Evidence map›Paper›PMID 41792279›Full record

ArticleNature structural & molecular biology2026

A proteome-wide dependency map of protein interaction motifs.

Sara M Ambjørn, Bob Meeusen, Johanna Kliche, Juanjuan Wang, Dimitriya H Garvanska, Thomas Kruse, Blanca Lopez Mendez, Matthias Mann, Niels Mailand, Emil P T Hertz and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature structural & molecular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. A SLiM view of the human proteome.Nature structural & molecular biology · 2026
    Article
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

12 authors.

Sara M Ambjørn *Center for Epigenetic Cell Memory, Danish Cancer Institute, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-5571-1382
Bob Meeusen *Center for Epigenetic Cell Memory, Danish Cancer Institute, Copenhagen, Denmark.ORCID http://orcid.org/0000-0003-3997-223X
Johanna KlicheCenter for Epigenetic Cell Memory, Danish Cancer Institute, Copenhagen, Denmark.
Juanjuan WangNovo Nordisk Foundation Center for Protein Research, ICMM, University of Copenhagen, Copenhagen, Denmark.
Dimitriya H GarvanskaCenter for Epigenetic Cell Memory, Danish Cancer Institute, Copenhagen, Denmark.
Thomas KruseCenter for Epigenetic Cell Memory, Danish Cancer Institute, Copenhagen, Denmark.
Blanca Lopez MendezNovo Nordisk Foundation Center for Protein Research, ICMM, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0001-8541-4904
Matthias MannNovo Nordisk Foundation Center for Protein Research, ICMM, University of Copenhagen, Copenhagen, Denmark.
Niels MailandCenter for Epigenetic Cell Memory, Danish Cancer Institute, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-6623-709X
Emil P T HertzNovo Nordisk Foundation Center for Protein Research, ICMM, University of Copenhagen, Copenhagen, Denmark. emil.hertz@skape.bio.ORCID http://orcid.org/0000-0001-6996-3559
Norman E DaveyDivision of Cancer Biology, The Institute of Cancer Research, London, UK. norman.davey@stjude.org.ORCID http://orcid.org/0000-0001-6988-4850
Jakob NilssonCenter for Epigenetic Cell Memory, Danish Cancer Institute, Copenhagen, Denmark. jaknil@cancer.dk.ORCID http://orcid.org/0000-0003-4100-1125

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Short linear motifs (SLiMs) are the most ubiquitous protein interaction motifs within unstructured regions of the human proteome, yet their contribution to cellular homeostasis remains poorly understood. Here, to systematically assess SLiM function, we applied base editing to mutate all reported and a set of computationally predicted SLiMs defined by SLiM-like evolutionary patterns. By screening 7,293 SLiM-containing regions with 80,473 mutations in HAP1 cells, we define a SLiM dependency map identifying 450 reported and 264 predicted SLiMs required for normal cell proliferation. Mutational consequences were highly reproducible in RPE1 cells, with differences attributed to cell-line-specific gene essentiality. We show that many predicted SLiMs affecting proliferation do not belong to existing classes and identify binding partners for several of these, providing mechanistic insight into a disease-associated ANKRD17 mutation. Our study provides a proteome-wide resource on SLiM essentiality uncovering numerous uncharacterized essential SLiMs.

Indexed as

Protein Interaction Domains and MotifsProteomeAmino Acid MotifsCell LineCell ProliferationHumansMutationProteome

Identifiers

What OpenQuestion holds

Textmetadata
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.