternative splicing.

Marinella G Callow, Colin Watanabe, Katherine E Wickliffe, Russell Bainer, Sarah Kummerfield, Julie Weng, Trinna Cuellar, Vasantharajan Janakiraman, Honglin Chen, Ben Chih and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  6. Raver1 linksProceedings of the National Academy of Sciences of the United States of America · 2025
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  9. mCellular & molecular biology letters · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 1 institution in 1 country.

Marinella G CallowDepartment of Discovery Oncology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Colin WatanabeDepartment of Bioinformatics and Computational Biology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Katherine E WickliffeDepartment of Physiological Chemistry, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Russell BainerDepartment of Bioinformatics and Computational Biology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Sarah KummerfieldDepartment of Bioinformatics and Computational Biology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Julie WengDepartment of Discovery Oncology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Trinna CuellarDepartment of Molecular Biology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Vasantharajan JanakiramanDepartment of Molecular Biology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Honglin ChenDepartment of Molecular Biology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Ben ChihDepartment of Biochemical and Cellular Pharmacology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Yuxin LiangDepartment of Molecular Biology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Benjamin HaleyDepartment of Molecular Biology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Kim NewtonDepartment of Physiological Chemistry, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA.
Michael R CostaDepartment of Discovery Oncology, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA. mcosta@gene.com.
Princeton University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The necroptotic cell death pathway is a key component of human pathogen defense that can become aberrantly derepressed during tissue homeostasis to contribute to multiple types of tissue damage and disease. While formation of the necrosome kinase signaling complex containing RIPK1, RIPK3, and MLKL has been extensively characterized, additional mechanisms of its regulation and effector functions likely remain to be discovered. We screened 19,883 mouse protein-coding genes by CRISPR/Cas9-mediated gene knockout for resistance to cytokine-induced necroptosis and identified 112 regulators and mediators of necroptosis, including 59 new candidate pathway components with minimal or no effect on cell growth in the absence of necroptosis induction. Among these, we further characterized the function of PTBP1, an RNA binding protein whose activity is required to maintain RIPK1 protein abundance by regulating alternative splice-site selection.

Indexed as

Alternative SplicingClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsNecroptosisAnimalsCRISPR-Associated Protein 9FibroblastsGene Expression Regulation, EnzymologicGene TargetingHEK293 CellsHeterogeneous-Nuclear RibonucleoproteinsHT29 CellsHumansMicePolypyrimidine Tract-Binding ProteinReceptor-Interacting Protein Serine-Threonine KinasesCRISPR-Associated Protein 9Heterogeneous-Nuclear RibonucleoproteinsPolypyrimidine Tract-Binding ProteinPtbp1 protein, mouseReceptor-Interacting Protein Serine-Threonine KinasesRipk1 protein, mouse

Identifiers

PMID29449584
PMCPMC5833675
OpenAlexW2792837471

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.