Evidence map›Paper›PMID 31010829›Full record

ArticleThe Journal of biological chemistry2019

Systematic proteomics of endogenous human cohesin reveals an interaction with diverse splicing factors and RNA-binding proteins required for mitotic progression.

Jung-Sik Kim, Xiaoyuan He, Jie Liu, Zhijun Duan, Taeyeon Kim, Julia Gerard, Brian Kim, Manoj M Pillai, William S Lane, William S Noble and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Cohesin mutations and chromatin changes in cancer.International journal of cancer · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. ANKRD11 binding to cohesin suggests a connection between KBG syndrome and Cornelia de Lange syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Article
  10. A STAG2-PAXIP1/PAGR1 axis suppresses lung tumorigenesis.The Journal of experimental medicine · 2025
    Article
  11. Addressing the tissue specificity of U5 snRNP spliceosomopathies.Frontiers in cell and developmental biology · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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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

12 authors at 5 institutions in 2 countries.

Jung-Sik KimFrom the Departments of Oncology and Biochemistry & Molecular Biology, Georgetown University School of Medicine, Washington, D. C. 20057.
Xiaoyuan HeFrom the Departments of Oncology and Biochemistry & Molecular Biology, Georgetown University School of Medicine, Washington, D. C. 20057.
Jie Liuthe Department of Genome Sciences.
Zhijun DuanInstitute for Stem Cell and Regenerative Medicine, and.
Taeyeon KimFrom the Departments of Oncology and Biochemistry & Molecular Biology, Georgetown University School of Medicine, Washington, D. C. 20057.
Julia GerardFrom the Departments of Oncology and Biochemistry & Molecular Biology, Georgetown University School of Medicine, Washington, D. C. 20057.
Brian KimFrom the Departments of Oncology and Biochemistry & Molecular Biology, Georgetown University School of Medicine, Washington, D. C. 20057.
Manoj M Pillaithe Section of Hematology, Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut 06510, and.ORCID 0000-0002-7835-0145
William S Lanethe Mass Spectrometry and Proteomics Resource Laboratory, Harvard University, Cambridge, Massachusetts 02138.
William S Noblethe Department of Genome Sciences.
Bogdan Budnikthe Mass Spectrometry and Proteomics Resource Laboratory, Harvard University, Cambridge, Massachusetts 02138.ORCID 0000-0003-3622-2003
Todd WaldmanFrom the Departments of Oncology and Biochemistry & Molecular Biology, Georgetown University School of Medicine, Washington, D. C. 20057, waldmant@georgetown.edu.
Georgetown University · USHarvard University · USHuman Genome Sciences (United States) · USCalifornia Institute for Regenerative Medicine · USYale Cancer Center · US

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI Louis M Weiner · 1990 to 2026
$71.5M
University of Washington Center for Nuclear Organization and FunctionU54DK107979 · NIDDK · UNIVERSITY OF WASHINGTON · PI NOBLE, WILLIAM STAFFORD, SHENDURE, JAY ASHOK · 2015 to 2019
$11.8M
Deregulation of SF3B1 function by recurrent HEAT domain mutationsR01HL133406 · NHLBI · YALE UNIVERSITY · PI NEUGEBAUER, KARLA M, PILLAI, MANOJ M. · 2017 to 2020
$1.7M
Analysis of STAG2 Inactivation and Aneuploidy in Human CancerR01CA169345 · NCI · GEORGETOWN UNIVERSITY · PI WALDMAN, TODD A · 2013 to 2017
$1.6M
NCI NIH HHS P30 CA051008NCI NIH HHS R01 CA169345NHLBI NIH HHS R01 HL133406NIDDK NIH HHS U54 DK107979
6 · The paper itself

Abstract

The cohesin complex regulates sister chromatid cohesion, chromosome organization, gene expression, and DNA repair. Cohesin is a ring complex composed of four core subunits and seven regulatory subunits. In an effort to comprehensively identify additional cohesin-interacting proteins, we used gene editing to introduce a dual epitope tag into the endogenous allele of each of 11 known components of cohesin in cultured human cells, and we performed MS analyses on dual-affinity purifications. In addition to reciprocally identifying all known components of cohesin, we found that cohesin interacts with a panoply of splicing factors and RNA-binding proteins (RBPs). These included diverse components of the U4/U6.U5 tri-small nuclear ribonucleoprotein complex and several splicing factors that are commonly mutated in cancer. The interaction between cohesin and splicing factors/RBPs was RNA- and DNA-independent, occurred in chromatin, was enhanced during mitosis, and required RAD21. Furthermore, cohesin-interacting splicing factors and RBPs followed the cohesin cycle and prophase pathway of cell cycle-regulated interactions with chromatin. Depletion of cohesin-interacting splicing factors and RBPs resulted in aberrant mitotic progression. These results provide a comprehensive view of the endogenous human cohesin interactome and identify splicing factors and RBPs as functionally significant cohesin-interacting proteins.

Indexed as

MitosisProteomicsCell Cycle ProteinsCell Line, TumorChromatinChromosomal Proteins, Non-HistoneCohesinsDNA-Binding ProteinsHumansMicroscopy, FluorescenceProtein BindingProtein Interaction MapsRNA-Binding ProteinsRNA InterferenceRNA, Small InterferingRNA Splicing FactorsCell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneCohesinsDNA-Binding ProteinsRAD21 protein, humanRNA-Binding ProteinsRNA, Small InterferingRNA Splicing Factorscell cyclecell divisionCKAP5cohesingene editinggenome structureMGAmitosisprotein–protein interactionRNA-binding proteinRNA splicingSTAG2

Identifiers

PMID31010829
PMCPMC6552432
OpenAlexW2942370373

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.