Evidence map›Paper›PMID 33563994›Full record

ArticleNature communications2021

Programmable human histone phosphorylation and gene activation using a CRISPR/Cas9-based chromatin kinase.

Jing Li, Barun Mahata, Mario Escobar, Jacob Goell, Kaiyuan Wang, Pranav Khemka, Isaac B Hilton

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. The landscape and trajectory of global CRISPR therapeutics.Molecular therapy. Nucleic acids · 2026
    Review
  3. Article
  4. Review
  5. Clinical translation of epigenome editing technologies.Current opinion in biomedical engineering · 2026
    Article
  6. Review
  7. Epigenetic editing: from concept to clinic.Nature reviews. Drug discovery · 2026
    Review
  8. Review
  9. Article
  10. Sensitive and Selective Next-Generation FRET-based PKA Biosensors.bioRxiv : the preprint server for biology · 2026
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. On RNA-programmable gene modulation as a versatile set of principles targeting muscular dystrophies.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Review
  20. 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

7 authors at 1 institution in 1 country.

Jing LiDepartment of Bioengineering, Rice University, Houston, TX, USA.
Barun MahataDepartment of Bioengineering, Rice University, Houston, TX, USA.
Mario EscobarDepartment of BioSciences, Rice University, Houston, TX, USA.ORCID 0000-0003-2262-7800
Jacob GoellDepartment of Bioengineering, Rice University, Houston, TX, USA.
Kaiyuan WangDepartment of Bioengineering, Rice University, Houston, TX, USA.ORCID 0000-0001-9567-1410
Pranav KhemkaDepartment of Bioengineering, Rice University, Houston, TX, USA.
Isaac B HiltonDepartment of Bioengineering, Rice University, Houston, TX, USA. isaac.hilton@rice.edu.ORCID 0000-0002-3064-8532
Rice University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone phosphorylation is a ubiquitous post-translational modification that allows eukaryotic cells to rapidly respond to environmental stimuli. Despite correlative evidence linking histone phosphorylation to changes in gene expression, establishing the causal role of this key epigenomic modification at diverse loci within native chromatin has been hampered by a lack of technologies enabling robust, locus-specific deposition of endogenous histone phosphorylation. To address this technological gap, here we build a programmable chromatin kinase, called dCas9-dMSK1, by directly fusing nuclease-null CRISPR/Cas9 to a hyperactive, truncated variant of the human MSK1 histone kinase. Targeting dCas9-dMSK1 to human promoters results in increased target histone phosphorylation and gene activation and demonstrates that hyperphosphorylation of histone H3 serine 28 (H3S28ph) in particular plays a causal role in the transactivation of human promoters. In addition, we uncover mediators of resistance to the BRAF V600E inhibitor PLX-4720 in human melanoma cells using genome-scale screening with dCas9-dMSK1. Collectively, our findings enable a facile way to reshape human chromatin using CRISPR/Cas9-based epigenome editing and further define the causal link between histone phosphorylation and human gene activation.

Indexed as

CRISPR-Cas SystemsAcetylationCell Line, TumorChromatinCRISPR-Associated Protein 9Drug Resistance, NeoplasmEpigenomicsHistonesHumansIndolesPhosphorylationPromoter Regions, GeneticRibosomal Protein S6 Kinases, 90-kDaSulfonamidesTranscriptional ActivationChromatinCRISPR-Associated Protein 9HistonesIndolesmitogen and stress-activated protein kinase 1PLX 4720Ribosomal Protein S6 Kinases, 90-kDaSulfonamides

Identifiers

PMID33563994
PMCPMC7873277
OpenAlexW3127215166

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.