Evidence map›Paper›PMID 31320642›Full record

ArticleNature communications2019

Reconstitution of recombinant human CCR4-NOT reveals molecular insights into regulated deadenylation.

Tobias Raisch, Chung-Te Chang, Yevgen Levdansky, Sowndarya Muthukumar, Stefan Raunser, Eugene Valkov

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

78 citing papers in PubMed, 101 citations in OpenAlex.

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18 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Tobias RaischDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076, Tübingen, Germany.ORCID http://orcid.org/0000-0002-6531-3812
Chung-Te ChangDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076, Tübingen, Germany.
Yevgen LevdanskyDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076, Tübingen, Germany.
Sowndarya MuthukumarDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076, Tübingen, Germany.ORCID http://orcid.org/0000-0002-9110-722X
Stefan RaunserDepartment of Structural Biochemistry, Max Planck Institute of Molecular Physiology, Otto-Hahn-Strasse 11, 44227, Dortmund, Germany.ORCID http://orcid.org/0000-0001-9373-3016
Eugene ValkovDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076, Tübingen, Germany. eugene.valkov@tuebingen.mpg.de.ORCID http://orcid.org/0000-0002-3721-1739
Max Planck Institute for Developmental Biology · DEMax Planck Institute of Molecular Physiology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CCR4-NOT is a conserved multiprotein complex which regulates eukaryotic gene expression principally via shortening of poly(A) tails of messenger RNA or deadenylation. Here, we reconstitute a complete, recombinant human CCR4-NOT complex. Our reconstitution strategy permits strict compositional control to test mechanistic hypotheses with purified component variants. CCR4-NOT is more active and selective for poly(A) than the isolated exonucleases, CCR4a and CAF1, which have distinct deadenylation profiles in vitro. The exonucleases require at least two out of three conserved non-enzymatic modules (CAF40, NOT10:NOT11 or NOT) for full activity in CCR4-NOT. CAF40 and the NOT10:NOT11 module both bind RNA directly and stimulate deadenylation in a partially redundant manner. Linear motifs from different RNA-binding factors that recruit CCR4-NOT to specific mRNAs via protein-protein interactions with CAF40 can inhibit bulk deadenylation. We reveal an additional layer of regulatory complexity to the human deadenylation machinery, which may prime it either for general or target-specific degradation.

Indexed as

ExoribonucleasesHumansMultiprotein ComplexesNuclear Receptor Subfamily 4, Group A, Member 2Poly AReceptors, CCR4Recombinant ProteinsRibonucleasesRNA, MessengerTranscription FactorsCCR4 protein, humanCNOT6L protein, humanCNOT8 protein, humanExoribonucleasesMultiprotein ComplexesNR4A2 protein, humanNuclear Receptor Subfamily 4, Group A, Member 2Poly AReceptors, CCR4Recombinant ProteinsRibonucleasesRNA, MessengerTranscription Factors

Identifiers

PMID31320642
PMCPMC6639331
OpenAlexW2959219826

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.